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  • Female  (258)
  • Time Factors  (109)
  • Mice, Inbred C57BL  (73)
  • Nature Publishing Group (NPG)  (389)
  • American Institute of Physics (AIP)
  • 2010-2014  (389)
  • 1985-1989
  • 2012  (389)
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  • 2010-2014  (389)
  • 1985-1989
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  • 1
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    Myocardial infarction accelerates atherosclerosis (2012)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2012-07-06
    Description: During progression of atherosclerosis, myeloid cells destabilize lipid-rich plaques in the arterial wall and cause their rupture, thus triggering myocardial infarction and stroke. Survivors of acute coronary syndromes have a high risk of recurrent events for unknown reasons. Here we show that the systemic response to ischaemic injury aggravates chronic atherosclerosis. After myocardial infarction or stroke, Apoe-/- mice developed larger atherosclerotic lesions with a more advanced morphology. This disease acceleration persisted over many weeks and was associated with markedly increased monocyte recruitment. Seeking the source of surplus monocytes in plaques, we found that myocardial infarction liberated haematopoietic stem and progenitor cells from bone marrow niches via sympathetic nervous system signalling. The progenitors then seeded the spleen, yielding a sustained boost in monocyte production. These observations provide new mechanistic insight into atherogenesis and provide a novel therapeutic opportunity to mitigate disease progression.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3401326/" 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/PMC3401326/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dutta, Partha -- Courties, Gabriel -- Wei, Ying -- Leuschner, Florian -- Gorbatov, Rostic -- Robbins, Clinton S -- Iwamoto, Yoshiko -- Thompson, Brian -- Carlson, Alicia L -- Heidt, Timo -- Majmudar, Maulik D -- Lasitschka, Felix -- Etzrodt, Martin -- Waterman, Peter -- Waring, Michael T -- Chicoine, Adam T -- van der Laan, Anja M -- Niessen, Hans W M -- Piek, Jan J -- Rubin, Barry B -- Butany, Jagdish -- Stone, James R -- Katus, Hugo A -- Murphy, Sabina A -- Morrow, David A -- Sabatine, Marc S -- Vinegoni, Claudio -- Moskowitz, Michael A -- Pittet, Mikael J -- Libby, Peter -- Lin, Charles P -- Swirski, Filip K -- Weissleder, Ralph -- Nahrendorf, Matthias -- P50-CA086355/CA/NCI NIH HHS/ -- R01 AI084880/AI/NIAID NIH HHS/ -- R01 EB006432/EB/NIBIB NIH HHS/ -- R01 HL095612/HL/NHLBI NIH HHS/ -- R01 HL095629/HL/NHLBI NIH HHS/ -- R01 HL096576/HL/NHLBI NIH HHS/ -- R01-EB006432/EB/NIBIB NIH HHS/ -- R01-HL095629/HL/NHLBI NIH HHS/ -- R01-HL096576/HL/NHLBI NIH HHS/ -- T32 CA079443/CA/NCI NIH HHS/ -- T32-CA79443/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2012 Jul 19;487(7407):325-9. doi: 10.1038/nature11260.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22763456" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apolipoproteins E/genetics ; Atherosclerosis/*etiology/*pathology ; Hematopoietic Stem Cells/cytology ; Inflammation/complications ; Mice ; Mice, Inbred C57BL ; Monocytes/cytology ; Myocardial Infarction/*complications/*pathology ; Spleen/cytology ; Stem Cells/cytology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 2
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    Lab flu may not aid vaccines (2012)
    Nature Publishing Group (NPG)
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    Publication Date: 2012-02-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Butler, Declan -- England -- Nature. 2012 Feb 8;482(7384):142-3. doi: 10.1038/482142a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22318581" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Humans ; Influenza A Virus, H5N1 Subtype/*genetics/*pathogenicity ; *Influenza Vaccines/economics/immunology/supply & distribution ; Influenza, Human/*epidemiology/prevention & control/transmission/virology ; Laboratories ; Mutagenesis ; Pandemics/*prevention & control ; Time Factors ; Zoonoses/epidemiology/*transmission/*virology
    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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    NLRP6 negatively regulates innate immunity and host defence against bacterial pathogens (2012)
    Nature Publishing Group (NPG)
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    Publication Date: 2012-07-06
    Description: Members of the intracellular nucleotide-binding and oligomerization domain (NOD)-like receptor (NLR) family contribute to immune responses through activation of nuclear factor-kappaB (NF-kappaB), type I interferon and inflammasome signalling. Mice lacking the NLR family member NLRP6 were recently shown to be susceptible to colitis and colorectal tumorigenesis, but the role of NLRP6 in microbial infections and the nature of the inflammatory signalling pathways regulated by NLRP6 remain unclear. Here we show that Nlrp6-deficient mice are highly resistant to infection with the bacterial pathogens Listeria monocytogenes, Salmonella typhimurium and Escherichia coli. Infected Nlrp6-deficient mice had increased numbers of monocytes and neutrophils in circulation, and NLRP6 signalling in both haematopoietic and radioresistant cells contributed to increased susceptibility. Nlrp6 deficiency enhanced activation of mitogen-activated protein kinase (MAPK) and the canonical NF-kappaB pathway after Toll-like receptor ligation, but not cytosolic NOD1/2 ligation, in vitro. Consequently, infected Nlrp6-deficient cells produced increased levels of NF-kappaB- and MAPK-dependent cytokines and chemokines. Thus, our results reveal NLRP6 as a negative regulator of inflammatory signalling, and demonstrate a role for this NLR in impeding clearance of both Gram-positive and -negative bacterial pathogens.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3422416/" 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/PMC3422416/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Anand, Paras K -- Malireddi, R K Subbarao -- Lukens, John R -- Vogel, Peter -- Bertin, John -- Lamkanfi, Mohamed -- Kanneganti, Thirumala-Devi -- AI101935/AI/NIAID NIH HHS/ -- AR056296/AR/NIAMS NIH HHS/ -- R01 AI101935/AI/NIAID NIH HHS/ -- R01 AR056296/AR/NIAMS NIH HHS/ -- England -- Nature. 2012 Aug 16;488(7411):389-93. doi: 10.1038/nature11250.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, St. Jude Children's Research Hospital, Memphis, Tennessee 38105, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22763455" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Disease Susceptibility/immunology ; Escherichia coli/*immunology ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Female ; Immunity, Innate/*immunology ; Listeria monocytogenes/*immunology ; MAP Kinase Signaling System ; Mice ; Monocytes/cytology/enzymology/immunology/metabolism ; NF-kappa B/metabolism ; Neutrophils/cytology/enzymology/immunology/metabolism ; Receptors, Cell Surface/deficiency/genetics/immunology/*metabolism ; Salmonella typhimurium/*immunology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 4
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    US advisers seek research overhaul (2012)
    Nature Publishing Group (NPG)
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    Publication Date: 2012-12-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hand, Eric -- England -- Nature. 2012 Dec 6;492(7427):18. doi: 10.1038/492018a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23222584" target="_blank"〉PubMed〈/a〉
    Keywords: Budgets/*legislation & jurisprudence ; Federal Government ; Industry/economics/organization & administration ; Public-Private Sector Partnerships/economics/organization & administration ; Research/*economics/*legislation & jurisprudence ; Research Support as Topic/economics/*legislation & jurisprudence/*organization & ; administration ; Time Factors ; United States
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
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    Toxicology: The learning curve (2012)
    Nature Publishing Group (NPG)
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    Publication Date: 2012-10-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fagin, Dan -- England -- Nature. 2012 Oct 25;490(7421):462-5. doi: 10.1038/490462a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23099381" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Benzhydryl Compounds ; Diethylhexyl Phthalate/administration & dosage/toxicity ; Diethylstilbestrol/administration & dosage/toxicity ; Dose-Response Relationship, Drug ; Endocrine Disruptors/*administration & dosage/*toxicity ; Estradiol/administration & dosage/toxicity ; Female ; Humans ; Male ; Mice ; National Institute of Environmental Health Sciences (U.S.) ; Phenols/administration & dosage/toxicity ; Risk Assessment/*methods ; Tamoxifen/administration & dosage/adverse effects/pharmacology ; Toxicology/*methods ; United States
    Print ISSN: 0028-0836
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 6
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    IFITM3 restricts the morbidity and mortality associated with influenza (2012)
    Nature Publishing Group (NPG)
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    Publication Date: 2012-03-27
    Description: The 2009 H1N1 influenza pandemic showed the speed with which a novel respiratory virus can spread and the ability of a generally mild infection to induce severe morbidity and mortality in a subset of the population. Recent in vitro studies show that the interferon-inducible transmembrane (IFITM) protein family members potently restrict the replication of multiple pathogenic viruses. Both the magnitude and breadth of the IFITM proteins' in vitro effects suggest that they are critical for intrinsic resistance to such viruses, including influenza viruses. Using a knockout mouse model, we now test this hypothesis directly and find that IFITM3 is essential for defending the host against influenza A virus in vivo. Mice lacking Ifitm3 display fulminant viral pneumonia when challenged with a normally low-pathogenicity influenza virus, mirroring the destruction inflicted by the highly pathogenic 1918 'Spanish' influenza. Similar increased viral replication is seen in vitro, with protection rescued by the re-introduction of Ifitm3. To test the role of IFITM3 in human influenza virus infection, we assessed the IFITM3 alleles of individuals hospitalized with seasonal or pandemic influenza H1N1/09 viruses. We find that a statistically significant number of hospitalized subjects show enrichment for a minor IFITM3 allele (SNP rs12252-C) that alters a splice acceptor site, and functional assays show the minor CC genotype IFITM3 has reduced influenza virus restriction in vitro. Together these data reveal that the action of a single intrinsic immune effector, IFITM3, profoundly alters the course of influenza virus infection in mouse and humans.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3648786/" 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/PMC3648786/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Everitt, Aaron R -- Clare, Simon -- Pertel, Thomas -- John, Sinu P -- Wash, Rachael S -- Smith, Sarah E -- Chin, Christopher R -- Feeley, Eric M -- Sims, Jennifer S -- Adams, David J -- Wise, Helen M -- Kane, Leanne -- Goulding, David -- Digard, Paul -- Anttila, Verneri -- Baillie, J Kenneth -- Walsh, Tim S -- Hume, David A -- Palotie, Aarno -- Xue, Yali -- Colonna, Vincenza -- Tyler-Smith, Chris -- Dunning, Jake -- Gordon, Stephen B -- GenISIS Investigators -- MOSAIC Investigators -- Smyth, Rosalind L -- Openshaw, Peter J -- Dougan, Gordon -- Brass, Abraham L -- Kellam, Paul -- 090382/Wellcome Trust/United Kingdom -- 090382/Z/09/Z/Wellcome Trust/United Kingdom -- 090385/Z/09/Z/Wellcome Trust/United Kingdom -- 098051/Wellcome Trust/United Kingdom -- 13031/Cancer Research UK/United Kingdom -- DHCS/04/G121/68/Department of Health/United Kingdom -- G0600371/Medical Research Council/United Kingdom -- G0600511/Medical Research Council/United Kingdom -- G0800767/Medical Research Council/United Kingdom -- G0800777/Medical Research Council/United Kingdom -- G0802752/Medical Research Council/United Kingdom -- G0901697/Medical Research Council/United Kingdom -- G1000758/Medical Research Council/United Kingdom -- MC_G1001212/Medical Research Council/United Kingdom -- MC_U122785833/Medical Research Council/United Kingdom -- P30 DK043351/DK/NIDDK NIH HHS/ -- R01 AI091786/AI/NIAID NIH HHS/ -- R01AI091786/AI/NIAID NIH HHS/ -- Chief Scientist Office/United Kingdom -- Medical Research Council/United Kingdom -- England -- Nature. 2012 Mar 25;484(7395):519-23. doi: 10.1038/nature10921.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton CB10 1SA, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22446628" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Amino Acid Sequence ; Animals ; Cytokines/immunology ; England/epidemiology ; Gene Deletion ; Humans ; Influenza A Virus, H1N1 Subtype/classification/growth & development/pathogenicity ; Influenza A Virus, H3N2 Subtype/classification/growth & development/pathogenicity ; Influenza A virus/classification/growth & development/*pathogenicity ; Influenza B virus/classification/growth & development/pathogenicity ; Influenza, Human/complications/epidemiology/mortality/virology ; Leukocytes/immunology ; Lung/pathology/virology ; Membrane Proteins/chemistry/deficiency/genetics/*metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Molecular Sequence Data ; Orthomyxoviridae Infections/complications/*mortality/pathology ; Pneumonia, Viral/etiology/pathology/prevention & control ; Polymorphism, Single Nucleotide/genetics ; RNA-Binding Proteins/chemistry/genetics/*metabolism ; Scotland/epidemiology ; Virus Replication
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 7
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    Q&A: A slow-motion crisis. Interview by Michael Eisenstein (2012)
    Nature Publishing Group (NPG)
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    Publication Date: 2012-03-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Falkowski, Paul -- England -- Nature. 2012 Feb 29;483(7387):S21. doi: 10.1038/483S21a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22378124" target="_blank"〉PubMed〈/a〉
    Keywords: Aquatic Organisms/*metabolism ; Environmental Restoration and Remediation ; Eutrophication ; Extinction, Biological ; *Global Warming ; *Human Activities ; Interdisciplinary Studies ; Marine Biology ; Photosynthesis ; Phytoplankton/*metabolism ; Seawater/chemistry/microbiology ; Time Factors
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 8
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    Microbiology: Learning about who we are (2012)
    Nature Publishing Group (NPG)
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    Publication Date: 2012-06-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Relman, David A -- England -- Nature. 2012 Jun 13;486(7402):194-5. doi: 10.1038/486194a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22699602" target="_blank"〉PubMed〈/a〉
    Keywords: Bacteria/*classification/*genetics ; *Biodiversity ; Female ; *Health ; Humans ; Male ; *Metagenome ; Metagenomics/*methods
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 9
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    Sustained translational repression by eIF2alpha-P mediates prion neurodegeneration (2012)
    Nature Publishing Group (NPG)
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    Publication Date: 2012-05-25
    Description: The mechanisms leading to neuronal death in neurodegenerative disease are poorly understood. Many of these disorders, including Alzheimer's, Parkinson's and prion diseases, are associated with the accumulation of misfolded disease-specific proteins. The unfolded protein response is a protective cellular mechanism triggered by rising levels of misfolded proteins. One arm of this pathway results in the transient shutdown of protein translation, through phosphorylation of the alpha-subunit of eukaryotic translation initiation factor, eIF2. Activation of the unfolded protein response and/or increased eIF2alpha-P levels are seen in patients with Alzheimer's, Parkinson's and prion diseases, but how this links to neurodegeneration is unknown. Here we show that accumulation of prion protein during prion replication causes persistent translational repression of global protein synthesis by eIF2alpha-P, associated with synaptic failure and neuronal loss in prion-diseased mice. Further, we show that promoting translational recovery in hippocampi of prion-infected mice is neuroprotective. Overexpression of GADD34, a specific eIF2alpha-P phosphatase, as well as reduction of levels of prion protein by lentivirally mediated RNA interference, reduced eIF2alpha-P levels. As a result, both approaches restored vital translation rates during prion disease, rescuing synaptic deficits and neuronal loss, thereby significantly increasing survival. In contrast, salubrinal, an inhibitor of eIF2alpha-P dephosphorylation, increased eIF2alpha-P levels, exacerbating neurotoxicity and significantly reducing survival in prion-diseased mice. Given the prevalence of protein misfolding and activation of the unfolded protein response in several neurodegenerative diseases, our results suggest that manipulation of common pathways such as translational control, rather than disease-specific approaches, may lead to new therapies preventing synaptic failure and neuronal loss across the spectrum of these disorders.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3378208/" 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/PMC3378208/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Moreno, Julie A -- Radford, Helois -- Peretti, Diego -- Steinert, Joern R -- Verity, Nicholas -- Martin, Maria Guerra -- Halliday, Mark -- Morgan, Jason -- Dinsdale, David -- Ortori, Catherine A -- Barrett, David A -- Tsaytler, Pavel -- Bertolotti, Anne -- Willis, Anne E -- Bushell, Martin -- Mallucci, Giovanna R -- MC_U105185860/Medical Research Council/United Kingdom -- MC_U123160654/Medical Research Council/United Kingdom -- MC_U132692719/Medical Research Council/United Kingdom -- MC_UP_A600_1023/Medical Research Council/United Kingdom -- MC_UP_A600_1024/Medical Research Council/United Kingdom -- U.1051.02.011.00001.01 (85860)/Medical Research Council/United Kingdom -- Medical Research Council/United Kingdom -- England -- Nature. 2012 May 6;485(7399):507-11. doi: 10.1038/nature11058.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉MRC Toxicology Unit, Hodgkin Building, University of Leicester, Lancaster Road, Leicester LE1 9HN, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22622579" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Death/drug effects ; Cinnamates/pharmacology ; Eukaryotic Initiation Factor-2/analysis/*chemistry/*metabolism ; Hippocampus/cytology/metabolism/pathology ; Kaplan-Meier Estimate ; Mice ; Mice, Inbred C57BL ; Neurodegenerative Diseases/etiology/*metabolism/pathology ; Neurons/drug effects/pathology ; Neuroprotective Agents ; Phosphoproteins/analysis/*metabolism ; Phosphorylation ; PrPSc Proteins/analysis/metabolism/toxicity ; Prion Diseases/pathology ; Prions/biosynthesis/genetics/*metabolism ; *Protein Biosynthesis/drug effects ; Protein Folding/drug effects ; Protein Phosphatase 1/genetics/metabolism ; Repressor Proteins/analysis/chemistry/*metabolism ; Synapses/drug effects/metabolism/pathology ; Synaptic Transmission/drug effects ; Thiourea/analogs & derivatives/pharmacology ; Unfolded Protein Response/physiology
    Print ISSN: 0028-0836
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 10
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    Haste not speed (2012)
    Nature Publishing Group (NPG)
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    Publication Date: 2012-12-14
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉England -- Nature. 2012 Dec 6;492(7427):8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23236613" target="_blank"〉PubMed〈/a〉
    Keywords: Budgets/*legislation & jurisprudence/organization & administration ; Europe ; *Federal Government ; National Institutes of Health (U.S.)/economics ; Research Support as Topic/economics/*legislation & jurisprudence/organization & ; administration ; Time Factors ; United States ; United States Government Agencies/*economics/organization & administration
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 11
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    The split brain: a tale of two halves (2012)
    Nature Publishing Group (NPG)
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    Publication Date: 2012-03-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wolman, David -- England -- Nature. 2012 Mar 14;483(7389):260-3. doi: 10.1038/483260a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22422242" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Age Factors ; Animals ; Brain/*physiology/*physiopathology/surgery ; Cohort Studies ; Corpus Callosum/physiology/physiopathology/*surgery ; Epilepsy/history/surgery ; Female ; Functional Laterality/*physiology ; History, 20th Century ; History, 21st Century ; Humans ; Magnetic Resonance Imaging ; Male ; Morals ; Neurosciences/*history ; Seizures/history/surgery
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 12
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    Ageing: Mixed results for dieting monkeys (2012)
    Nature Publishing Group (NPG)
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    Publication Date: 2012-08-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Austad, Steven N -- England -- Nature. 2012 Sep 13;489(7415):210-11. doi: 10.1038/nature11484.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22932269" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/*physiology ; Animals ; *Caloric Restriction ; Female ; *Health ; Humans ; Longevity/*physiology ; Male ; *National Institute on Aging (U.S.)
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  • 13
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    Non-invasive prenatal measurement of the fetal genome (2012)
    Nature Publishing Group (NPG)
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    Publication Date: 2012-07-06
    Description: The vast majority of prenatal genetic testing requires invasive sampling. However, this poses a risk to the fetus, so one must make a decision that weighs the desire for genetic information against the risk of an adverse outcome due to hazards of the testing process. These issues are not required to be coupled, and it would be desirable to discover genetic information about the fetus without incurring a health risk. Here we demonstrate that it is possible to non-invasively sequence the entire prenatal genome. Our results show that molecular counting of parental haplotypes in maternal plasma by shotgun sequencing of maternal plasma DNA allows the inherited fetal genome to be deciphered non-invasively. We also applied the counting principle directly to each allele in the fetal exome by performing exome capture on maternal plasma DNA before shotgun sequencing. This approach enables non-invasive exome screening of clinically relevant and deleterious alleles that were paternally inherited or had arisen as de novo germline mutations, and complements the haplotype counting approach to provide a comprehensive view of the fetal genome. Non-invasive determination of the fetal genome may ultimately facilitate the diagnosis of all inherited and de novo genetic disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3561905/" 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/PMC3561905/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fan, H Christina -- Gu, Wei -- Wang, Jianbin -- Blumenfeld, Yair J -- El-Sayed, Yasser Y -- Quake, Stephen R -- DP1 OD000251/OD/NIH HHS/ -- U54 CA151459/CA/NCI NIH HHS/ -- England -- Nature. 2012 Jul 19;487(7407):320-4. doi: 10.1038/nature11251.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Bioengineering, Stanford University, Clark Center Rm E300, 318 Campus Drive, Stanford, California 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22763444" target="_blank"〉PubMed〈/a〉
    Keywords: Chromosomes, Human/genetics ; DNA/*analysis/blood ; Exome/genetics ; Female ; Fetus ; *Genome, Human ; Haplotypes ; Humans ; Male ; Pregnancy ; Prenatal Diagnosis/*methods ; Sensitivity and Specificity
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    Fetal tests spur legal battle (2012)
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    Publication Date: 2012-06-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hayden, Erika Check -- England -- Nature. 2012 Jun 27;486(7404):454. doi: 10.1038/486454a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22739292" target="_blank"〉PubMed〈/a〉
    Keywords: California ; Female ; Fetus/blood supply/*metabolism ; Genetic Testing/economics/*legislation & jurisprudence/utilization ; Humans ; Patents as Topic/legislation & jurisprudence ; Pregnancy/*blood ; *Prenatal Diagnosis/economics/utilization
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    Contest to sequence centenarians kicks off (2012)
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    Publication Date: 2012-07-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Baker, Monya -- England -- Nature. 2012 Jul 23;487(7408):417. doi: 10.1038/487417a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22836978" target="_blank"〉PubMed〈/a〉
    Keywords: Aged, 80 and over ; *Awards and Prizes ; California ; Foundations/economics ; Genome, Human/*genetics ; Genomics/*economics/instrumentation/*methods/trends ; Humans ; Hydrogen-Ion Concentration ; Longevity/genetics ; Semiconductors ; Time Factors
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    Autistic-like social behaviour in Shank2-mutant mice improved by restoring NMDA receptor function (2012)
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    Publication Date: 2012-06-16
    Description: Autism spectrum disorder (ASD) is a group of conditions characterized by impaired social interaction and communication, and restricted and repetitive behaviours. ASD is a highly heritable disorder involving various genetic determinants. Shank2 (also known as ProSAP1) is a multi-domain scaffolding protein and signalling adaptor enriched at excitatory neuronal synapses, and mutations in the human SHANK2 gene have recently been associated with ASD and intellectual disability. Although ASD-associated genes are being increasingly identified and studied using various approaches, including mouse genetics, further efforts are required to delineate important causal mechanisms with the potential for therapeutic application. Here we show that Shank2-mutant (Shank2(-/-)) mice carrying a mutation identical to the ASD-associated microdeletion in the human SHANK2 gene exhibit ASD-like behaviours including reduced social interaction, reduced social communication by ultrasonic vocalizations, and repetitive jumping. These mice show a marked decrease in NMDA (N-methyl-D-aspartate) glutamate receptor (NMDAR) function. Direct stimulation of NMDARs with D-cycloserine, a partial agonist of NMDARs, normalizes NMDAR function and improves social interaction in Shank2(-/-) mice. Furthermore, treatment of Shank2(-/-) mice with a positive allosteric modulator of metabotropic glutamate receptor 5 (mGluR5), which enhances NMDAR function via mGluR5 activation, also normalizes NMDAR function and markedly enhances social interaction. These results suggest that reduced NMDAR function may contribute to the development of ASD-like phenotypes in Shank2(-/-) mice, and mGluR modulation of NMDARs offers a potential strategy to treat ASD.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Won, Hyejung -- Lee, Hye-Ryeon -- Gee, Heon Yung -- Mah, Won -- Kim, Jae-Ick -- Lee, Jiseok -- Ha, Seungmin -- Chung, Changuk -- Jung, Eun Suk -- Cho, Yi Sul -- Park, Sae-Geun -- Lee, Jung-Soo -- Lee, Kyungmin -- Kim, Daesoo -- Bae, Yong Chul -- Kaang, Bong-Kiun -- Lee, Min Goo -- Kim, Eunjoon -- England -- Nature. 2012 Jun 13;486(7402):261-5. doi: 10.1038/nature11208.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, KAIST, Daejeon 305-701, Korea.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22699620" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing/*genetics ; Animals ; Antimetabolites/pharmacology ; *Autistic Disorder/genetics/metabolism ; Behavior, Animal/*drug effects/physiology ; Benzamides/*pharmacology ; Cycloserine/*pharmacology ; Disease Models, Animal ; Female ; Male ; Mice ; Mice, Inbred C57BL ; Nerve Tissue Proteins/*genetics ; Pyrazoles/*pharmacology ; Receptors, N-Methyl-D-Aspartate/*agonists/*metabolism
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    The aged niche disrupts muscle stem cell quiescence (2012)
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    Publication Date: 2012-10-02
    Description: The niche is a conserved regulator of stem cell quiescence and function. During ageing, stem cell function declines. To what extent and by what means age-related changes within the niche contribute to this phenomenon are unknown. Here we demonstrate that the aged muscle stem cell niche, the muscle fibre, expresses Fgf2 under homeostatic conditions, driving a subset of satellite cells to break quiescence and lose their self-renewing capacity. We show in mice that relatively dormant aged satellite cells robustly express sprouty 1 (Spry1), an inhibitor of fibroblast growth factor (FGF) signalling. Increasing FGF signalling in aged satellite cells under homeostatic conditions by removing Spry1 results in the loss of quiescence, satellite cell depletion and diminished regenerative capacity. Conversely, reducing niche-derived FGF activity through inhibition of Fgfr1 signalling or overexpression of Spry1 in satellite cells prevents their depletion. These experiments identify an age-dependent change in the stem cell niche that directly influences stem cell quiescence and function.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3605795/" 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/PMC3605795/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chakkalakal, Joe V -- Jones, Kieran M -- Basson, M Albert -- Brack, Andrew S -- 091475/Wellcome Trust/United Kingdom -- BB/F017626/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- R01 AR060868/AR/NIAMS NIH HHS/ -- R01 AR061002/AR/NIAMS NIH HHS/ -- WT091475/Wellcome Trust/United Kingdom -- England -- Nature. 2012 Oct 18;490(7420):355-60. doi: 10.1038/nature11438. Epub 2012 Sep 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center of Regenerative Medicine, Massachusetts General Hospital, Boston, Massachusetts 02114, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23023126" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; Aging/*physiology ; Animals ; Cell Aging ; Cell Count ; *Cell Cycle ; Cell Differentiation ; Cyclin-Dependent Kinase Inhibitor p27/metabolism ; Fibroblast Growth Factor 2/genetics/metabolism ; Flow Cytometry ; Homeostasis ; Membrane Proteins/metabolism ; Mice ; Mice, Inbred C57BL ; Muscle Cells/*cytology ; Muscle, Skeletal/cytology ; PAX7 Transcription Factor/metabolism ; Phosphoproteins/metabolism ; Satellite Cells, Skeletal Muscle/*cytology/metabolism/transplantation ; Signal Transduction ; Stem Cell Niche/*physiology ; Time Factors
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    Metastasis: The rude awakening (2012)
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    Publication Date: 2012-06-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rice, Jocelyn -- England -- Nature. 2012 May 30;485(7400):S55-7. doi: 10.1038/485S55a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22648500" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Breast Neoplasms/*pathology/therapy ; Female ; Humans ; Mice ; Neoplasm Metastasis/*pathology/therapy ; Neoplastic Cells, Circulating/pathology ; Recurrence
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    Sensory science: partners in flavour (2012)
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    Publication Date: 2012-06-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bakalar, Nicholas -- England -- Nature. 2012 Jun 20;486(7403):S4-5. doi: 10.1038/486S4a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22717401" target="_blank"〉PubMed〈/a〉
    Keywords: Amniotic Fluid/chemistry ; Electroencephalography ; Female ; Fetus/drug effects/physiology ; Flavoring Agents/*pharmacology ; *Food ; Food Habits/physiology ; Hearing/physiology ; Humans ; Odors ; Pregnancy ; Smell/physiology ; Taste/drug effects/*physiology ; Temperature ; Vision, Ocular/physiology
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    Increase in observed net carbon dioxide uptake by land and oceans during the past 50 years (2012)
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    Publication Date: 2012-08-04
    Description: One of the greatest sources of uncertainty for future climate predictions is the response of the global carbon cycle to climate change. Although approximately one-half of total CO(2) emissions is at present taken up by combined land and ocean carbon reservoirs, models predict a decline in future carbon uptake by these reservoirs, resulting in a positive carbon-climate feedback. Several recent studies suggest that rates of carbon uptake by the land and ocean have remained constant or declined in recent decades. Other work, however, has called into question the reported decline. Here we use global-scale atmospheric CO(2) measurements, CO(2) emission inventories and their full range of uncertainties to calculate changes in global CO(2) sources and sinks during the past 50 years. Our mass balance analysis shows that net global carbon uptake has increased significantly by about 0.05 billion tonnes of carbon per year and that global carbon uptake doubled, from 2.4 +/- 0.8 to 5.0 +/- 0.9 billion tonnes per year, between 1960 and 2010. Therefore, it is very unlikely that both land and ocean carbon sinks have decreased on a global scale. Since 1959, approximately 350 billion tonnes of carbon have been emitted by humans to the atmosphere, of which about 55 per cent has moved into the land and oceans. Thus, identifying the mechanisms and locations responsible for increasing global carbon uptake remains a critical challenge in constraining the modern global carbon budget and predicting future carbon-climate interactions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ballantyne, A P -- Alden, C B -- Miller, J B -- Tans, P P -- White, J W C -- England -- Nature. 2012 Aug 2;488(7409):70-2. doi: 10.1038/nature11299.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Geology, University of Colorado, Boulder, Colorado 80309, USA. apballantyne@gmail.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22859203" target="_blank"〉PubMed〈/a〉
    Keywords: Atmosphere/*chemistry ; Carbon/analysis ; Carbon Dioxide/*analysis/history ; *Carbon Sequestration ; Climate Change/*statistics & numerical data ; History, 20th Century ; History, 21st Century ; Human Activities ; Models, Theoretical ; Oceans and Seas ; Seawater/*chemistry ; Time Factors ; Uncertainty
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    Synthetic homeostatic materials with chemo-mechano-chemical self-regulation (2012)
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    Publication Date: 2012-07-13
    Description: Living organisms have unique homeostatic abilities, maintaining tight control of their local environment through interconversions of chemical and mechanical energy and self-regulating feedback loops organized hierarchically across many length scales. In contrast, most synthetic materials are incapable of continuous self-monitoring and self-regulating behaviour owing to their limited single-directional chemomechanical or mechanochemical modes. Applying the concept of homeostasis to the design of autonomous materials would have substantial impacts in areas ranging from medical implants that help stabilize bodily functions to 'smart' materials that regulate energy usage. Here we present a versatile strategy for creating self-regulating, self-powered, homeostatic materials capable of precisely tailored chemo-mechano-chemical feedback loops on the nano- or microscale. We design a bilayer system with hydrogel-supported, catalyst-bearing microstructures, which are separated from a reactant-containing 'nutrient' layer. Reconfiguration of the gel in response to a stimulus induces the reversible actuation of the microstructures into and out of the nutrient layer, and serves as a highly precise 'on/off' switch for chemical reactions. We apply this design to trigger organic, inorganic and biochemical reactions that undergo reversible, repeatable cycles synchronized with the motion of the microstructures and the driving external chemical stimulus. By exploiting a continuous feedback loop between various exothermic catalytic reactions in the nutrient layer and the mechanical action of the temperature-responsive gel, we then create exemplary autonomous, self-sustained homeostatic systems that maintain a user-defined parameter--temperature--in a narrow range. The experimental results are validated using computational modelling that qualitatively captures the essential features of the self-regulating behaviour and provides additional criteria for the optimization of the homeostatic function, subsequently confirmed experimentally. This design is highly customizable owing to the broad choice of chemistries, tunable mechanics and its physical simplicity, and may lead to a variety of applications in autonomous systems with chemo-mechano-chemical transduction at their core.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉He, Ximin -- Aizenberg, Michael -- Kuksenok, Olga -- Zarzar, Lauren D -- Shastri, Ankita -- Balazs, Anna C -- Aizenberg, Joanna -- England -- Nature. 2012 Jul 11;487(7406):214-8. doi: 10.1038/nature11223.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Engineering and Applied Sciences, Harvard University, Cambridge, Massachusetts 02138, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22785318" target="_blank"〉PubMed〈/a〉
    Keywords: *Chemical Engineering ; Click Chemistry ; Computer Simulation ; *Feedback ; *Homeostasis ; Hydrogen-Ion Concentration ; Manufactured Materials/standards ; Temperature ; Time Factors
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    Neuroscience: Sibling neurons bond to share sensations (2012)
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    Publication Date: 2012-06-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mrsic-Flogel, Thomas D -- Bonhoeffer, Tobias -- 095074/Wellcome Trust/United Kingdom -- England -- Nature. 2012 Jun 6;486(7401):41-2. doi: 10.1038/486041a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22678277" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Communication ; *Cell Lineage ; *Electric Conductivity ; Electrical Synapses/*physiology ; Female ; Gap Junctions/*metabolism ; Male ; Neocortex/*cytology ; Neurons/*cytology/*physiology ; Visual Cortex/*cytology
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    Stem cells: a sporadic super state (2012)
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    Publication Date: 2012-07-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Surani, Azim -- Tischler, Julia -- 079249/Wellcome Trust/United Kingdom -- 092096/Wellcome Trust/United Kingdom -- G0800784/Medical Research Council/United Kingdom -- England -- Nature. 2012 Jul 4;487(7405):43-5. doi: 10.1038/487043a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wellcome Trust Cancer Research UK Gurdon Institute, University of Cambridge, Cambridge CB2 1QN, UK. a.surani@gurdon.cam.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22763548" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Dedifferentiation/*genetics ; Embryonic Stem Cells/*cytology/*metabolism ; Endogenous Retroviruses/*genetics ; Female ; Pluripotent Stem Cells/*cytology ; Totipotent Stem Cells/*cytology/*metabolism
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    Melanomas resist T-cell therapy through inflammation-induced reversible dedifferentiation (2012)
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    Publication Date: 2012-10-12
    Description: Adoptive cell transfer therapies (ACTs) with cytotoxic T cells that target melanocytic antigens can achieve remissions in patients with metastatic melanomas, but tumours frequently relapse. Hypotheses explaining the acquired resistance to ACTs include the selection of antigen-deficient tumour cell variants and the induction of T-cell tolerance. However, the lack of appropriate experimental melanoma models has so far impeded clear insights into the underlying mechanisms. Here we establish an effective ACT protocol in a genetically engineered mouse melanoma model that recapitulates tumour regression, remission and relapse as seen in patients. We report the unexpected observation that melanomas acquire ACT resistance through an inflammation-induced reversible loss of melanocytic antigens. In serial transplantation experiments, melanoma cells switch between a differentiated and a dedifferentiated phenotype in response to T-cell-driven inflammatory stimuli. We identified the proinflammatory cytokine tumour necrosis factor (TNF)-alpha as a crucial factor that directly caused reversible dedifferentiation of mouse and human melanoma cells. Tumour cells exposed to TNF-alpha were poorly recognized by T cells specific for melanocytic antigens, whereas recognition by T cells specific for non-melanocytic antigens was unaffected or even increased. Our results demonstrate that the phenotypic plasticity of melanoma cells in an inflammatory microenvironment contributes to tumour relapse after initially successful T-cell immunotherapy. On the basis of our work, we propose that future ACT protocols should simultaneously target melanocytic and non-melanocytic antigens to ensure broad recognition of both differentiated and dedifferentiated melanoma cells, and include strategies to sustain T-cell effector functions by blocking immune-inhibitory mechanisms in the tumour microenvironment.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Landsberg, Jennifer -- Kohlmeyer, Judith -- Renn, Marcel -- Bald, Tobias -- Rogava, Meri -- Cron, Mira -- Fatho, Martina -- Lennerz, Volker -- Wolfel, Thomas -- Holzel, Michael -- Tuting, Thomas -- England -- Nature. 2012 Oct 18;490(7420):412-6. doi: 10.1038/nature11538. Epub 2012 Oct 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Experimental Dermatology, Department of Dermatology and Allergy, University of Bonn, D-53105 Bonn, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23051752" target="_blank"〉PubMed〈/a〉
    Keywords: Adoptive Transfer ; Animals ; *Cell Dedifferentiation ; Cell Differentiation ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Disease Models, Animal ; Humans ; *Immunotherapy ; Inflammation/immunology/*pathology ; Melanoma/immunology/metabolism/*pathology/*therapy ; Mice ; Mice, Inbred C57BL ; Neoplasm Transplantation ; T-Lymphocytes, Cytotoxic/*immunology/*transplantation ; Tumor Microenvironment/immunology ; Tumor Necrosis Factor-alpha/immunology/pharmacology ; gp100 Melanoma Antigen/metabolism
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    Sequence analysis of mutations and translocations across breast cancer subtypes (2012)
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    Publication Date: 2012-06-23
    Description: Breast carcinoma is the leading cause of cancer-related mortality in women worldwide, with an estimated 1.38 million new cases and 458,000 deaths in 2008 alone. This malignancy represents a heterogeneous group of tumours with characteristic molecular features, prognosis and responses to available therapy. Recurrent somatic alterations in breast cancer have been described, including mutations and copy number alterations, notably ERBB2 amplifications, the first successful therapy target defined by a genomic aberration. Previous DNA sequencing studies of breast cancer genomes have revealed additional candidate mutations and gene rearrangements. Here we report the whole-exome sequences of DNA from 103 human breast cancers of diverse subtypes from patients in Mexico and Vietnam compared to matched-normal DNA, together with whole-genome sequences of 22 breast cancer/normal pairs. Beyond confirming recurrent somatic mutations in PIK3CA, TP53, AKT1, GATA3 and MAP3K1, we discovered recurrent mutations in the CBFB transcription factor gene and deletions of its partner RUNX1. Furthermore, we have identified a recurrent MAGI3-AKT3 fusion enriched in triple-negative breast cancer lacking oestrogen and progesterone receptors and ERBB2 expression. The MAGI3-AKT3 fusion leads to constitutive activation of AKT kinase, which is abolished by treatment with an ATP-competitive AKT small-molecule inhibitor.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4148686/" 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/PMC4148686/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Banerji, Shantanu -- Cibulskis, Kristian -- Rangel-Escareno, Claudia -- Brown, Kristin K -- Carter, Scott L -- Frederick, Abbie M -- Lawrence, Michael S -- Sivachenko, Andrey Y -- Sougnez, Carrie -- Zou, Lihua -- Cortes, Maria L -- Fernandez-Lopez, Juan C -- Peng, Shouyong -- Ardlie, Kristin G -- Auclair, Daniel -- Bautista-Pina, Veronica -- Duke, Fujiko -- Francis, Joshua -- Jung, Joonil -- Maffuz-Aziz, Antonio -- Onofrio, Robert C -- Parkin, Melissa -- Pho, Nam H -- Quintanar-Jurado, Valeria -- Ramos, Alex H -- Rebollar-Vega, Rosa -- Rodriguez-Cuevas, Sergio -- Romero-Cordoba, Sandra L -- Schumacher, Steven E -- Stransky, Nicolas -- Thompson, Kristin M -- Uribe-Figueroa, Laura -- Baselga, Jose -- Beroukhim, Rameen -- Polyak, Kornelia -- Sgroi, Dennis C -- Richardson, Andrea L -- Jimenez-Sanchez, Gerardo -- Lander, Eric S -- Gabriel, Stacey B -- Garraway, Levi A -- Golub, Todd R -- Melendez-Zajgla, Jorge -- Toker, Alex -- Getz, Gad -- Hidalgo-Miranda, Alfredo -- Meyerson, Matthew -- CA089393/CA/NCI NIH HHS/ -- CA122099/CA/NCI NIH HHS/ -- R01 CA122099/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2012 Jun 20;486(7403):405-9. doi: 10.1038/nature11154.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Broad Institute of MIT and Harvard, Cambridge, Massachusetts 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22722202" target="_blank"〉PubMed〈/a〉
    Keywords: Algorithms ; Breast Neoplasms/*classification/*genetics/pathology ; Core Binding Factor Alpha 2 Subunit/genetics ; Core Binding Factor beta Subunit/genetics ; DNA Mutational Analysis ; Exome/genetics ; Female ; Gene Fusion/genetics ; Humans ; Membrane Proteins/genetics ; Mexico ; Mutation/*genetics ; Proto-Oncogene Proteins c-akt/antagonists & inhibitors/genetics/metabolism ; Translocation, Genetic/*genetics ; Vietnam
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    Nonlinear dendritic integration of sensory and motor input during an active sensing task (2012)
    Nature Publishing Group (NPG)
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    Publication Date: 2012-11-13
    Description: Active dendrites provide neurons with powerful processing capabilities. However, little is known about the role of neuronal dendrites in behaviourally related circuit computations. Here we report that a novel global dendritic nonlinearity is involved in the integration of sensory and motor information within layer 5 pyramidal neurons during an active sensing behaviour. Layer 5 pyramidal neurons possess elaborate dendritic arborizations that receive functionally distinct inputs, each targeted to spatially separate regions. At the cellular level, coincident input from these segregated pathways initiates regenerative dendritic electrical events that produce bursts of action potential output and circuits featuring this powerful dendritic nonlinearity can implement computations based on input correlation. To examine this in vivo we recorded dendritic activity in layer 5 pyramidal neurons in the barrel cortex using two-photon calcium imaging in mice performing an object-localization task. Large-amplitude, global calcium signals were observed throughout the apical tuft dendrites when active touch occurred at particular object locations or whisker angles. Such global calcium signals are produced by dendritic plateau potentials that require both vibrissal sensory input and primary motor cortex activity. These data provide direct evidence of nonlinear dendritic processing of correlated sensory and motor information in the mammalian neocortex during active sensation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Xu, Ning-long -- Harnett, Mark T -- Williams, Stephen R -- Huber, Daniel -- O'Connor, Daniel H -- Svoboda, Karel -- Magee, Jeffrey C -- Howard Hughes Medical Institute/ -- England -- Nature. 2012 Dec 13;492(7428):247-51. doi: 10.1038/nature11601. Epub 2012 Nov 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Janelia Farm Research Campus, Ashburn, Virginia 20147, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23143335" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Behavior, Animal/*physiology ; Calcium/metabolism ; Dendrites/*physiology ; Male ; Mice ; Mice, Inbred C57BL ; Motor Activity/*physiology ; Patch-Clamp Techniques ; Pyramidal Cells/physiology ; Sensation/*physiology ; Signal Transduction
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    A restricted cell population propagates glioblastoma growth after chemotherapy (2012)
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    Publication Date: 2012-08-03
    Description: Glioblastoma multiforme is the most common primary malignant brain tumour, with a median survival of about one year. This poor prognosis is due to therapeutic resistance and tumour recurrence after surgical removal. Precisely how recurrence occurs is unknown. Using a genetically engineered mouse model of glioma, here we identify a subset of endogenous tumour cells that are the source of new tumour cells after the drug temozolomide (TMZ) is administered to transiently arrest tumour growth. A nestin-DeltaTK-IRES-GFP (Nes-DeltaTK-GFP) transgene that labels quiescent subventricular zone adult neural stem cells also labels a subset of endogenous glioma tumour cells. On arrest of tumour cell proliferation with TMZ, pulse-chase experiments demonstrate a tumour re-growth cell hierarchy originating with the Nes-DeltaTK-GFP transgene subpopulation. Ablation of the GFP+ cells with chronic ganciclovir administration significantly arrested tumour growth, and combined TMZ and ganciclovir treatment impeded tumour development. Thus, a relatively quiescent subset of endogenous glioma cells, with properties similar to those proposed for cancer stem cells, is responsible for sustaining long-term tumour growth through the production of transient populations of highly proliferative cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3427400/" 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/PMC3427400/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Jian -- Li, Yanjiao -- Yu, Tzong-Shiue -- McKay, Renee M -- Burns, Dennis K -- Kernie, Steven G -- Parada, Luis F -- R01 CA131313/CA/NCI NIH HHS/ -- R01 NS048192-01/NS/NINDS NIH HHS/ -- England -- Nature. 2012 Aug 23;488(7412):522-6. doi: 10.1038/nature11287.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Developmental Biology, University of Texas Southwestern Medical Center, Dallas, Texas 75390-9133, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22854781" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antineoplastic Agents, Alkylating/pharmacology/therapeutic use ; Brain Neoplasms/*drug therapy/*pathology ; Cell Proliferation/drug effects ; Cell Tracking ; Dacarbazine/*analogs & derivatives/pharmacology/therapeutic use ; Disease Models, Animal ; Disease Progression ; Female ; Ganciclovir/pharmacology ; Glioblastoma/*drug therapy/*pathology ; Green Fluorescent Proteins/genetics/metabolism ; Male ; Mice ; Mice, Transgenic ; Neoplastic Stem Cells/*drug effects/*pathology ; Neural Stem Cells/drug effects/pathology ; Transgenes/genetics
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    Cancer metabolism: Tumour friend or foe (2012)
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    Publication Date: 2012-06-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Svensson, Robert U -- Shaw, Reuben J -- England -- Nature. 2012 May 31;485(7400):590-1. doi: 10.1038/485590a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22660317" target="_blank"〉PubMed〈/a〉
    Keywords: AMP-Activated Protein Kinases/*metabolism ; Animals ; *Energy Metabolism ; Female ; *Homeostasis ; Male ; NADP/*metabolism ; Neoplasms/*metabolism/*pathology ; *Oxidative Stress
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    Evolutionary anthropology: Homo 'incendius' (2012)
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    Publication Date: 2012-06-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roberts, Richard G -- Bird, Michael I -- England -- Nature. 2012 May 23;485(7400):586-7. doi: 10.1038/nature11195.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22660314" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anthropology ; Caves ; Fires/*history ; Geologic Sediments ; History, Ancient ; *Hominidae/psychology ; South Africa ; Time Factors
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    Tet1 controls meiosis by regulating meiotic gene expression (2012)
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    Publication Date: 2012-11-16
    Description: Meiosis is a germ-cell-specific cell division process through which haploid gametes are produced for sexual reproduction. Before the initiation of meiosis, mouse primordial germ cells undergo a series of epigenetic reprogramming steps, including the global erasure of DNA methylation at the 5-position of cytosine (5mC) in CpG-rich DNA. Although several epigenetic regulators, such as Dnmt3l and the histone methyltransferases G9a and Prdm9, have been reported to be crucial for meiosis, little is known about how the expression of meiotic genes is regulated and how their expression contributes to normal meiosis. Using a loss-of-function approach in mice, here we show that the 5mC-specific dioxygenase Tet1 has an important role in regulating meiosis in mouse oocytes. Tet1 deficiency significantly reduces female germ-cell numbers and fertility. Univalent chromosomes and unresolved DNA double-strand breaks are also observed in Tet1-deficient oocytes. Tet1 deficiency does not greatly affect the genome-wide demethylation that takes place in primordial germ cells, but leads to defective DNA demethylation and decreased expression of a subset of meiotic genes. Our study thus establishes a function for Tet1 in meiosis and meiotic gene activation in female germ cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3528851/" 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/PMC3528851/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yamaguchi, Shinpei -- Hong, Kwonho -- Liu, Rui -- Shen, Li -- Inoue, Azusa -- Diep, Dinh -- Zhang, Kun -- Zhang, Yi -- R01GM097253/GM/NIGMS NIH HHS/ -- U01 DK089565/DK/NIDDK NIH HHS/ -- U01DK089565/DK/NIDDK NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2012 Dec 20;492(7429):443-7. doi: 10.1038/nature11709. Epub 2012 Nov 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Harvard Medical School, WAB-149G, 200 Longwood Avenue, Boston, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23151479" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Cell Count ; DNA Breaks, Double-Stranded ; DNA Methylation/genetics ; DNA-Binding Proteins/deficiency/genetics/*metabolism ; Embryo, Mammalian/cytology/pathology ; Female ; Gene Expression Regulation/*genetics ; Infertility, Female/pathology ; Male ; Meiosis/*genetics ; Mice ; Mice, Knockout ; Oocytes/cytology/*metabolism/pathology ; Proto-Oncogene Proteins/deficiency/genetics/*metabolism ; Transcriptome
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    An RNA interference screen uncovers a new molecule in stem cell self-renewal and long-term regeneration (2012)
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    Publication Date: 2012-04-13
    Description: Adult stem cells sustain tissue maintenance and regeneration throughout the lifetime of an animal. These cells often reside in specific signalling niches that orchestrate the stem cell's balancing act between quiescence and cell-cycle re-entry based on the demand for tissue regeneration. How stem cells maintain their capacity to replenish themselves after tissue regeneration is poorly understood. Here we use RNA-interference-based loss-of-function screening as a powerful approach to uncover transcriptional regulators that govern the self-renewal capacity and regenerative potential of stem cells. Hair follicle stem cells provide an ideal model. These cells have been purified and characterized from their native niche in vivo and, in contrast to their rapidly dividing progeny, they can be maintained and passaged long-term in vitro. Focusing on the nuclear proteins and/or transcription factors that are enriched in stem cells compared with their progeny, we screened approximately 2,000 short hairpin RNAs for their effect on long-term, but not short-term, stem cell self-renewal in vitro. To address the physiological relevance of our findings, we selected one candidate that was uncovered in the screen: TBX1. This transcription factor is expressed in many tissues but has not been studied in the context of stem cell biology. By conditionally ablating Tbx1 in vivo, we showed that during homeostasis, tissue regeneration occurs normally but is markedly delayed. We then devised an in vivo assay for stem cell replenishment and found that when challenged with repetitive rounds of regeneration, the Tbx1-deficient stem cell niche becomes progressively depleted. Addressing the mechanism of TBX1 action, we discovered that TBX1 acts as an intrinsic rheostat of BMP signalling: it is a gatekeeper that governs the transition between stem cell quiescence and proliferation in hair follicles. Our results validate the RNA interference screen and underscore its power in unearthing new molecules that govern stem cell self-renewal and tissue-regenerative potential.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3600643/" 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/PMC3600643/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Ting -- Heller, Evan -- Beronja, Slobodan -- Oshimori, Naoki -- Stokes, Nicole -- Fuchs, Elaine -- R01 AR050452/AR/NIAMS NIH HHS/ -- R01-AR050452/AR/NIAMS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2012 Apr 4;485(7396):104-8. doi: 10.1038/nature10940.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, The Rockefeller University, New York, New York 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22495305" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bone Morphogenetic Proteins/metabolism ; Cell Proliferation ; Epidermis/cytology ; Female ; Hair Follicle/cytology ; Male ; Mice ; *RNA Interference ; Regeneration/genetics/*physiology ; Signal Transduction ; Stem Cells/*cytology/metabolism ; T-Box Domain Proteins/deficiency/genetics/*metabolism
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    Publishing: Handful of papers dominates citation (2012)
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    Publication Date: 2012-11-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barabasi, Albert-Laszlo -- Song, Chaoming -- Wang, Dashun -- England -- Nature. 2012 Nov 1;491(7422):40. doi: 10.1038/491040a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23128218" target="_blank"〉PubMed〈/a〉
    Keywords: *Bibliometrics ; Crowdsourcing ; Publishing/*statistics & numerical data ; Research/*statistics & numerical data ; *Research Personnel ; Time Factors
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    Pulsed electron paramagnetic resonance spectroscopy powered by a free-electron laser (2012)
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    Publication Date: 2012-09-22
    Description: Electron paramagnetic resonance (EPR) spectroscopy interrogates unpaired electron spins in solids and liquids to reveal local structure and dynamics; for example, EPR has elucidated parts of the structure of protein complexes that other techniques in structural biology have not been able to reveal. EPR can also probe the interplay of light and electricity in organic solar cells and light-emitting diodes, and the origin of decoherence in condensed matter, which is of fundamental importance to the development of quantum information processors. Like nuclear magnetic resonance, EPR spectroscopy becomes more powerful at high magnetic fields and frequencies, and with excitation by coherent pulses rather than continuous waves. However, the difficulty of generating sequences of powerful pulses at frequencies above 100 gigahertz has, until now, confined high-power pulsed EPR to magnetic fields of 3.5 teslas and below. Here we demonstrate that one-kilowatt pulses from a free-electron laser can power a pulsed EPR spectrometer at 240 gigahertz (8.5 teslas), providing transformative enhancements over the alternative, a state-of-the-art approximately 30-milliwatt solid-state source. Our spectrometer can rotate spin-1/2 electrons through pi/2 in only 6 nanoseconds (compared to 300 nanoseconds with the solid-state source). Fourier-transform EPR on nitrogen impurities in diamond demonstrates excitation and detection of EPR lines separated by about 200 megahertz. We measured decoherence times as short as 63 nanoseconds, in a frozen solution of nitroxide free-radicals at temperatures as high as 190 kelvin. Both free-electron lasers and the quasi-optical technology developed for the spectrometer are scalable to frequencies well in excess of one terahertz, opening the way to high-power pulsed EPR spectroscopy up to the highest static magnetic fields currently available.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Takahashi, S -- Brunel, L-C -- Edwards, D T -- van Tol, J -- Ramian, G -- Han, S -- Sherwin, M S -- England -- Nature. 2012 Sep 20;489(7416):409-13. doi: 10.1038/nature11437.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry, University of Southern California, Los Angeles, California 90089, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22996555" target="_blank"〉PubMed〈/a〉
    Keywords: Allyl Compounds/chemistry ; Benzene/chemistry ; Cyclic N-Oxides/chemistry ; Diamond/chemistry ; Electron Spin Resonance Spectroscopy/*instrumentation/*methods ; *Electrons ; Fourier Analysis ; Free Radicals/chemistry ; *Lasers ; Nitrogen Oxides/chemistry ; Temperature ; Time Factors
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    Atmospheric CO2 forces abrupt vegetation shifts locally, but not globally (2012)
    Nature Publishing Group (NPG)
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    Publication Date: 2012-07-06
    Description: It is possible that anthropogenic climate change will drive the Earth system into a qualitatively different state. Although different types of uncertainty limit our capacity to assess this risk, Earth system scientists are particularly concerned about tipping elements, large-scale components of the Earth system that can be switched into qualitatively different states by small perturbations. Despite growing evidence that tipping elements exist in the climate system, whether large-scale vegetation systems can tip into alternative states is poorly understood. Here we show that tropical grassland, savanna and forest ecosystems, areas large enough to have powerful impacts on the Earth system, are likely to shift to alternative states. Specifically, we show that increasing atmospheric CO2 concentration will force transitions to vegetation states characterized by higher biomass and/or woody-plant dominance. The timing of these critical transitions varies as a result of between-site variance in the rate of temperature increase, as well as a dependence on stochastic variation in fire severity and rainfall. We further show that the locations of bistable vegetation zones (zones where alternative vegetation states can exist) will shift as climate changes. We conclude that even though large-scale directional regime shifts in terrestrial ecosystems are likely, asynchrony in the timing of these shifts may serve to dampen, but not nullify, the shock that these changes may represent to the Earth system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Higgins, Steven I -- Scheiter, Simon -- England -- Nature. 2012 Aug 9;488(7410):209-12. doi: 10.1038/nature11238.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut fur Physische Geographie, Goethe Universitat Frankfurt am Main, 60438 Frankfurt am Main, Germany. higgins@em.uni-frankfurt.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22763447" target="_blank"〉PubMed〈/a〉
    Keywords: Africa ; Atmosphere/*chemistry ; Biomass ; Carbon/metabolism ; Carbon Dioxide/analysis/*metabolism ; Climate Change/*statistics & numerical data ; *Ecosystem ; Fires ; Geography ; History, 19th Century ; History, 20th Century ; History, 21st Century ; Hot Temperature ; Models, Biological ; Photosynthesis/physiology ; Poaceae/growth & development/metabolism ; Probability ; Rain ; Stochastic Processes ; Time Factors ; Trees/*growth & development/metabolism ; Wood
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    FTO genotype is associated with phenotypic variability of body mass index (2012)
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    Publication Date: 2012-09-18
    Description: There is evidence across several species for genetic control of phenotypic variation of complex traits, such that the variance among phenotypes is genotype dependent. Understanding genetic control of variability is important in evolutionary biology, agricultural selection programmes and human medicine, yet for complex traits, no individual genetic variants associated with variance, as opposed to the mean, have been identified. Here we perform a meta-analysis of genome-wide association studies of phenotypic variation using approximately 170,000 samples on height and body mass index (BMI) in human populations. We report evidence that the single nucleotide polymorphism (SNP) rs7202116 at the FTO gene locus, which is known to be associated with obesity (as measured by mean BMI for each rs7202116 genotype), is also associated with phenotypic variability. We show that the results are not due to scale effects or other artefacts, and find no other experiment-wise significant evidence for effects on variability, either at loci other than FTO for BMI or at any locus for height. The difference in variance for BMI among individuals with opposite homozygous genotypes at the FTO locus is approximately 7%, corresponding to a difference of approximately 0.5 kilograms in the standard deviation of weight. Our results indicate that genetic variants can be discovered that are associated with variability, and that between-person variability in obesity can partly be explained by the genotype at the FTO locus. The results are consistent with reported FTO by environment interactions for BMI, possibly mediated by DNA methylation. Our BMI results for other SNPs and our height results for all SNPs suggest that most genetic variants, including those that influence mean height or mean BMI, are not associated with phenotypic variance, or that their effects on variability are too small to detect even with samples sizes greater than 100,000.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3564953/" 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/PMC3564953/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yang, Jian -- Loos, Ruth J F -- Powell, Joseph E -- Medland, Sarah E -- Speliotes, Elizabeth K -- Chasman, Daniel I -- Rose, Lynda M -- Thorleifsson, Gudmar -- Steinthorsdottir, Valgerdur -- Magi, Reedik -- Waite, Lindsay -- Smith, Albert Vernon -- Yerges-Armstrong, Laura M -- Monda, Keri L -- Hadley, David -- Mahajan, Anubha -- Li, Guo -- Kapur, Karen -- Vitart, Veronique -- Huffman, Jennifer E -- Wang, Sophie R -- Palmer, Cameron -- Esko, Tonu -- Fischer, Krista -- Zhao, Jing Hua -- Demirkan, Ayse -- Isaacs, Aaron -- Feitosa, Mary F -- Luan, Jian'an -- Heard-Costa, Nancy L -- White, Charles -- Jackson, Anne U -- Preuss, Michael -- Ziegler, Andreas -- Eriksson, Joel -- Kutalik, Zoltan -- Frau, Francesca -- Nolte, Ilja M -- Van Vliet-Ostaptchouk, Jana V -- Hottenga, Jouke-Jan -- Jacobs, Kevin B -- Verweij, Niek -- Goel, Anuj -- Medina-Gomez, Carolina -- Estrada, Karol -- Bragg-Gresham, Jennifer Lynn -- Sanna, Serena -- Sidore, Carlo -- Tyrer, Jonathan -- Teumer, Alexander -- Prokopenko, Inga -- Mangino, Massimo -- Lindgren, Cecilia M -- Assimes, Themistocles L -- Shuldiner, Alan R -- Hui, Jennie -- Beilby, John P -- McArdle, Wendy L -- Hall, Per -- Haritunians, Talin -- Zgaga, Lina -- Kolcic, Ivana -- Polasek, Ozren -- Zemunik, Tatijana -- Oostra, Ben A -- Junttila, M Juhani -- Gronberg, Henrik -- Schreiber, Stefan -- Peters, Annette -- Hicks, Andrew A -- Stephens, Jonathan -- Foad, Nicola S -- Laitinen, Jaana -- Pouta, Anneli -- Kaakinen, Marika -- Willemsen, Gonneke -- Vink, Jacqueline M -- Wild, Sarah H -- Navis, Gerjan -- Asselbergs, Folkert W -- Homuth, Georg -- John, Ulrich -- Iribarren, Carlos -- Harris, Tamara -- Launer, Lenore -- Gudnason, Vilmundur -- O'Connell, Jeffrey R -- Boerwinkle, Eric -- Cadby, Gemma -- Palmer, Lyle J -- James, Alan L -- Musk, Arthur W -- Ingelsson, Erik -- Psaty, Bruce M -- Beckmann, Jacques S -- Waeber, Gerard -- Vollenweider, Peter -- Hayward, Caroline -- Wright, Alan F -- Rudan, Igor -- Groop, Leif C -- Metspalu, Andres -- Khaw, Kay Tee -- van Duijn, Cornelia M -- Borecki, Ingrid B -- Province, Michael A -- Wareham, Nicholas J -- Tardif, Jean-Claude -- Huikuri, Heikki V -- Cupples, L Adrienne -- Atwood, Larry D -- Fox, Caroline S -- Boehnke, Michael -- Collins, Francis S -- Mohlke, Karen L -- Erdmann, Jeanette -- Schunkert, Heribert -- Hengstenberg, Christian -- Stark, Klaus -- Lorentzon, Mattias -- Ohlsson, Claes -- Cusi, Daniele -- Staessen, Jan A -- Van der Klauw, Melanie M -- Pramstaller, Peter P -- Kathiresan, Sekar -- Jolley, Jennifer D -- Ripatti, Samuli -- Jarvelin, Marjo-Riitta -- de Geus, Eco J C -- Boomsma, Dorret I -- Penninx, Brenda -- Wilson, James F -- Campbell, Harry -- Chanock, Stephen J -- van der Harst, Pim -- Hamsten, Anders -- Watkins, Hugh -- Hofman, Albert -- Witteman, Jacqueline C -- Zillikens, M Carola -- Uitterlinden, Andre G -- Rivadeneira, Fernando -- Kiemeney, Lambertus A -- Vermeulen, Sita H -- Abecasis, Goncalo R -- Schlessinger, David -- Schipf, Sabine -- Stumvoll, Michael -- Tonjes, Anke -- Spector, Tim D -- North, Kari E -- Lettre, Guillaume -- McCarthy, Mark I -- Berndt, Sonja I -- Heath, Andrew C -- Madden, Pamela A F -- Nyholt, Dale R -- Montgomery, Grant W -- Martin, Nicholas G -- McKnight, Barbara -- Strachan, David P -- Hill, William G -- Snieder, Harold -- Ridker, Paul M -- Thorsteinsdottir, Unnur -- Stefansson, Kari -- Frayling, Timothy M -- Hirschhorn, Joel N -- Goddard, Michael E -- Visscher, Peter M -- 090532/Wellcome Trust/United Kingdom -- 14136/Cancer Research UK/United Kingdom -- AA014041/AA/NIAAA NIH HHS/ -- AA07535/AA/NIAAA NIH HHS/ -- AA10248/AA/NIAAA NIH HHS/ -- AA13320/AA/NIAAA NIH HHS/ -- AA13321/AA/NIAAA NIH HHS/ -- AA13326/AA/NIAAA NIH HHS/ -- CZB/4/710/Chief Scientist Office/United Kingdom -- DA12854/DA/NIDA NIH HHS/ -- F32 AR059469/AR/NIAMS NIH HHS/ -- F32 DK079466/DK/NIDDK NIH HHS/ -- G0601261/Medical Research Council/United Kingdom -- G1000143/Medical Research Council/United Kingdom -- GM057091/GM/NIGMS NIH HHS/ -- HHSN268201100005C/HL/NHLBI NIH HHS/ -- HHSN268201100006C/HL/NHLBI NIH HHS/ -- HHSN268201100007C/HL/NHLBI NIH HHS/ -- HHSN268201100008C/HL/NHLBI NIH HHS/ -- HHSN268201100009C/HL/NHLBI NIH HHS/ -- HHSN268201100010C/HL/NHLBI NIH HHS/ -- HHSN268201100011C/HL/NHLBI NIH HHS/ -- HHSN268201100012C/HL/NHLBI NIH HHS/ -- K05 AA017688/AA/NIAAA NIH HHS/ -- K23 DK080145/DK/NIDDK NIH HHS/ -- MC_PC_U127561128/Medical Research Council/United Kingdom -- MC_U106179471/Medical Research Council/United Kingdom -- MC_U127561128/Medical Research Council/United Kingdom -- N01 AG012100/AG/NIA NIH HHS/ -- N01 HC015103/HC/NHLBI NIH HHS/ -- N01 HC025195/HC/NHLBI NIH HHS/ -- N01 HC035129/HC/NHLBI NIH HHS/ -- N01 HC045133/HC/NHLBI NIH HHS/ -- N01 HC055222/HC/NHLBI NIH HHS/ -- N01 HC075150/HC/NHLBI NIH HHS/ -- N01 HC085079/HC/NHLBI NIH HHS/ -- N01 HG065403/HG/NHGRI NIH HHS/ -- N01HC85086/HL/NHLBI NIH HHS/ -- N02 HL64278/HL/NHLBI NIH HHS/ -- P30 DK063491/DK/NIDDK NIH HHS/ -- P30 DK072488/DK/NIDDK NIH HHS/ -- R01 AA007535/AA/NIAAA NIH HHS/ -- R01 AA013320/AA/NIAAA NIH HHS/ -- R01 AA013321/AA/NIAAA NIH HHS/ -- R01 AA013326/AA/NIAAA NIH HHS/ -- R01 AA014041/AA/NIAAA NIH HHS/ -- R01 AG015928/AG/NIA NIH HHS/ -- R01 AG020098/AG/NIA NIH HHS/ -- R01 AG023629/AG/NIA NIH HHS/ -- R01 AG027058/AG/NIA NIH HHS/ -- R01 DA012854/DA/NIDA NIH HHS/ -- R01 DK062370/DK/NIDDK NIH HHS/ -- R01 DK072193/DK/NIDDK NIH HHS/ -- R01 DK073490/DK/NIDDK NIH HHS/ -- R01 DK075681/DK/NIDDK NIH HHS/ -- R01 DK075787/DK/NIDDK NIH HHS/ -- R01 HG002651/HG/NHGRI NIH HHS/ -- R01 HL043851/HL/NHLBI NIH HHS/ -- R01 HL059367/HL/NHLBI NIH HHS/ -- R01 HL075366/HL/NHLBI NIH HHS/ -- R01 HL080295/HL/NHLBI NIH HHS/ -- R01 HL086694/HL/NHLBI NIH HHS/ -- R01 HL087641/HL/NHLBI NIH HHS/ -- R01 HL087647/HL/NHLBI NIH HHS/ -- R01 HL087652/HL/NHLBI NIH HHS/ -- R01 HL087676/HL/NHLBI NIH HHS/ -- R01 HL087679/HL/NHLBI NIH HHS/ -- R01 HL105756/HL/NHLBI NIH HHS/ -- R01 LM010098/LM/NLM NIH HHS/ -- R01 MH063706/MH/NIMH NIH HHS/ -- RL1 MH083268/MH/NIMH NIH HHS/ -- U01 DK062418/DK/NIDDK NIH HHS/ -- U01 HG004402/HG/NHGRI NIH HHS/ -- U01 HL054527/HL/NHLBI NIH HHS/ -- U01 HL069757/HL/NHLBI NIH HHS/ -- U01 HL072515/HL/NHLBI NIH HHS/ -- U01 HL084729/HL/NHLBI NIH HHS/ -- U01 HL084756/HL/NHLBI NIH HHS/ -- U54 RR020278/RR/NCRR NIH HHS/ -- UL1 RR033176/RR/NCRR NIH HHS/ -- Z01 HG000024-14/Intramural NIH HHS/ -- England -- Nature. 2012 Oct 11;490(7419):267-72. doi: 10.1038/nature11401. Epub 2012 Sep 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of Queensland Diamantina Institute, The University of Queensland, Princess Alexandra Hospital, Brisbane, Queensland 4102, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22982992" target="_blank"〉PubMed〈/a〉
    Keywords: Body Height/genetics ; *Body Mass Index ; Co-Repressor Proteins ; Female ; *Genetic Variation ; Genome-Wide Association Study ; Humans ; Male ; Nerve Tissue Proteins/genetics ; *Phenotype ; Polymorphism, Single Nucleotide ; Proteins/*genetics ; Repressor Proteins/genetics
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    Microbiology: Antibiotics and adiposity (2012)
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    Publication Date: 2012-08-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Flint, Harry J -- England -- Nature. 2012 Aug 30;488(7413):601-2. doi: 10.1038/488601a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22932383" target="_blank"〉PubMed〈/a〉
    Keywords: Adiposity/*drug effects ; Animals ; Anti-Bacterial Agents/*administration & dosage/*pharmacology ; Colon/*drug effects/*microbiology ; Female ; Male ; Metagenome/*drug effects
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    Circadian rhythms: No lazing on sunny afternoons (2012)
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    Publication Date: 2012-04-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rouyer, Francois -- England -- Nature. 2012 Apr 18;484(7394):325-6. doi: 10.1038/484325a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22517159" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Circadian Rhythm/*physiology ; Drosophila melanogaster/*physiology ; *Environment ; Female ; Male
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    Outreach: Field hospitality (2012)
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    Publication Date: 2012-01-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Laursen, Lucas -- England -- Nature. 2012 Jan 19;481(7381):399-401.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22263234" target="_blank"〉PubMed〈/a〉
    Keywords: Administrative Personnel ; *Communication ; *Expeditions ; Faculty ; *Journalism ; Paleontology/education ; *Public Relations ; *Research Personnel/psychology ; Science/*education ; Time Factors
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    Alzheimer's: Put patients and researchers in touch (2012)
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    Publication Date: 2012-08-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Murray, Matt -- England -- Nature. 2012 Aug 9;488(7410):157. doi: 10.1038/488157c.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22874953" target="_blank"〉PubMed〈/a〉
    Keywords: *Biomedical Research ; Female ; Humans ; Male ; *Motivation ; Patients/*psychology ; Research Personnel/*psychology
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    Afternoon rain more likely over drier soils (2012)
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    Publication Date: 2012-09-14
    Description: Land surface properties, such as vegetation cover and soil moisture, influence the partitioning of radiative energy between latent and sensible heat fluxes in daytime hours. During dry periods, soil-water deficit can limit evapotranspiration, leading to warmer and drier conditions in the lower atmosphere. Soil moisture can influence the development of convective storms through such modifications of low-level atmospheric temperature and humidity, which in turn feeds back on soil moisture. Yet there is considerable uncertainty in how soil moisture affects convective storms across the world, owing to a lack of observational evidence and uncertainty in large-scale models. Here we present a global-scale observational analysis of the coupling between soil moisture and precipitation. We show that across all six continents studied, afternoon rain falls preferentially over soils that are relatively dry compared to the surrounding area. The signal emerges most clearly in the observations over semi-arid regions, where surface fluxes are sensitive to soil moisture, and convective events are frequent. Mechanistically, our results are consistent with enhanced afternoon moist convection driven by increased sensible heat flux over drier soils, and/or mesoscale variability in soil moisture. We find no evidence in our analysis of a positive feedback--that is, a preference for rain over wetter soils-at the spatial scale (50-100 kilometres) studied. In contrast, we find that a positive feedback of soil moisture on simulated precipitation does dominate in six state-of-the-art global weather and climate models--a difference that may contribute to excessive simulated droughts in large-scale models.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Taylor, Christopher M -- de Jeu, Richard A M -- Guichard, Francoise -- Harris, Phil P -- Dorigo, Wouter A -- England -- Nature. 2012 Sep 20;489(7416):423-6. doi: 10.1038/nature11377. Epub 2012 Sep 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉NERC Centre for Ecology and Hydrology, Maclean Building, Benson Lane, Crowmarsh Gifford, Wallingford OX10 8BB, UK. cmt@ceh.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22972193" target="_blank"〉PubMed〈/a〉
    Keywords: Atmosphere/chemistry ; Climate ; Desert Climate ; *Desiccation ; Droughts ; Ecosystem ; Feedback ; Geography ; Hot Temperature ; *Humidity ; Models, Theoretical ; *Rain ; Soil/*chemistry ; Time Factors ; Water/*analysis
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    Human gut microbiome viewed across age and geography (2012)
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    Publication Date: 2012-06-16
    Description: Gut microbial communities represent one source of human genetic and metabolic diversity. To examine how gut microbiomes differ among human populations, here we characterize bacterial species in fecal samples from 531 individuals, plus the gene content of 110 of them. The cohort encompassed healthy children and adults from the Amazonas of Venezuela, rural Malawi and US metropolitan areas and included mono- and dizygotic twins. Shared features of the functional maturation of the gut microbiome were identified during the first three years of life in all three populations, including age-associated changes in the genes involved in vitamin biosynthesis and metabolism. Pronounced differences in bacterial assemblages and functional gene repertoires were noted between US residents and those in the other two countries. These distinctive features are evident in early infancy as well as adulthood. Our findings underscore the need to consider the microbiome when evaluating human development, nutritional needs, physiological variations and the impact of westernization.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3376388/" 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/PMC3376388/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yatsunenko, Tanya -- Rey, Federico E -- Manary, Mark J -- Trehan, Indi -- Dominguez-Bello, Maria Gloria -- Contreras, Monica -- Magris, Magda -- Hidalgo, Glida -- Baldassano, Robert N -- Anokhin, Andrey P -- Heath, Andrew C -- Warner, Barbara -- Reeder, Jens -- Kuczynski, Justin -- Caporaso, J Gregory -- Lozupone, Catherine A -- Lauber, Christian -- Clemente, Jose Carlos -- Knights, Dan -- Knight, Rob -- Gordon, Jeffrey I -- DK078669/DK/NIDDK NIH HHS/ -- K01 DK090285/DK/NIDDK NIH HHS/ -- K05 AA017688/AA/NIAAA NIH HHS/ -- P01 DK078669/DK/NIDDK NIH HHS/ -- P01 DK078669-05/DK/NIDDK NIH HHS/ -- T32 HD049338-06/HD/NICHD NIH HHS/ -- T32-HD049338/HD/NICHD NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2012 May 9;486(7402):222-7. doi: 10.1038/nature11053.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Genome Sciences and Systems Biology, Washington University School of Medicine, St Louis, Missouri 63108, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22699611" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Age Factors ; Aged ; Bacteria/*classification/*genetics ; *Biodiversity ; Child ; Child, Preschool ; Feces/microbiology ; Female ; Geography ; Humans ; Infant ; Intestines/*microbiology ; Malawi ; Male ; *Metagenome ; Middle Aged ; Phylogeny ; RNA, Ribosomal, 16S/genetics ; Twins, Dizygotic ; Twins, Monozygotic ; United States ; Venezuela ; Young Adult
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    Resurrection of endogenous retroviruses in antibody-deficient mice (2012)
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    Publication Date: 2012-10-30
    Description: The mammalian host has developed a long-standing symbiotic relationship with a considerable number of microbial species. These include the microbiota on environmental surfaces, such as the respiratory and gastrointestinal tracts, and also endogenous retroviruses (ERVs), comprising a substantial fraction of the mammalian genome. The long-term consequences for the host of interactions with these microbial species can range from mutualism to parasitism and are not always completely understood. The potential effect of one microbial symbiont on another is even less clear. Here we study the control of ERVs in the commonly used C57BL/6 (B6) mouse strain, which lacks endogenous murine leukaemia viruses (MLVs) able to replicate in murine cells. We demonstrate the spontaneous emergence of fully infectious ecotropic MLV in B6 mice with a range of distinct immune deficiencies affecting antibody production. These recombinant retroviruses establish infection of immunodeficient mouse colonies, and ultimately result in retrovirus-induced lymphomas. Notably, ERV activation in immunodeficient mice is prevented in husbandry conditions associated with reduced or absent intestinal microbiota. Our results shed light onto a previously unappreciated role for immunity in the control of ERVs and provide a potential mechanistic link between immune activation by microbial triggers and a range of pathologies associated with ERVs, including cancer.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3511586/" 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/PMC3511586/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Young, George R -- Eksmond, Urszula -- Salcedo, Rosalba -- Alexopoulou, Lena -- Stoye, Jonathan P -- Kassiotis, George -- MC_U117512710/Medical Research Council/United Kingdom -- MC_U117581330/Medical Research Council/United Kingdom -- U.1175.02.005.00005(60891)/Medical Research Council/United Kingdom -- U.1175.02.006.00007(81330)/Medical Research Council/United Kingdom -- U117512710/Medical Research Council/United Kingdom -- U117581330/Medical Research Council/United Kingdom -- England -- Nature. 2012 Nov 29;491(7426):774-8. doi: 10.1038/nature11599. Epub 2012 Oct 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Immunoregulation, MRC National Institute for Medical Research, The Ridgeway, London NW7 1AA, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23103862" target="_blank"〉PubMed〈/a〉
    Keywords: Animal Husbandry ; Animals ; Antibodies, Viral/*biosynthesis/immunology ; Cell Transformation, Viral ; Endogenous Retroviruses/genetics/growth & development/immunology/*physiology ; Female ; Immunocompromised Host/*immunology ; Leukemia/virology ; Leukemia Virus, Murine/genetics/growth & development/immunology/physiology ; Lymphoma/virology ; Male ; Mice ; Mice, Inbred C57BL ; Receptors, Antigen, T-Cell/deficiency/genetics ; Recombination, Genetic ; Viremia/immunology/virology ; *Virus Activation
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    Translational research: A UK tissue bank for breast tumours (2012)
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    Publication Date: 2012-05-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thompson, Alastair M -- England -- Nature. 2012 May 9;485(7397):174. doi: 10.1038/485174d.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22575950" target="_blank"〉PubMed〈/a〉
    Keywords: Breast Neoplasms/classification/*pathology ; Female ; Great Britain ; Humans ; Ireland ; *Tissue Banks ; *Translational Medical Research/trends
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    PPAR-gamma is a major driver of the accumulation and phenotype of adipose tissue Treg cells (2012)
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    Publication Date: 2012-06-23
    Description: Obesity and type-2 diabetes have increased markedly over the past few decades, in parallel. One of the major links between these two disorders is chronic, low-grade inflammation. Prolonged nutrient excess promotes the accumulation and activation of leukocytes in visceral adipose tissue (VAT) and ultimately other tissues, leading to metabolic abnormalities such as insulin resistance, type-2 diabetes and fatty-liver disease. Although invasion of VAT by pro-inflammatory macrophages is considered to be a key event driving adipose-tissue inflammation and insulin resistance, little is known about the roles of other immune system cell types in these processes. A unique population of VAT-resident regulatory T (Treg) cells was recently implicated in control of the inflammatory state of adipose tissue and, thereby, insulin sensitivity. Here we identify peroxisome proliferator-activated receptor (PPAR)-gamma, the 'master regulator' of adipocyte differentiation, as a crucial molecular orchestrator of VAT Treg cell accumulation, phenotype and function. Unexpectedly, PPAR-gamma expression by VAT Treg cells was necessary for complete restoration of insulin sensitivity in obese mice by the thiazolidinedione drug pioglitazone. These findings suggest a previously unknown cellular mechanism for this important class of thiazolidinedione drugs, and provide proof-of-principle that discrete populations of Treg cells with unique functions can be precisely targeted to therapeutic ends.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3387339/" 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/PMC3387339/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cipolletta, Daniela -- Feuerer, Markus -- Li, Amy -- Kamei, Nozomu -- Lee, Jongsoon -- Shoelson, Steven E -- Benoist, Christophe -- Mathis, Diane -- DK092541/DK/NIDDK NIH HHS/ -- DK51729/DK/NIDDK NIH HHS/ -- P30DK36836/DK/NIDDK NIH HHS/ -- R01 DK051729/DK/NIDDK NIH HHS/ -- R01 DK092541/DK/NIDDK NIH HHS/ -- R01 DK092541-02/DK/NIDDK NIH HHS/ -- R37 DK051729/DK/NIDDK NIH HHS/ -- T32 GM007753/GM/NIGMS NIH HHS/ -- England -- Nature. 2012 Jun 28;486(7404):549-53. doi: 10.1038/nature11132.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Immunology, Department of Microbiology and Immunobiology, Harvard Medical School, Boston, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22722857" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue/*cytology/immunology/pathology ; Animals ; Cell Differentiation ; Diabetes Mellitus, Type 2/drug therapy/metabolism/pathology ; Epididymis/cytology/immunology ; Forkhead Transcription Factors/metabolism ; Gene Expression ; Hypoglycemic Agents/pharmacology ; Inflammation/immunology/metabolism/pathology ; Insulin Resistance/physiology ; Lymphocyte Count ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Obese ; Obesity/metabolism/pathology ; PPAR gamma/*metabolism ; Phenotype ; RNA, Messenger/genetics/metabolism ; T-Lymphocytes, Regulatory/*cytology/drug effects/*metabolism ; Thiazolidinediones/pharmacology ; Transcription, Genetic
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    Fracking boom spurs environmental audit (2012)
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    Publication Date: 2012-06-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thompson, Helen -- England -- Nature. 2012 May 29;485(7400):556-7. doi: 10.1038/485556a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22660293" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Confidentiality ; *Environment ; Environmental Exposure/*adverse effects/legislation & jurisprudence ; Environmental Monitoring ; Extraction and Processing Industry/economics/*legislation & jurisprudence ; Female ; Humans ; Livestock ; Ohio ; *Oil and Gas Fields ; Pregnancy ; *Public Health/legislation & jurisprudence ; Sentinel Surveillance ; United States ; United States Environmental Protection Agency
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    Plans stall for biodefence lab (2012)
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    Publication Date: 2012-03-03
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Young, Susan -- England -- Nature. 2012 Feb 28;483(7387):18-9. doi: 10.1038/483018a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22382957" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bioterrorism/*prevention & control ; Budgets/legislation & jurisprudence ; Cattle ; Cattle Diseases/transmission/virology ; *Facility Design and Construction/economics ; Foot-and-Mouth Disease/prevention & control/transmission/virology ; Horse Diseases/prevention & control/transmission/virology ; Horses/virology ; Humans ; Kansas ; *Laboratories/economics ; National Academy of Sciences (U.S.) ; Risk Assessment ; Time Factors ; United States ; United States Department of Homeland Security ; Viral Vaccines/immunology ; Zoonoses/transmission/virology
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    Policy: take direct action on climate inaction (2012)
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    Publication Date: 2012-07-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Frid, Alejandro -- Quarmby, Lynne -- England -- Nature. 2012 Jul 4;487(7405):38. doi: 10.1038/487038a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22763536" target="_blank"〉PubMed〈/a〉
    Keywords: Canada ; Carbon Dioxide ; Coal ; *Environmental Policy/trends ; *Federal Government ; Global Warming/*prevention & control/statistics & numerical data ; Mining/legislation & jurisprudence ; Research Personnel/*legislation & jurisprudence ; Social Change ; Time Factors
    Print ISSN: 0028-0836
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    Romania: Misconduct rule is not retroactive (2012)
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    Publication Date: 2012-08-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ciuparu, Dragos -- England -- Nature. 2012 Aug 9;488(7410):157. doi: 10.1038/488157b.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22874951" target="_blank"〉PubMed〈/a〉
    Keywords: Plagiarism ; Romania ; Scientific Misconduct/*legislation & jurisprudence ; Time Factors
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    Comprehensive molecular portraits of human breast tumours (2012)
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    Publication Date: 2012-09-25
    Description: We analysed primary breast cancers by genomic DNA copy number arrays, DNA methylation, exome sequencing, messenger RNA arrays, microRNA sequencing and reverse-phase protein arrays. Our ability to integrate information across platforms provided key insights into previously defined gene expression subtypes and demonstrated the existence of four main breast cancer classes when combining data from five platforms, each of which shows significant molecular heterogeneity. Somatic mutations in only three genes (TP53, PIK3CA and GATA3) occurred at 〉10% incidence across all breast cancers; however, there were numerous subtype-associated and novel gene mutations including the enrichment of specific mutations in GATA3, PIK3CA and MAP3K1 with the luminal A subtype. We identified two novel protein-expression-defined subgroups, possibly produced by stromal/microenvironmental elements, and integrated analyses identified specific signalling pathways dominant in each molecular subtype including a HER2/phosphorylated HER2/EGFR/phosphorylated EGFR signature within the HER2-enriched expression subtype. Comparison of basal-like breast tumours with high-grade serous ovarian tumours showed many molecular commonalities, indicating a related aetiology and similar therapeutic opportunities. The biological finding of the four main breast cancer subtypes caused by different subsets of genetic and epigenetic abnormalities raises the hypothesis that much of the clinically observable plasticity and heterogeneity occurs within, and not across, these major biological subtypes of breast cancer.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3465532/" 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/PMC3465532/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cancer Genome Atlas Network -- K08 CA148912/CA/NCI NIH HHS/ -- P30 CA016058/CA/NCI NIH HHS/ -- P30 CA016086/CA/NCI NIH HHS/ -- P30 CA016672/CA/NCI NIH HHS/ -- P50 CA058223/CA/NCI NIH HHS/ -- P50 CA116201/CA/NCI NIH HHS/ -- P50CA116201/CA/NCI NIH HHS/ -- P50CA58223/CA/NCI NIH HHS/ -- R01 LM009722/LM/NLM NIH HHS/ -- U01 CA084955/CA/NCI NIH HHS/ -- U24 CA143799/CA/NCI NIH HHS/ -- U24 CA143848/CA/NCI NIH HHS/ -- U24 CA143866/CA/NCI NIH HHS/ -- U24 CA143882/CA/NCI NIH HHS/ -- U24CA143799/CA/NCI NIH HHS/ -- U24CA143835/CA/NCI NIH HHS/ -- U24CA143840/CA/NCI NIH HHS/ -- U24CA143845/CA/NCI NIH HHS/ -- U24CA143848/CA/NCI NIH HHS/ -- U24CA143858/CA/NCI NIH HHS/ -- U24CA143866/CA/NCI NIH HHS/ -- U24CA143867/CA/NCI NIH HHS/ -- U24CA143882/CA/NCI NIH HHS/ -- U24CA143883/CA/NCI NIH HHS/ -- U24CA144025/CA/NCI NIH HHS/ -- U54 HG004028/HG/NHGRI NIH HHS/ -- U54HG003079/HG/NHGRI NIH HHS/ -- England -- Nature. 2012 Oct 4;490(7418):61-70. doi: 10.1038/nature11412. Epub 2012 Sep 23.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23000897" target="_blank"〉PubMed〈/a〉
    Keywords: Breast Neoplasms/classification/*genetics/metabolism/*pathology ; DNA Copy Number Variations/genetics ; DNA Methylation ; DNA Mutational Analysis ; Exome/genetics ; Female ; GATA3 Transcription Factor/genetics ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Genes, BRCA1 ; Genes, Neoplasm/*genetics ; Genes, erbB-2/genetics ; Genes, p53/genetics ; *Genetic Heterogeneity ; Genome, Human/genetics ; Genomics ; Humans ; MAP Kinase Kinase Kinase 1/genetics ; MicroRNAs/genetics ; Mutation/*genetics ; Oligonucleotide Array Sequence Analysis ; Ovarian Neoplasms/genetics/pathology ; Phosphatidylinositol 3-Kinases/genetics ; Protein Array Analysis ; Proteomics ; RNA, Messenger/genetics ; RNA, Neoplasm/genetics ; Receptors, Estrogen/metabolism ; Retinoblastoma Protein/genetics/metabolism
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    Extended leaf phenology and the autumn niche in deciduous forest invasions (2012)
    Nature Publishing Group (NPG)
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    Publication Date: 2012-04-27
    Description: The phenology of growth in temperate deciduous forests, including the timing of leaf emergence and senescence, has strong control over ecosystem properties such as productivity and nutrient cycling, and has an important role in the carbon economy of understory plants. Extended leaf phenology, whereby understory species assimilate carbon in early spring before canopy closure or in late autumn after canopy fall, has been identified as a key feature of many forest species invasions, but it remains unclear whether there are systematic differences in the growth phenology of native and invasive forest species or whether invaders are more responsive to warming trends that have lengthened the duration of spring or autumn growth. Here, in a 3-year monitoring study of 43 native and 30 non-native shrub and liana species common to deciduous forests in the eastern United States, I show that extended autumn leaf phenology is a common attribute of eastern US forest invasions, where non-native species are extending the autumn growing season by an average of 4 weeks compared with natives. In contrast, there was no consistent evidence that non-natives as a group show earlier spring growth phenology, and non-natives were not better able to track interannual variation in spring temperatures. Seasonal leaf production and photosynthetic data suggest that most non-native species capture a significant proportion of their annual carbon assimilate after canopy leaf fall, a behaviour that was virtually absent in natives and consistent across five phylogenetic groups. Pronounced differences in how native and non-native understory species use pre- and post-canopy environments suggest eastern US invaders are driving a seasonal redistribution of forest productivity that may rival climate change in its impact on forest processes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fridley, Jason D -- England -- Nature. 2012 May 17;485(7398):359-62. doi: 10.1038/nature11056.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Syracuse University, 107 College Place, Syracuse, New York 13244, USA. fridley@syr.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22535249" target="_blank"〉PubMed〈/a〉
    Keywords: Carbon/metabolism ; *Ecosystem ; *Introduced Species ; Photosynthesis ; Plant Leaves/classification/*growth & development ; *Seasons ; Temperature ; Time Factors ; Trees/classification/*growth & development ; United States
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    Reach and grasp by people with tetraplegia using a neurally controlled robotic arm (2012)
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    Publication Date: 2012-05-19
    Description: Paralysis following spinal cord injury, brainstem stroke, amyotrophic lateral sclerosis and other disorders can disconnect the brain from the body, eliminating the ability to perform volitional movements. A neural interface system could restore mobility and independence for people with paralysis by translating neuronal activity directly into control signals for assistive devices. We have previously shown that people with long-standing tetraplegia can use a neural interface system to move and click a computer cursor and to control physical devices. Able-bodied monkeys have used a neural interface system to control a robotic arm, but it is unknown whether people with profound upper extremity paralysis or limb loss could use cortical neuronal ensemble signals to direct useful arm actions. Here we demonstrate the ability of two people with long-standing tetraplegia to use neural interface system-based control of a robotic arm to perform three-dimensional reach and grasp movements. Participants controlled the arm and hand over a broad space without explicit training, using signals decoded from a small, local population of motor cortex (MI) neurons recorded from a 96-channel microelectrode array. One of the study participants, implanted with the sensor 5 years earlier, also used a robotic arm to drink coffee from a bottle. Although robotic reach and grasp actions were not as fast or accurate as those of an able-bodied person, our results demonstrate the feasibility for people with tetraplegia, years after injury to the central nervous system, to recreate useful multidimensional control of complex devices directly from a small sample of neural signals.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3640850/" 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/PMC3640850/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hochberg, Leigh R -- Bacher, Daniel -- Jarosiewicz, Beata -- Masse, Nicolas Y -- Simeral, John D -- Vogel, Joern -- Haddadin, Sami -- Liu, Jie -- Cash, Sydney S -- van der Smagt, Patrick -- Donoghue, John P -- HHSN275201100018C/HD/NICHD NIH HHS/ -- N01 HD053403/HD/NICHD NIH HHS/ -- N01HD10018/HD/NICHD NIH HHS/ -- N01HD53403/HD/NICHD NIH HHS/ -- NS25074/NS/NINDS NIH HHS/ -- R01 DC009899/DC/NIDCD NIH HHS/ -- R01 DC009899-02/DC/NIDCD NIH HHS/ -- R01 EB007401/EB/NIBIB NIH HHS/ -- R01 EB007401-05/EB/NIBIB NIH HHS/ -- R01DC009899/DC/NIDCD NIH HHS/ -- R01EB007401/EB/NIBIB NIH HHS/ -- R56 NS025074/NS/NINDS NIH HHS/ -- R56 NS025074-23/NS/NINDS NIH HHS/ -- RC1 HD063931/HD/NICHD NIH HHS/ -- RC1 HD063931-02/HD/NICHD NIH HHS/ -- RC1HD063931/HD/NICHD NIH HHS/ -- England -- Nature. 2012 May 16;485(7398):372-5. doi: 10.1038/nature11076.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Rehabilitation Research & Development Service, Department of Veterans Affairs, Providence, Rhode Island 02908, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22596161" target="_blank"〉PubMed〈/a〉
    Keywords: Aged ; Arm/*physiology ; Calibration ; Drinking/physiology ; Female ; Hand/physiology ; Hand Strength/*physiology ; Humans ; Male ; *Man-Machine Systems ; Microelectrodes ; Middle Aged ; Motor Cortex/cytology/physiology ; Movement/*physiology ; Psychomotor Performance ; Quadriplegia/*physiopathology ; Robotics/*instrumentation/*methods ; Time Factors
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    Control of a Salmonella virulence locus by an ATP-sensing leader messenger RNA (2012)
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    Publication Date: 2012-06-16
    Description: The facultative intracellular pathogen Salmonella enterica resides within a membrane-bound compartment inside macrophages. This compartment must be acidified for Salmonella to survive within macrophages, possibly because acidic pH promotes expression of Salmonella virulence proteins. We reasoned that Salmonella might sense its surroundings have turned acidic not only upon protonation of the extracytoplasmic domain of a protein sensor but also by an increase in cytosolic ATP levels, because conditions that enhance the proton gradient across the bacterial inner membrane stimulate ATP synthesis. Here we report that an increase in cytosolic ATP promotes transcription of the coding region for the virulence gene mgtC, which is the most highly induced horizontally acquired gene when Salmonella is inside macrophages. This transcript is induced both upon media acidification and by physiological conditions that increase ATP levels independently of acidification. ATP is sensed by the coupling/uncoupling of transcription of the unusually long mgtC leader messenger RNA and translation of a short open reading frame located in this region. A mutation in the mgtC leader messenger RNA that eliminates the response to ATP hinders mgtC expression inside macrophages and attenuates Salmonella virulence in mice. Our results define a singular example of an ATP-sensing leader messenger RNA. Moreover, they indicate that pathogens can interpret extracellular cues by the impact they have on cellular metabolites.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3711680/" 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/PMC3711680/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, Eun-Jin -- Groisman, Eduardo A -- AI49561/AI/NIAID NIH HHS/ -- R01 AI049561/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2012 Jun 13;486(7402):271-5. doi: 10.1038/nature11090.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Yale School of Medicine, Section of Microbial Pathogenesis, New Haven, Connecticut 06536-0812, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22699622" target="_blank"〉PubMed〈/a〉
    Keywords: 5' Untranslated Regions/genetics/*physiology ; Adenosine Triphosphate/*metabolism ; Animals ; *Bacterial Proteins/genetics/metabolism ; Base Sequence ; *Cation Transport Proteins/genetics/metabolism ; Female ; Gene Expression Regulation, Bacterial ; Hydrogen-Ion Concentration ; Macrophages/microbiology ; Mice ; Mice, Inbred C3H ; Molecular Sequence Data ; Mutation/genetics ; Salmonella Infections/mortality/pathology ; Salmonella typhimurium/genetics/metabolism/*pathogenicity ; Sequence Alignment ; Virulence/*genetics
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    Wild flower blooms again after 30,000 years on ice (2012)
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    Publication Date: 2012-02-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Levy, Sharon -- England -- Nature. 2012 Feb 21;482(7386):454. doi: 10.1038/482454a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22358807" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cryopreservation ; *Ecosystem ; Extinction, Biological ; Flowers/*growth & development ; *Freezing ; Germination ; History, Ancient ; *Ice ; Sciuridae/physiology ; Seeds/growth & development ; Time Factors
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    Hsp72 preserves muscle function and slows progression of severe muscular dystrophy (2012)
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    Publication Date: 2012-04-13
    Description: Duchenne muscular dystrophy (DMD) is a severe and progressive muscle wasting disorder caused by mutations in the dystrophin gene that result in the absence of the membrane-stabilizing protein dystrophin. Dystrophin-deficient muscle fibres are fragile and susceptible to an influx of Ca(2+), which activates inflammatory and muscle degenerative pathways. At present there is no cure for DMD, and existing therapies are ineffective. Here we show that increasing the expression of intramuscular heat shock protein 72 (Hsp72) preserves muscle strength and ameliorates the dystrophic pathology in two mouse models of muscular dystrophy. Treatment with BGP-15 (a pharmacological inducer of Hsp72 currently in clinical trials for diabetes) improved muscle architecture, strength and contractile function in severely affected diaphragm muscles in mdx dystrophic mice. In dko mice, a phenocopy of DMD that results in severe spinal curvature (kyphosis), muscle weakness and premature death, BGP-15 decreased kyphosis, improved the dystrophic pathophysiology in limb and diaphragm muscles and extended lifespan. We found that the sarcoplasmic/endoplasmic reticulum Ca(2+)-ATPase (SERCA, the main protein responsible for the removal of intracellular Ca(2+)) is dysfunctional in severely affected muscles of mdx and dko mice, and that Hsp72 interacts with SERCA to preserve its function under conditions of stress, ultimately contributing to the decreased muscle degeneration seen with Hsp72 upregulation. Treatment with BGP-15 similarly increased SERCA activity in dystrophic skeletal muscles. Our results provide evidence that increasing the expression of Hsp72 in muscle (through the administration of BGP-15) has significant therapeutic potential for DMD and related conditions, either as a self-contained therapy or as an adjuvant with other potential treatments, including gene, cell and pharmacological therapies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gehrig, Stefan M -- van der Poel, Chris -- Sayer, Timothy A -- Schertzer, Jonathan D -- Henstridge, Darren C -- Church, Jarrod E -- Lamon, Severine -- Russell, Aaron P -- Davies, Kay E -- Febbraio, Mark A -- Lynch, Gordon S -- GTB07001/Telethon/Italy -- MC_U137761449/Medical Research Council/United Kingdom -- England -- Nature. 2012 Apr 4;484(7394):394-8. doi: 10.1038/nature10980.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Basic and Clinical Myology Laboratory, Department of Physiology, University of Melbourne, Victoria, 3010, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22495301" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium-Transporting ATPases/metabolism ; Diaphragm/drug effects/physiology ; Disease Models, Animal ; *Disease Progression ; Female ; Gene Expression Regulation/drug effects ; HSP72 Heat-Shock Proteins/biosynthesis/genetics/*metabolism ; Kyphosis/drug therapy ; Longevity/drug effects ; Male ; Mice ; Mice, Inbred mdx ; Mice, Transgenic ; Muscle, Skeletal/drug effects/*physiology/physiopathology ; Muscular Dystrophy, Duchenne/genetics/*metabolism/pathology/*physiopathology ; Oximes/pharmacology ; Piperidines/pharmacology ; Rats
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    Prenatal diagnostics: Fetal genes in mother's blood (2012)
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    Details
    Publication Date: 2012-07-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bianchi, Diana W -- England -- Nature. 2012 Jul 18;487(7407):304-5. doi: 10.1038/487304a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22810690" target="_blank"〉PubMed〈/a〉
    Keywords: DNA/*analysis ; Female ; *Genome, Human ; Humans ; Male ; Pregnancy ; Prenatal Diagnosis/*methods
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    Vision: Looking to develop sight (2012)
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    Publication Date: 2012-07-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Birch, Eileen -- R01 EY022313/EY/NEI NIH HHS/ -- England -- Nature. 2012 Jul 25;487(7408):441-2. doi: 10.1038/487441a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22836997" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cats ; Critical Period (Psychology) ; Dominance, Ocular/physiology ; Environment ; Humans ; Infant, Newborn ; Infant, Premature/growth & development/physiology ; Models, Neurological ; Photic Stimulation ; Primates/physiology ; Time Factors ; Vision, Binocular/*physiology ; Visual Cortex/*growth & development/*physiology ; Visual Pathways/embryology/growth & development/physiology
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    Genome-wide protein-DNA binding dynamics suggest a molecular clutch for transcription factor function (2012)
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    Publication Date: 2012-04-14
    Description: Dynamic access to genetic information is central to organismal development and environmental response. Consequently, genomic processes must be regulated by mechanisms that alter genome function relatively rapidly. Conventional chromatin immunoprecipitation (ChIP) experiments measure transcription factor occupancy, but give no indication of kinetics and are poor predictors of transcription factor function at a given locus. To measure transcription-factor-binding dynamics across the genome, we performed competition ChIP (refs 6, 7) with a sequence-specific Saccharomyces cerevisiae transcription factor, Rap1 (ref. 8). Rap1-binding dynamics and Rap1 occupancy were only weakly correlated (R(2) = 0.14), but binding dynamics were more strongly linked to function than occupancy. Long Rap1 residence was coupled to transcriptional activation, whereas fast binding turnover, which we refer to as 'treadmilling', was linked to low transcriptional output. Thus, DNA-binding events that seem identical by conventional ChIP may have different underlying modes of interaction that lead to opposing functional outcomes. We propose that transcription factor binding turnover is a major point of regulation in determining the functional consequences of transcription factor binding, and is mediated mainly by control of competition between transcription factors and nucleosomes. Our model predicts a clutch-like mechanism that rapidly engages a treadmilling transcription factor into a stable binding state, or vice versa, to modulate transcription factor function.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3341663/" 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/PMC3341663/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lickwar, Colin R -- Mueller, Florian -- Hanlon, Sean E -- McNally, James G -- Lieb, Jason D -- R01 GM072518/GM/NIGMS NIH HHS/ -- R01 GM072518-05/GM/NIGMS NIH HHS/ -- R01-GM072518/GM/NIGMS NIH HHS/ -- Intramural NIH HHS/ -- England -- Nature. 2012 Apr 11;484(7393):251-5. doi: 10.1038/nature10985.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599-3280, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22498630" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Binding Sites ; Binding, Competitive ; Chromatin Immunoprecipitation ; DNA, Fungal/genetics/*metabolism ; Gene Expression Regulation, Fungal ; *Genome, Fungal ; Histone Acetyltransferases/metabolism ; *Models, Biological ; Nucleosomes/genetics/metabolism ; Protein Binding ; RNA Polymerase II/metabolism ; RNA, Messenger/biosynthesis/genetics ; Saccharomyces cerevisiae/classification/*genetics/*metabolism ; Saccharomyces cerevisiae Proteins/*metabolism ; Telomere-Binding Proteins/*metabolism ; Time Factors ; Transcription Factors/*metabolism
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    Strict evolutionary conservation followed rapid gene loss on human and rhesus Y chromosomes (2012)
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    Publication Date: 2012-03-01
    Description: The human X and Y chromosomes evolved from an ordinary pair of autosomes during the past 200-300 million years. The human MSY (male-specific region of Y chromosome) retains only three percent of the ancestral autosomes' genes owing to genetic decay. This evolutionary decay was driven by a series of five 'stratification' events. Each event suppressed X-Y crossing over within a chromosome segment or 'stratum', incorporated that segment into the MSY and subjected its genes to the erosive forces that attend the absence of crossing over. The last of these events occurred 30 million years ago, 5 million years before the human and Old World monkey lineages diverged. Although speculation abounds regarding ongoing decay and looming extinction of the human Y chromosome, remarkably little is known about how many MSY genes were lost in the human lineage in the 25 million years that have followed its separation from the Old World monkey lineage. To investigate this question, we sequenced the MSY of the rhesus macaque, an Old World monkey, and compared it to the human MSY. We discovered that during the last 25 million years MSY gene loss in the human lineage was limited to the youngest stratum (stratum 5), which comprises three percent of the human MSY. In the older strata, which collectively comprise the bulk of the human MSY, gene loss evidently ceased more than 25 million years ago. Likewise, the rhesus MSY has not lost any older genes (from strata 1-4) during the past 25 million years, despite its major structural differences to the human MSY. The rhesus MSY is simpler, with few amplified gene families or palindromes that might enable intrachromosomal recombination and repair. We present an empirical reconstruction of human MSY evolution in which each stratum transitioned from rapid, exponential loss of ancestral genes to strict conservation through purifying selection.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3292678/" 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/PMC3292678/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hughes, Jennifer F -- Skaletsky, Helen -- Brown, Laura G -- Pyntikova, Tatyana -- Graves, Tina -- Fulton, Robert S -- Dugan, Shannon -- Ding, Yan -- Buhay, Christian J -- Kremitzki, Colin -- Wang, Qiaoyan -- Shen, Hua -- Holder, Michael -- Villasana, Donna -- Nazareth, Lynne V -- Cree, Andrew -- Courtney, Laura -- Veizer, Joelle -- Kotkiewicz, Holland -- Cho, Ting-Jan -- Koutseva, Natalia -- Rozen, Steve -- Muzny, Donna M -- Warren, Wesley C -- Gibbs, Richard A -- Wilson, Richard K -- Page, David C -- R01 HG000257/HG/NHGRI NIH HHS/ -- R01 HG000257-17/HG/NHGRI NIH HHS/ -- U54 HG003273/HG/NHGRI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2012 Feb 22;483(7387):82-6. doi: 10.1038/nature10843.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Biology, Massachusetts Institute of Technology, 9 Cambridge Center, Cambridge, Massachusetts 02142, USA. jhughes@wi.mit.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22367542" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromosomes, Human, Y/*genetics ; Conserved Sequence/*genetics ; Crossing Over, Genetic/genetics ; *Evolution, Molecular ; Gene Amplification/genetics ; *Gene Deletion ; Humans ; In Situ Hybridization, Fluorescence ; Macaca mulatta/*genetics ; Male ; Models, Genetic ; Molecular Sequence Data ; Pan troglodytes/genetics ; Radiation Hybrid Mapping ; Selection, Genetic/genetics ; Time Factors ; Y Chromosome/*genetics
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    Neuroscience: Genes and human brain evolution (2012)
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    Publication Date: 2012-06-23
    Description: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3636765/" 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/PMC3636765/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Geschwind, Daniel H -- Konopka, Genevieve -- R00 MH090238/MH/NIMH NIH HHS/ -- R37 MH060233/MH/NIMH NIH HHS/ -- England -- Nature. 2012 Jun 28;486(7404):481-2. doi: 10.1038/nature11380.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22722844" target="_blank"〉PubMed〈/a〉
    Keywords: *Biological Evolution ; Brain/*anatomy & histology/*metabolism ; Evolution, Molecular ; Female ; GTPase-Activating Proteins/*genetics ; Gene Duplication/genetics ; Genes, Duplicate/*genetics ; Humans ; Hydatidiform Mole/genetics ; Male ; Pregnancy
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    Translational medicine: Double protection for weakened bones (2012)
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    Publication Date: 2012-05-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zaidi, Mone -- Iqbal, Jameel -- England -- Nature. 2012 May 2;485(7396):47-8. doi: 10.1038/485047a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22552091" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Bone Resorption ; *Cytoprotection ; Female ; Male ; Osteoblasts/*cytology ; Osteoclasts/*cytology ; *Osteogenesis ; Semaphorin-3A/*metabolism
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    Glycolytic oligodendrocytes maintain myelin and long-term axonal integrity (2012)
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    Publication Date: 2012-05-25
    Description: Oligodendrocytes, the myelin-forming glial cells of the central nervous system, maintain long-term axonal integrity. However, the underlying support mechanisms are not understood. Here we identify a metabolic component of axon-glia interactions by generating conditional Cox10 (protoheme IX farnesyltransferase) mutant mice, in which oligodendrocytes and Schwann cells fail to assemble stable mitochondrial cytochrome c oxidase (COX, also known as mitochondrial complex IV). In the peripheral nervous system, Cox10 conditional mutants exhibit severe neuropathy with dysmyelination, abnormal Remak bundles, muscle atrophy and paralysis. Notably, perturbing mitochondrial respiration did not cause glial cell death. In the adult central nervous system, we found no signs of demyelination, axonal degeneration or secondary inflammation. Unlike cultured oligodendrocytes, which are sensitive to COX inhibitors, post-myelination oligodendrocytes survive well in the absence of COX activity. More importantly, by in vivo magnetic resonance spectroscopy, brain lactate concentrations in mutants were increased compared with controls, but were detectable only in mice exposed to volatile anaesthetics. This indicates that aerobic glycolysis products derived from oligodendrocytes are rapidly metabolized within white matter tracts. Because myelinated axons can use lactate when energy-deprived, our findings suggest a model in which axon-glia metabolic coupling serves a physiological function.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3613737/" 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/PMC3613737/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Funfschilling, Ursula -- Supplie, Lotti M -- Mahad, Don -- Boretius, Susann -- Saab, Aiman S -- Edgar, Julia -- Brinkmann, Bastian G -- Kassmann, Celia M -- Tzvetanova, Iva D -- Mobius, Wiebke -- Diaz, Francisca -- Meijer, Dies -- Suter, Ueli -- Hamprecht, Bernd -- Sereda, Michael W -- Moraes, Carlos T -- Frahm, Jens -- Goebbels, Sandra -- Nave, Klaus-Armin -- 078415/Wellcome Trust/United Kingdom -- England -- Nature. 2012 Apr 29;485(7399):517-21. doi: 10.1038/nature11007.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max Planck Institute of Experimental Medicine, Department of Neurogenetics, Hermann-Rein-Strasse 3, D-37075 Gottingen, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22622581" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Alkyl and Aryl Transferases/deficiency/genetics/metabolism ; Animals ; Axons/*physiology ; Brain/cytology/metabolism ; Cell Respiration ; Cell Survival ; Demyelinating Diseases/enzymology/genetics/metabolism/pathology ; Electron Transport Complex IV/antagonists & inhibitors/genetics/metabolism ; *Glycolysis ; Lactic Acid/metabolism ; Magnetic Resonance Spectroscopy ; Membrane Proteins/deficiency/genetics/metabolism ; Mice ; Mitochondria/enzymology/genetics/metabolism/pathology ; Mutant Proteins/genetics/metabolism ; Myelin Sheath/*metabolism ; Oligodendroglia/cytology/drug effects/enzymology/*metabolism ; Protons ; Schwann Cells/enzymology/metabolism ; Time Factors
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    The let-7-Imp axis regulates ageing of the Drosophila testis stem-cell niche (2012)
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    Publication Date: 2012-06-05
    Description: Adult stem cells support tissue homeostasis and repair throughout the life of an individual. During ageing, numerous intrinsic and extrinsic changes occur that result in altered stem-cell behaviour and reduced tissue maintenance and regeneration. In the Drosophila testis, ageing results in a marked decrease in the self-renewal factor Unpaired (Upd), leading to a concomitant loss of germline stem cells. Here we demonstrate that IGF-II messenger RNA binding protein (Imp) counteracts endogenous small interfering RNAs to stabilize upd (also known as os) RNA. However, similar to upd, Imp expression decreases in the hub cells of older males, which is due to the targeting of Imp by the heterochronic microRNA let-7. In the absence of Imp, upd mRNA therefore becomes unprotected and susceptible to degradation. Understanding the mechanistic basis for ageing-related changes in stem-cell behaviour will lead to the development of strategies to treat age-onset diseases and facilitate stem-cell-based therapies in older individuals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Toledano, Hila -- D'Alterio, Cecilia -- Czech, Benjamin -- Levine, Erel -- Jones, D Leanne -- R01 AG028092/AG/NIA NIH HHS/ -- R01 AG040288/AG/NIA NIH HHS/ -- England -- Nature. 2012 May 23;485(7400):605-10. doi: 10.1038/nature11061.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Genetics, The Salk Institute for Biological Studies, La Jolla, California 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22660319" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Argonaute Proteins/metabolism ; Base Sequence ; Cell Aging/*physiology ; Drosophila Proteins/biosynthesis/genetics/*metabolism ; Drosophila melanogaster/*cytology/genetics/*metabolism ; Female ; Male ; MicroRNAs/*genetics ; Organ Specificity ; RNA Helicases/metabolism ; RNA, Messenger/genetics/metabolism ; RNA, Small Interfering/antagonists & inhibitors/genetics/metabolism ; RNA-Binding Proteins/biosynthesis/genetics/*metabolism ; Ribonuclease III/metabolism ; Stem Cell Niche/genetics/*physiology ; Testis/*cytology ; Transcription Factors/genetics/metabolism
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    Keith H. Campbell (1954-2012) (2012)
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    Publication Date: 2012-11-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Trounson, Alan -- England -- Nature. 2012 Nov 8;491(7423):193. doi: 10.1038/491193a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉California Institute for Regenerative Medicine, San Francisco, California 94107, USA. atrounson@cirm.ca.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23135461" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Awards and Prizes ; Cellular Reprogramming ; Cloning, Organism/*history ; Embryonic Stem Cells/physiology ; Female ; Great Britain ; History, 20th Century ; Induced Pluripotent Stem Cells/physiology ; Sheep ; Swine
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    Autistic-like behaviour and cerebellar dysfunction in Purkinje cell Tsc1 mutant mice (2012)
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    Publication Date: 2012-07-06
    Description: Autism spectrum disorders (ASDs) are highly prevalent neurodevelopmental disorders, but the underlying pathogenesis remains poorly understood. Recent studies have implicated the cerebellum in these disorders, with post-mortem studies in ASD patients showing cerebellar Purkinje cell (PC) loss, and isolated cerebellar injury has been associated with a higher incidence of ASDs. However, the extent of cerebellar contribution to the pathogenesis of ASDs remains unclear. Tuberous sclerosis complex (TSC) is a genetic disorder with high rates of comorbid ASDs that result from mutation of either TSC1 or TSC2, whose protein products dimerize and negatively regulate mammalian target of rapamycin (mTOR) signalling. TSC is an intriguing model to investigate the cerebellar contribution to the underlying pathogenesis of ASDs, as recent studies in TSC patients demonstrate cerebellar pathology and correlate cerebellar pathology with increased ASD symptomatology. Functional imaging also shows that TSC patients with ASDs display hypermetabolism in deep cerebellar structures, compared to TSC patients without ASDs. However, the roles of Tsc1 and the sequelae of Tsc1 dysfunction in the cerebellum have not been investigated so far. Here we show that both heterozygous and homozygous loss of Tsc1 in mouse cerebellar PCs results in autistic-like behaviours, including abnormal social interaction, repetitive behaviour and vocalizations, in addition to decreased PC excitability. Treatment of mutant mice with the mTOR inhibitor, rapamycin, prevented the pathological and behavioural deficits. These findings demonstrate new roles for Tsc1 in PC function and define a molecular basis for a cerebellar contribution to cognitive disorders such as autism.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3615424/" 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/PMC3615424/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tsai, Peter T -- Hull, Court -- Chu, YunXiang -- Greene-Colozzi, Emily -- Sadowski, Abbey R -- Leech, Jarrett M -- Steinberg, Jason -- Crawley, Jacqueline N -- Regehr, Wade G -- Sahin, Mustafa -- K12 NS079414/NS/NINDS NIH HHS/ -- P30HD18655/HD/NICHD NIH HHS/ -- R01 NS032405/NS/NINDS NIH HHS/ -- R01NS032405/NS/NINDS NIH HHS/ -- R01NS58956/NS/NINDS NIH HHS/ -- T32 MH020017/MH/NIMH NIH HHS/ -- T32 NS007473/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- Intramural NIH HHS/ -- England -- Nature. 2012 Aug 30;488(7413):647-51. doi: 10.1038/nature11310.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The F.M. Kirby Neurobiology Center, Department of Neurology, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA. peter.tsai@childrens.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22763451" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autistic Disorder/complications/genetics/pathology/*physiopathology ; Behavior, Animal/drug effects ; Cell Count ; Cell Shape/drug effects ; Cerebellum/drug effects/pathology/*physiopathology ; Grooming/drug effects/physiology ; Heterozygote ; Maze Learning/drug effects/physiology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mutation/genetics ; Purkinje Cells/drug effects/*metabolism ; Rotarod Performance Test ; Sirolimus/pharmacology ; Synapses/metabolism ; TOR Serine-Threonine Kinases/antagonists & inhibitors/metabolism ; Tuberous Sclerosis/complications/genetics ; Tumor Suppressor Proteins/deficiency/*genetics/*metabolism ; Vocalization, Animal/drug effects/physiology
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    A FOXO3-IRF7 gene regulatory circuit limits inflammatory sequelae of antiviral responses (2012)
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    Publication Date: 2012-09-18
    Description: Antiviral responses must be tightly regulated to defend rapidly against infection while minimizing inflammatory damage. Type 1 interferons (IFN-I) are crucial mediators of antiviral responses and their transcription is regulated by a variety of transcription factors; principal among these is the family of interferon regulatory factors (IRFs). The IRF gene regulatory networks are complex and contain multiple feedback loops. The tools of systems biology are well suited to elucidate the complex interactions that give rise to precise coordination of the interferon response. Here we have used an unbiased systems approach to predict that a member of the forkhead family of transcription factors, FOXO3, is a negative regulator of a subset of antiviral genes. This prediction was validated using macrophages isolated from Foxo3-null mice. Genome-wide location analysis combined with gene deletion studies identified the Irf7 gene as a critical target of FOXO3. FOXO3 was identified as a negative regulator of Irf7 transcription and we have further demonstrated that FOXO3, IRF7 and IFN-I form a coherent feed-forward regulatory circuit. Our data suggest that the FOXO3-IRF7 regulatory circuit represents a novel mechanism for establishing the requisite set points in the interferon pathway that balances the beneficial effects and deleterious sequelae of the antiviral response.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3556990/" 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/PMC3556990/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Litvak, Vladimir -- Ratushny, Alexander V -- Lampano, Aaron E -- Schmitz, Frank -- Huang, Albert C -- Raman, Ayush -- Rust, Alistair G -- Bergthaler, Andreas -- Aitchison, John D -- Aderem, Alan -- HHSN272200700038C/AI/NIAID NIH HHS/ -- HHSN272200700038C/PHS HHS/ -- HHSN272200800058C/AI/NIAID NIH HHS/ -- HSN272200800058C/PHS HHS/ -- R01 AI025032/AI/NIAID NIH HHS/ -- R01 AI032972/AI/NIAID NIH HHS/ -- R01AI025032/AI/NIAID NIH HHS/ -- R01AI032972/AI/NIAID NIH HHS/ -- U19 AI100627/AI/NIAID NIH HHS/ -- U54 GM103511/GM/NIGMS NIH HHS/ -- U54 RR022220/RR/NCRR NIH HHS/ -- U54GM103511/GM/NIGMS NIH HHS/ -- England -- Nature. 2012 Oct 18;490(7420):421-5. doi: 10.1038/nature11428. Epub 2012 Sep 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Seattle Biomedical Research Institute, Seattle, Washington 98109, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22982991" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Female ; Forkhead Transcription Factors/deficiency/genetics/*metabolism ; Gene Deletion ; Gene Expression Regulation/*immunology ; Inflammation/genetics/*immunology/*pathology ; Interferon Regulatory Factor-7/deficiency/genetics/*metabolism ; Interferon Type I/immunology ; Lung/immunology/pathology/virology ; Macrophages/immunology ; Mice ; Mice, Inbred C57BL ; Reproducibility of Results ; Vesiculovirus/*immunology
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    Novel Foxo1-dependent transcriptional programs control T(reg) cell function (2012)
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    Publication Date: 2012-11-09
    Description: Regulatory T (T(reg)) cells, characterized by expression of the transcription factor forkhead box P3 (Foxp3), maintain immune homeostasis by suppressing self-destructive immune responses. Foxp3 operates as a late-acting differentiation factor controlling T(reg) cell homeostasis and function, whereas the early T(reg)-cell-lineage commitment is regulated by the Akt kinase and the forkhead box O (Foxo) family of transcription factors. However, whether Foxo proteins act beyond the T(reg)-cell-commitment stage to control T(reg) cell homeostasis and function remains largely unexplored. Here we show that Foxo1 is a pivotal regulator of T(reg )cell function. T(reg) cells express high amounts of Foxo1 and display reduced T-cell-receptor-induced Akt activation, Foxo1 phosphorylation and Foxo1 nuclear exclusion. Mice with T(reg)-cell-specific deletion of Foxo1 develop a fatal inflammatory disorder similar in severity to that seen in Foxp3-deficient mice, but without the loss of T(reg) cells. Genome-wide analysis of Foxo1 binding sites reveals ~300 Foxo1-bound target genes, including the pro-inflammatory cytokine Ifng, that do not seem to be directly regulated by Foxp3. These findings show that the evolutionarily ancient Akt-Foxo1 signalling module controls a novel genetic program indispensable for T(reg) cell function.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3771531/" 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/PMC3771531/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ouyang, Weiming -- Liao, Will -- Luo, Chong T -- Yin, Na -- Huse, Morgan -- Kim, Myoungjoo V -- Peng, Min -- Chan, Pamela -- Ma, Qian -- Mo, Yifan -- Meijer, Dies -- Zhao, Keji -- Rudensky, Alexander Y -- Atwal, Gurinder -- Zhang, Michael Q -- Li, Ming O -- HG001696/HG/NHGRI NIH HHS/ -- R01 HG001696/HG/NHGRI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2012 Nov 22;491(7425):554-9. doi: 10.1038/nature11581. Epub 2012 Nov 7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immunology Program, Memorial Sloan-Kettering Cancer Center, New York, New York 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23135404" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites ; Cell Nucleus/metabolism/pathology ; Female ; Forkhead Transcription Factors/*metabolism ; Gene Expression Regulation/genetics ; Genome/genetics ; Immune Tolerance/genetics/immunology ; Interferon-gamma/deficiency/genetics ; Male ; Mice ; Mice, Inbred C57BL ; Proto-Oncogene Proteins c-akt/metabolism ; Receptors, Antigen, T-Cell/immunology/metabolism ; Signal Transduction ; T-Lymphocytes, Regulatory/*immunology/*metabolism/pathology ; *Transcription, Genetic
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    Environmental science: The hidden costs of flexible fertility (2012)
    Nature Publishing Group (NPG)
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    Publication Date: 2012-05-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Owen, Richard -- Jobling, Susan -- England -- Nature. 2012 May 23;485(7399):441. doi: 10.1038/485441a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of Exeter Business School, Exeter EX4 4PU, UK. r.j.owen@exeter.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22622553" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Wild ; Aquatic Organisms/*drug effects ; Contraceptives, Oral, Hormonal/adverse effects/chemistry ; Disorders of Sex Development/*chemically induced ; Endocrine Disruptors/*adverse effects/analysis ; Environmental Monitoring/economics ; Environmental Policy/*economics ; Ethinyl Estradiol/*adverse effects/analysis ; Europe ; Female ; Fishes ; Fresh Water/chemistry ; Humans
    Print ISSN: 0028-0836
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    Drug-pollution law all washed up (2012)
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    Publication Date: 2012-11-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gilbert, Natasha -- England -- Nature. 2012 Nov 22;491(7425):503-4. doi: 10.1038/491503a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23172189" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aquatic Organisms/drug effects ; Disorders of Sex Development/chemically induced/epidemiology/*veterinary ; Endocrine Disruptors/*adverse effects/*isolation & purification/poisoning ; Environmental Restoration and Remediation/economics/*legislation & jurisprudence ; Ethinyl Estradiol/adverse effects/isolation & purification/poisoning ; European Union/economics ; Female ; Fishes/abnormalities ; Great Britain ; Male ; Rivers/chemistry ; Water Pollution/*adverse effects/economics/*legislation & jurisprudence ; Water Purification/economics/*legislation & jurisprudence/methods
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    The microRNA miR-34 modulates ageing and neurodegeneration in Drosophila (2012)
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    Publication Date: 2012-02-22
    Description: Human neurodegenerative diseases have the temporal hallmark of afflicting the elderly population. Ageing is one of the most prominent factors to influence disease onset and progression, yet little is known about the molecular pathways that connect these processes. To understand this connection it is necessary to identify the pathways that functionally integrate ageing, chronic maintenance of the brain and modulation of neurodegenerative disease. MicroRNAs (miRNA) are emerging as critical factors in gene regulation during development; however, their role in adult-onset, age-associated processes is only beginning to be revealed. Here we report that the conserved miRNA miR-34 regulates age-associated events and long-term brain integrity in Drosophila, providing a molecular link between ageing and neurodegeneration. Fly mir-34 expression exhibits adult-onset, brain-enriched and age-modulated characteristics. Whereas mir-34 loss triggers a gene profile of accelerated brain ageing, late-onset brain degeneration and a catastrophic decline in survival, mir-34 upregulation extends median lifespan and mitigates neurodegeneration induced by human pathogenic polyglutamine disease protein. Some of the age-associated effects of miR-34 require adult-onset translational repression of Eip74EF, an essential ETS domain transcription factor involved in steroid hormone pathways. Our studies indicate that miRNA-dependent pathways may have an impact on adult-onset, age-associated events by silencing developmental genes that later have a deleterious influence on adult life cycle and disease, and highlight fly miR-34 as a key miRNA with a role in this process.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3326599/" 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/PMC3326599/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liu, Nan -- Landreh, Michael -- Cao, Kajia -- Abe, Masashi -- Hendriks, Gert-Jan -- Kennerdell, Jason R -- Zhu, Yongqing -- Wang, Li-San -- Bonini, Nancy M -- AG010124/AG/NIA NIH HHS/ -- R01 NS043578/NS/NINDS NIH HHS/ -- R01 NS043578-05/NS/NINDS NIH HHS/ -- R01-NS043578/NS/NINDS NIH HHS/ -- RC2 AG036528/AG/NIA NIH HHS/ -- RC2 AG036528-01/AG/NIA NIH HHS/ -- RC2-AG036528-01/AG/NIA NIH HHS/ -- T32 AG000255/AG/NIA NIH HHS/ -- T32 AG000255-02/AG/NIA NIH HHS/ -- T32 AG00255/AG/NIA NIH HHS/ -- U01 AG032984/AG/NIA NIH HHS/ -- U01 AG032984-02/AG/NIA NIH HHS/ -- U01-AG-032984-02/AG/NIA NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2012 Feb 15;482(7386):519-23. doi: 10.1038/nature10810.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22343898" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/*genetics ; Animals ; Brain/metabolism/pathology ; *Disease Models, Animal ; Down-Regulation ; Drosophila Proteins/biosynthesis/genetics ; Drosophila melanogaster/*genetics/*physiology ; Female ; Gene Expression Regulation/*genetics ; Hot Temperature ; Humans ; Longevity/genetics ; Male ; MicroRNAs/*genetics ; Mutation ; Neurodegenerative Diseases/*genetics/pathology ; Protein Biosynthesis ; RNA, Messenger/analysis/genetics ; Survival Analysis ; Time Factors ; Transcription Factors/biosynthesis/genetics ; Up-Regulation
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    Optogenetic stimulation of a hippocampal engram activates fear memory recall (2012)
    Nature Publishing Group (NPG)
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    Publication Date: 2012-03-24
    Description: A specific memory is thought to be encoded by a sparse population of neurons. These neurons can be tagged during learning for subsequent identification and manipulation. Moreover, their ablation or inactivation results in reduced memory expression, suggesting their necessity in mnemonic processes. However, the question of sufficiency remains: it is unclear whether it is possible to elicit the behavioural output of a specific memory by directly activating a population of neurons that was active during learning. Here we show in mice that optogenetic reactivation of hippocampal neurons activated during fear conditioning is sufficient to induce freezing behaviour. We labelled a population of hippocampal dentate gyrus neurons activated during fear learning with channelrhodopsin-2 (ChR2) and later optically reactivated these neurons in a different context. The mice showed increased freezing only upon light stimulation, indicating light-induced fear memory recall. This freezing was not detected in non-fear-conditioned mice expressing ChR2 in a similar proportion of cells, nor in fear-conditioned mice with cells labelled by enhanced yellow fluorescent protein instead of ChR2. Finally, activation of cells labelled in a context not associated with fear did not evoke freezing in mice that were previously fear conditioned in a different context, suggesting that light-induced fear memory recall is context specific. Together, our findings indicate that activating a sparse but specific ensemble of hippocampal neurons that contribute to a memory engram is sufficient for the recall of that memory. Moreover, our experimental approach offers a general method of mapping cellular populations bearing memory engrams.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3331914/" 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/PMC3331914/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liu, Xu -- Ramirez, Steve -- Pang, Petti T -- Puryear, Corey B -- Govindarajan, Arvind -- Deisseroth, Karl -- Tonegawa, Susumu -- P50 MH058880/MH/NIMH NIH HHS/ -- P50 MH058880-10/MH/NIMH NIH HHS/ -- P50-MH58880/MH/NIMH NIH HHS/ -- R01 MH078821/MH/NIMH NIH HHS/ -- R01 MH078821-17/MH/NIMH NIH HHS/ -- R01-MH078821/MH/NIMH NIH HHS/ -- England -- Nature. 2012 Mar 22;484(7394):381-5. doi: 10.1038/nature11028.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉RIKEN-MIT Center for Neural Circuit Genetics at the Picower Institute for Learning and Memory, Department of Biology and Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22441246" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacterial Proteins/genetics/metabolism ; Conditioning (Psychology)/physiology/radiation effects ; Dentate Gyrus/cytology/physiology/radiation effects ; Fear/*physiology/*radiation effects ; Female ; Freezing Reaction, Cataleptic/physiology/radiation effects ; Gene Expression Regulation ; Hippocampus/cytology/*physiology/*radiation effects ; Light ; Luminescent Proteins/genetics/metabolism ; Male ; Mental Recall/*radiation effects ; Mice ; Mice, Transgenic ; Rhodopsin/genetics/metabolism
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    Error prone (2012)
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    Publication Date: 2012-07-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉England -- Nature. 2012 Jul 25;487(7408):406. doi: 10.1038/487406a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22836962" target="_blank"〉PubMed〈/a〉
    Keywords: *Artifacts ; Competitive Behavior ; Genome, Human/genetics ; Genomics/methods/*standards ; Humans ; Quality Control ; *Research Design/standards ; Time Factors
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    Multi-isotope imaging mass spectrometry reveals slow protein turnover in hair-cell stereocilia (2012)
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    Publication Date: 2012-01-17
    Description: Hair cells of the inner ear are not normally replaced during an animal's life, and must continually renew components of their various organelles. Among these are the stereocilia, each with a core of several hundred actin filaments that arise from their apical surfaces and that bear the mechanotransduction apparatus at their tips. Actin turnover in stereocilia has previously been studied by transfecting neonatal rat hair cells in culture with a beta-actin-GFP fusion, and evidence was found that actin is replaced, from the top down, in 2-3 days. Overexpression of the actin-binding protein espin causes elongation of stereocilia within 12-24 hours, also suggesting rapid regulation of stereocilia lengths. Similarly, the mechanosensory 'tip links' are replaced in 5-10 hours after cleavage in chicken and mammalian hair cells. In contrast, turnover in chick stereocilia in vivo is much slower. It might be that only certain components of stereocilia turn over quickly, that rapid turnover occurs only in neonatal animals, only in culture, or only in response to a challenge like breakage or actin overexpression. Here we quantify protein turnover by feeding animals with a (15)N-labelled precursor amino acid and using multi-isotope imaging mass spectrometry to measure appearance of new protein. Surprisingly, in adult frogs and mice and in neonatal mice, in vivo and in vitro, the stereocilia were remarkably stable, incorporating newly synthesized protein at 〈10% per day. Only stereocilia tips had rapid turnover and no treadmilling was observed. Other methods confirmed this: in hair cells expressing beta-actin-GFP we bleached fiducial lines across hair bundles, but they did not move in 6 days. When we stopped expression of beta- or gamma-actin with tamoxifen-inducible recombination, neither actin isoform left the stereocilia, except at the tips. Thus, rapid turnover in stereocilia occurs only at the tips and not by a treadmilling process.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3267870/" 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/PMC3267870/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Duan-Sun -- Piazza, Valeria -- Perrin, Benjamin J -- Rzadzinska, Agnieszka K -- Poczatek, J Collin -- Wang, Mei -- Prosser, Haydn M -- Ervasti, James M -- Corey, David P -- Lechene, Claude P -- 2P41RR0112553-12/RR/NCRR NIH HHS/ -- F32DC009539/DC/NIDCD NIH HHS/ -- P41EB001974/EB/NIBIB NIH HHS/ -- P41RR14579/RR/NCRR NIH HHS/ -- R01 AR042423/AR/NIAMS NIH HHS/ -- R01 AR042423-08/AR/NIAMS NIH HHS/ -- R01 AR049899/AR/NIAMS NIH HHS/ -- R01 DC000033/DC/NIDCD NIH HHS/ -- R01 DC002281/DC/NIDCD NIH HHS/ -- R01AR049899/AR/NIAMS NIH HHS/ -- R01D K58762/PHS HHS/ -- R01DC00033/DC/NIDCD NIH HHS/ -- R01DC02281/DC/NIDCD NIH HHS/ -- R01DC03463/DC/NIDCD NIH HHS/ -- R01DC04179/DC/NIDCD NIH HHS/ -- R01EY12963/EY/NEI NIH HHS/ -- R01GM47214/GM/NIGMS NIH HHS/ -- R37DK39773/DK/NIDDK NIH HHS/ -- WT079643/Wellcome Trust/United Kingdom -- Howard Hughes Medical Institute/ -- England -- Nature. 2012 Jan 15;481(7382):520-4. doi: 10.1038/nature10745.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Harvard Medical School and Howard Hughes Medical Institute, Boston, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22246323" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/metabolism ; Animals ; Animals, Newborn ; Bleaching Agents ; Chickens ; Epithelium/drug effects/metabolism ; Fiducial Markers ; Hair Cells, Auditory, Inner/*cytology ; Homologous Recombination/drug effects ; Mass Spectrometry/*methods ; Mice ; Mice, Inbred C57BL ; Proteins/*metabolism ; Rana catesbeiana ; Stereocilia/*metabolism ; Tamoxifen/pharmacology
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    Vaccination: A durable design (2012)
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    Publication Date: 2012-08-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sanderson, Katharine -- England -- Nature. 2012 Aug 30;488(7413):S7. doi: 10.1038/488S7a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22932439" target="_blank"〉PubMed〈/a〉
    Keywords: Antigens, Viral/immunology ; Developing Countries/economics/statistics & numerical data ; *Drug Design ; Drug Storage ; Female ; Human Papillomavirus Recombinant Vaccine Quadrivalent, Types 6, 11, 16, 18 ; Humans ; Immunization Schedule ; Immunotherapy, Active ; Papillomaviridae/classification/immunology/pathogenicity ; Papillomavirus Infections/epidemiology/immunology/*prevention & control/virology ; *Papillomavirus Vaccines/economics/immunology/supply & distribution/therapeutic ; use ; Uterine Cervical Neoplasms/epidemiology/immunology/*prevention & control/virology ; *Vaccination/economics
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    Combined pesticide exposure severely affects individual- and colony-level traits in bees (2012)
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    Publication Date: 2012-10-23
    Description: Reported widespread declines of wild and managed insect pollinators have serious consequences for global ecosystem services and agricultural production. Bees contribute approximately 80% of insect pollination, so it is important to understand and mitigate the causes of current declines in bee populations . Recent studies have implicated the role of pesticides in these declines, as exposure to these chemicals has been associated with changes in bee behaviour and reductions in colony queen production. However, the key link between changes in individual behaviour and the consequent impact at the colony level has not been shown. Social bee colonies depend on the collective performance of many individual workers. Thus, although field-level pesticide concentrations can have subtle or sublethal effects at the individual level, it is not known whether bee societies can buffer such effects or whether it results in a severe cumulative effect at the colony level. Furthermore, widespread agricultural intensification means that bees are exposed to numerous pesticides when foraging, yet the possible combinatorial effects of pesticide exposure have rarely been investigated. Here we show that chronic exposure of bumblebees to two pesticides (neonicotinoid and pyrethroid) at concentrations that could approximate field-level exposure impairs natural foraging behaviour and increases worker mortality leading to significant reductions in brood development and colony success. We found that worker foraging performance, particularly pollen collecting efficiency, was significantly reduced with observed knock-on effects for forager recruitment, worker losses and overall worker productivity. Moreover, we provide evidence that combinatorial exposure to pesticides increases the propensity of colonies to fail.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3495159/" 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/PMC3495159/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gill, Richard J -- Ramos-Rodriguez, Oscar -- Raine, Nigel E -- 094886/Wellcome Trust/United Kingdom -- BB/I000178/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- Biotechnology and Biological Sciences Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- England -- Nature. 2012 Nov 1;491(7422):105-8. doi: 10.1038/nature11585. Epub 2012 Oct 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Biological Sciences, Royal Holloway, University of London, Egham, Surrey, TW20 0EX, UK. richard.gill@rhul.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23086150" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bees/*drug effects/*physiology ; Behavior, Animal/*drug effects/physiology ; Feeding Behavior/drug effects ; Female ; Imidazoles/pharmacology ; Insecticides/*pharmacology ; Male ; Nitro Compounds/pharmacology ; Pollen/metabolism ; Pollination/drug effects ; Pyrethrins/pharmacology ; *Social Behavior ; Social Dominance ; Survival Analysis
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    Ageing: Sorting out the sirtuins (2012)
    Nature Publishing Group (NPG)
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    Publication Date: 2012-03-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lombard, David B -- Miller, Richard A -- R01 GM101171/GM/NIGMS NIH HHS/ -- England -- Nature. 2012 Mar 7;483(7388):166-7. doi: 10.1038/nature10950.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22367538" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Female ; Longevity/*physiology ; Male ; *Sex Characteristics ; Sirtuins/*metabolism
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    Regenerative medicine: Reprogramming the injured heart (2012)
    Nature Publishing Group (NPG)
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    Publication Date: 2012-06-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Palpant, Nathan J -- Murry, Charles E -- England -- Nature. 2012 May 31;485(7400):585-6. doi: 10.1038/485585a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22660313" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Transdifferentiation ; *Cellular Reprogramming ; Female ; Fibroblasts/*cytology ; Heart/*physiology ; Male ; Myocardial Infarction/*therapy ; Myocytes, Cardiac/*cytology/*physiology ; Regenerative Medicine/*methods ; Transcription Factors/*metabolism
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    Endospore abundance, microbial growth and necromass turnover in deep sub-seafloor sediment (2012)
    Nature Publishing Group (NPG)
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    Publication Date: 2012-03-20
    Description: Two decades of scientific ocean drilling have demonstrated widespread microbial life in deep sub-seafloor sediment, and surprisingly high microbial-cell numbers. Despite the ubiquity of life in the deep biosphere, the large community sizes and the low energy fluxes in this vast buried ecosystem are not yet understood. It is not known whether organisms of the deep biosphere are specifically adapted to extremely low energy fluxes or whether most of the observed cells are in a dormant, spore-like state. Here we apply a new approach--the D:L-amino-acid model--to quantify the distributions and turnover times of living microbial biomass, endospores and microbial necromass, as well as to determine their role in the sub-seafloor carbon budget. The approach combines sensitive analyses of unique bacterial markers (muramic acid and D-amino acids) and the bacterial endospore marker, dipicolinic acid, with racemization dynamics of stereo-isomeric amino acids. Endospores are as abundant as vegetative cells and microbial activity is extremely low, leading to microbial biomass turnover times of hundreds to thousands of years. We infer from model calculations that biomass production is sustained by organic carbon deposited from the surface photosynthetic world millions of years ago and that microbial necromass is recycled over timescales of hundreds of thousands of years.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lomstein, Bente Aa -- Langerhuus, Alice T -- D'Hondt, Steven -- Jorgensen, Bo B -- Spivack, Arthur J -- England -- Nature. 2012 Mar 18;484(7392):101-4. doi: 10.1038/nature10905.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Bioscience, Section for Microbiology, Aarhus University, Building 1540, Ny Munkegade 114, DK-8000 Aarhus C, Denmark. bente.lomstein@biology.au.dk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22425999" target="_blank"〉PubMed〈/a〉
    Keywords: Altitude ; Amino Acids/analysis/chemistry/metabolism ; Aquatic Organisms/chemistry/growth & development/*isolation & purification ; Archaea/chemistry/cytology/*growth & development/isolation & purification ; Bacteria/chemistry/cytology/*growth & development/isolation & purification ; Biomarkers/analysis ; *Biomass ; Carbon/metabolism ; Cell Wall/chemistry ; Geologic Sediments/*microbiology ; Muramic Acids/analysis ; Oceans and Seas ; Oxidation-Reduction ; Peru ; Photosynthesis ; Picolinic Acids/analysis ; Seawater/*microbiology ; Spores, Bacterial/chemistry/growth & development/isolation & purification ; Time Factors
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    Interventions: Live long and prosper (2012)
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    Publication Date: 2012-12-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bourzac, Katherine -- England -- Nature. 2012 Dec 6;492(7427):S18-20. doi: 10.1038/492S18a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23222670" target="_blank"〉PubMed〈/a〉
    Keywords: Age of Onset ; Aging/*drug effects/genetics/*physiology ; Animal Diseases/epidemiology/genetics/prevention & control ; Animals ; Biomedical Research ; *Caloric Restriction ; Cardiovascular Diseases/prevention & control ; Female ; Gene Expression Profiling ; Geriatrics/methods ; Humans ; Longevity/*drug effects/genetics/*physiology ; Macaca mulatta/physiology ; Male ; Mice ; Models, Animal ; Neoplasms/prevention & control ; Oligonucleotide Array Sequence Analysis ; Reproducibility of Results ; Sirolimus/adverse effects/analogs & derivatives/immunology/*pharmacology ; Sirtuins/deficiency/genetics/metabolism ; Somatomedins/genetics/metabolism ; Stilbenes/pharmacology ; TOR Serine-Threonine Kinases/metabolism
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    Climate policy: Deadline 2015 (2012)
    Nature Publishing Group (NPG)
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    Publication Date: 2012-01-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jacobs, Michael -- England -- Nature. 2012 Jan 11;481(7380):137-8. doi: 10.1038/481137a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Grantham Research Institute on Climate Change and the Environment, London School of Economics and Political Science, London WC2A 2AE, UK. m.u.jacobs@lse.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22237091" target="_blank"〉PubMed〈/a〉
    Keywords: *Climate Change ; Congresses as Topic/trends ; Environmental Policy/*legislation & jurisprudence ; Federal Government ; *International Cooperation ; Time Factors ; United Nations
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    The translational landscape of mTOR signalling steers cancer initiation and metastasis (2012)
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    Publication Date: 2012-03-01
    Description: The mammalian target of rapamycin (mTOR) kinase is a master regulator of protein synthesis that couples nutrient sensing to cell growth and cancer. However, the downstream translationally regulated nodes of gene expression that may direct cancer development are poorly characterized. Using ribosome profiling, we uncover specialized translation of the prostate cancer genome by oncogenic mTOR signalling, revealing a remarkably specific repertoire of genes involved in cell proliferation, metabolism and invasion. We extend these findings by functionally characterizing a class of translationally controlled pro-invasion messenger RNAs that we show direct prostate cancer invasion and metastasis downstream of oncogenic mTOR signalling. Furthermore, we develop a clinically relevant ATP site inhibitor of mTOR, INK128, which reprograms this gene expression signature with therapeutic benefit for prostate cancer metastasis, for which there is presently no cure. Together, these findings extend our understanding of how the 'cancerous' translation machinery steers specific cancer cell behaviours, including metastasis, and may be therapeutically targeted.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3663483/" 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/PMC3663483/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hsieh, Andrew C -- Liu, Yi -- Edlind, Merritt P -- Ingolia, Nicholas T -- Janes, Matthew R -- Sher, Annie -- Shi, Evan Y -- Stumpf, Craig R -- Christensen, Carly -- Bonham, Michael J -- Wang, Shunyou -- Ren, Pingda -- Martin, Michael -- Jessen, Katti -- Feldman, Morris E -- Weissman, Jonathan S -- Shokat, Kevan M -- Rommel, Christian -- Ruggero, Davide -- R01 CA140456/CA/NCI NIH HHS/ -- R01 CA154916/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2012 Feb 22;485(7396):55-61. doi: 10.1038/nature10912.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Medicine and Department of Urology, Helen Diller Family Comprehensive Cancer Center, 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/22367541" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing/metabolism ; Animals ; Benzoxazoles/pharmacology ; Cell Line, Tumor ; Cell Movement/drug effects/genetics ; Eukaryotic Initiation Factor-4E/metabolism ; Eukaryotic Initiation Factors/metabolism ; Gene Expression Regulation, Neoplastic/drug effects/genetics ; Genome/genetics ; Humans ; Male ; Mice ; Mice, Inbred C57BL ; Neoplasm Invasiveness/genetics ; *Neoplasm Metastasis/drug therapy/genetics ; Phosphoproteins/metabolism ; Prostatic Neoplasms/drug therapy/genetics/*pathology ; *Protein Biosynthesis ; Pyrimidines/pharmacology ; RNA, Messenger/genetics/metabolism ; Repressor Proteins/metabolism ; *Signal Transduction ; TOR Serine-Threonine Kinases/antagonists & inhibitors/*metabolism
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    Automated design of ligands to polypharmacological profiles (2012)
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    Publication Date: 2012-12-14
    Description: The clinical efficacy and safety of a drug is determined by its activity profile across many proteins in the proteome. However, designing drugs with a specific multi-target profile is both complex and difficult. Therefore methods to design drugs rationally a priori against profiles of several proteins would have immense value in drug discovery. Here we describe a new approach for the automated design of ligands against profiles of multiple drug targets. The method is demonstrated by the evolution of an approved acetylcholinesterase inhibitor drug into brain-penetrable ligands with either specific polypharmacology or exquisite selectivity profiles for G-protein-coupled receptors. Overall, 800 ligand-target predictions of prospectively designed ligands were tested experimentally, of which 75% were confirmed to be correct. We also demonstrate target engagement in vivo. The approach can be a useful source of drug leads when multi-target profiles are required to achieve either selectivity over other drug targets or a desired polypharmacology.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3653568/" 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/PMC3653568/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Besnard, Jeremy -- Ruda, Gian Filippo -- Setola, Vincent -- Abecassis, Keren -- Rodriguiz, Ramona M -- Huang, Xi-Ping -- Norval, Suzanne -- Sassano, Maria F -- Shin, Antony I -- Webster, Lauren A -- Simeons, Frederick R C -- Stojanovski, Laste -- Prat, Annik -- Seidah, Nabil G -- Constam, Daniel B -- Bickerton, G Richard -- Read, Kevin D -- Wetsel, William C -- Gilbert, Ian H -- Roth, Bryan L -- Hopkins, Andrew L -- 083481/Wellcome Trust/United Kingdom -- BB/FOF/PF/15/09/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/J010510/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- MH082441/MH/NIMH NIH HHS/ -- R01 DA017204/DA/NIDA NIH HHS/ -- R01 MH061887/MH/NIMH NIH HHS/ -- U19 MH082441/MH/NIMH NIH HHS/ -- WT 083481/Wellcome Trust/United Kingdom -- England -- Nature. 2012 Dec 13;492(7428):215-20. doi: 10.1038/nature11691.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biological Chemistry and Drug Discovery, College of Life Sciences, University of Dundee, Dundee DD1 5EH, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23235874" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Automation ; Drug Delivery Systems ; *Drug Design ; Female ; *Ligands ; Male ; Mice ; Mice, Inbred C57BL ; Models, Theoretical ; Pharmacological Phenomena ; Reproducibility of Results
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    Biophysical mechanism of T-cell receptor triggering in a reconstituted system (2012)
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    Publication Date: 2012-07-06
    Description: A T-cell-mediated immune response is initiated by the T-cell receptor (TCR) interacting with peptide-bound major histocompatibility complex (pMHC) on an infected cell. The mechanism by which this interaction triggers intracellular phosphorylation of the TCR, which lacks a kinase domain, remains poorly understood. Here, we have introduced the TCR and associated signalling molecules into a non-immune cell and reconstituted ligand-specific signalling when these cells are conjugated with antigen-presenting cells. We show that signalling requires the differential segregation of a phosphatase and kinase in the plasma membrane. An artificial, chemically controlled receptor system generates the same effect as TCR-pMHC, demonstrating that the binding energy of an extracellular protein-protein interaction can drive the spatial segregation of membrane proteins without a transmembrane conformational change. This general mechanism may extend to other receptors that rely on extrinsic kinases, including, as we demonstrate, chimaeric antigen receptors being developed for cancer immunotherapy.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3393772/" 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/PMC3393772/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉James, John R -- Vale, Ronald D -- Howard Hughes Medical Institute/ -- England -- Nature. 2012 Jul 5;487(7405):64-9. doi: 10.1038/nature11220.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Cellular and Molecular Pharmacology, University of California, San Francisco, 600 16th Street, San Francisco, California 94158, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22763440" target="_blank"〉PubMed〈/a〉
    Keywords: Antigen-Presenting Cells/immunology/metabolism ; Antigens, CD45/genetics/metabolism ; Cell Compartmentation ; Cell Membrane/enzymology ; Cell Transdifferentiation/*genetics ; *Genetic Engineering ; HEK293 Cells ; Histocompatibility Antigens Class II/immunology/metabolism ; Humans ; Lymphocyte Activation/*immunology ; Lymphocyte Specific Protein Tyrosine Kinase p56(lck)/metabolism ; Phosphorylation ; Receptors, Antigen, T-Cell/immunology/*metabolism ; Signal Transduction/immunology ; Synthetic Biology/*methods ; T-Lymphocytes/enzymology/immunology/*metabolism ; Time Factors ; *Transduction, Genetic
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    Stem-cell therapy takes off in Texas (2012)
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    Publication Date: 2012-03-03
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cyranoski, David -- England -- Nature. 2012 Feb 29;483(7387):13-4. doi: 10.1038/483013a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22382952" target="_blank"〉PubMed〈/a〉
    Keywords: Abdominal Fat/cytology ; *Adult Stem Cells/cytology ; Clinical Trials as Topic/ethics/legislation & jurisprudence ; Compassionate Use Trials ; Female ; Humans ; Male ; Stem Cell Transplantation/ethics/legislation & jurisprudence/*utilization ; Texas ; Tissue Banks ; United States ; United States Food and Drug Administration/legislation & jurisprudence
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    New evidence on testosterone and cooperation (2012)
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    Publication Date: 2012-05-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉van Honk, Jack -- Montoya, Estrella R -- Bos, Peter A -- van Vugt, Mark -- Terburg, David -- England -- Nature. 2012 May 23;485(7399):E4-5; discussion E5-6. doi: 10.1038/nature11136.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Experimental Psychology, Utrecht University, 3584CS Utrecht, Netherlands. j.vanhonk@uu.nl〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22622587" target="_blank"〉PubMed〈/a〉
    Keywords: Female ; *Game Theory ; Humans ; *Prejudice ; *Social Behavior ; Testosterone/*pharmacology
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    Novel role of PKR in inflammasome activation and HMGB1 release (2012)
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    Publication Date: 2012-07-18
    Description: The inflammasome regulates the release of caspase activation-dependent cytokines, including interleukin (IL)-1beta, IL-18 and high-mobility group box 1 (HMGB1). By studying HMGB1 release mechanisms, here we identify a role for double-stranded RNA-dependent protein kinase (PKR, also known as EIF2AK2) in inflammasome activation. Exposure of macrophages to inflammasome agonists induced PKR autophosphorylation. PKR inactivation by genetic deletion or pharmacological inhibition severely impaired inflammasome activation in response to double-stranded RNA, ATP, monosodium urate, adjuvant aluminium, rotenone, live Escherichia coli, anthrax lethal toxin, DNA transfection and Salmonella typhimurium infection. PKR deficiency significantly inhibited the secretion of IL-1beta, IL-18 and HMGB1 in E. coli-induced peritonitis. PKR physically interacts with several inflammasome components, including NOD-like receptor (NLR) family pyrin domain-containing 3 (NLRP3), NLRP1, NLR family CARD domain-containing protein 4 (NLRC4), absent in melanoma 2 (AIM2), and broadly regulates inflammasome activation. PKR autophosphorylation in a cell-free system with recombinant NLRP3, apoptosis-associated speck-like protein containing a CARD (ASC, also known as PYCARD) and pro-caspase-1 reconstitutes inflammasome activity. These results show a crucial role for PKR in inflammasome activation, and indicate that it should be possible to pharmacologically target this molecule to treat inflammation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4163918/" 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/PMC4163918/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lu, Ben -- Nakamura, Takahisa -- Inouye, Karen -- Li, Jianhua -- Tang, Yiting -- Lundback, Peter -- Valdes-Ferrer, Sergio I -- Olofsson, Peder S -- Kalb, Thomas -- Roth, Jesse -- Zou, Yongrui -- Erlandsson-Harris, Helena -- Yang, Huan -- Ting, Jenny P-Y -- Wang, Haichao -- Andersson, Ulf -- Antoine, Daniel J -- Chavan, Sangeeta S -- Hotamisligil, Gokhan S -- Tracey, Kevin J -- DK052539/DK/NIDDK NIH HHS/ -- G0700654/Medical Research Council/United Kingdom -- R01 DK052539/DK/NIDDK NIH HHS/ -- R01 GM057226/GM/NIGMS NIH HHS/ -- R01 GM062508/GM/NIGMS NIH HHS/ -- R01 GM62508/GM/NIGMS NIH HHS/ -- England -- Nature. 2012 Aug 30;488(7413):670-4. doi: 10.1038/nature11290.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Biomedical Science, The Feinstein Institute for Medical Research, 350 Community Drive, Manhasset, New York 11030, USA. blu@nshs.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22801494" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing/metabolism ; Adenosine Triphosphate/pharmacology ; Animals ; Antigens, Bacterial/pharmacology ; Apoptosis Regulatory Proteins/metabolism ; Bacterial Toxins/pharmacology ; CARD Signaling Adaptor Proteins/metabolism ; Calcium-Binding Proteins/metabolism ; Carrier Proteins/metabolism ; Cell Line ; Cells, Cultured ; Crystallins/metabolism ; Escherichia coli/immunology/physiology ; Escherichia coli Infections/immunology/metabolism ; Female ; HMGB1 Protein/blood/*secretion ; Humans ; Inflammasomes/agonists/*metabolism ; Interleukin-18/blood ; Interleukin-1beta/blood ; Interleukin-6/analysis/blood ; Macrophages, Peritoneal/drug effects/metabolism ; Male ; Membrane Proteins/metabolism ; Mice ; Mice, Inbred C57BL ; Peritonitis/metabolism ; Phosphorylation ; RNA, Double-Stranded/immunology/pharmacology ; Rotenone/pharmacology ; Salmonella Infections/immunology/metabolism ; Salmonella typhimurium/immunology/physiology ; Transfection ; Uric Acid/pharmacology ; eIF-2 Kinase/antagonists & inhibitors/deficiency/genetics/*metabolism
    Print ISSN: 0028-0836
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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    Environment and genetics: Making sense of the noise (2012)
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    Publication Date: 2012-06-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Petherick, Anna -- England -- Nature. 2012 May 30;485(7400):S64-5. doi: 10.1038/485S64a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22648504" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Age Factors ; Aged ; Breast Neoplasms/*etiology/*genetics/psychology ; Child ; *Disease Susceptibility ; Exercise/physiology ; Female ; *Gene-Environment Interaction ; Genes, BRCA1 ; Genes, BRCA2 ; Genetic Predisposition to Disease/genetics ; Genome-Wide Association Study ; Humans ; Menopause/physiology ; Middle Aged ; Obesity/complications ; Pedigree ; Risk Factors ; Siblings ; Stress, Psychological/complications ; Twin Studies as Topic
    Print ISSN: 0028-0836
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    Widespread adoption of Bt cotton and insecticide decrease promotes biocontrol services (2012)
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    Publication Date: 2012-06-23
    Description: Over the past 16 years, vast plantings of transgenic crops producing insecticidal proteins from the bacterium Bacillus thuringiensis (Bt) have helped to control several major insect pests and reduce the need for insecticide sprays. Because broad-spectrum insecticides kill arthropod natural enemies that provide biological control of pests, the decrease in use of insecticide sprays associated with Bt crops could enhance biocontrol services. However, this hypothesis has not been tested in terms of long-term landscape-level impacts. On the basis of data from 1990 to 2010 at 36 sites in six provinces of northern China, we show here a marked increase in abundance of three types of generalist arthropod predators (ladybirds, lacewings and spiders) and a decreased abundance of aphid pests associated with widespread adoption of Bt cotton and reduced insecticide sprays in this crop. We also found evidence that the predators might provide additional biocontrol services spilling over from Bt cotton fields onto neighbouring crops (maize, peanut and soybean). Our work extends results from general studies evaluating ecological effects of Bt crops by demonstrating that such crops can promote biocontrol services in agricultural landscapes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lu, Yanhui -- Wu, Kongming -- Jiang, Yuying -- Guo, Yuyuan -- Desneux, Nicolas -- England -- Nature. 2012 Jul 19;487(7407):362-5. doi: 10.1038/nature11153.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉State Key Laboratory for Biology of Plant Diseases and Insect Pests, Institute of Plant Protection, Chinese Academy of Agricultural Sciences, Beijing, 100193 China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22722864" target="_blank"〉PubMed〈/a〉
    Keywords: *Agriculture/trends ; Animals ; Aphids/physiology ; Arthropods/physiology ; Bacillus thuringiensis/genetics ; China ; Food Chain ; *Gossypium/genetics/parasitology ; *Insecticides ; Pest Control, Biological/*trends ; *Plants, Genetically Modified ; Population Density ; Time Factors
    Print ISSN: 0028-0836
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    Extrathymically generated regulatory T cells control mucosal TH2 inflammation (2012)
    Nature Publishing Group (NPG)
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    Publication Date: 2012-02-10
    Description: A balance between pro- and anti-inflammatory mechanisms at mucosal interfaces, which are sites of constitutive exposure to microbes and non-microbial foreign substances, allows for efficient protection against pathogens yet prevents adverse inflammatory responses associated with allergy, asthma and intestinal inflammation. Regulatory T (T(reg)) cells prevent systemic and tissue-specific autoimmunity and inflammatory lesions at mucosal interfaces. These cells are generated in the thymus (tT(reg) cells) and in the periphery (induced (i)T(reg) cells), and their dual origin implies a division of labour between tT(reg) and iT(reg) cells in immune homeostasis. Here we show that a highly selective blockage in differentiation of iT(reg) cells in mice did not lead to unprovoked multi-organ autoimmunity, exacerbation of induced tissue-specific autoimmune pathology, or increased pro-inflammatory responses of T helper 1 (T(H)1) and T(H)17 cells. However, mice deficient in iT(reg) cells spontaneously developed pronounced T(H)2-type pathologies at mucosal sites--in the gastrointestinal tract and lungs--with hallmarks of allergic inflammation and asthma. Furthermore, iT(reg)-cell deficiency altered gut microbial communities. These results suggest that whereas T(reg) cells generated in the thymus appear sufficient for control of systemic and tissue-specific autoimmunity, extrathymic differentiation of T(reg) cells affects commensal microbiota composition and serves a distinct, essential function in restraint of allergic-type inflammation at mucosal interfaces.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3485072/" 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/PMC3485072/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Josefowicz, Steven Z -- Niec, Rachel E -- Kim, Hye Young -- Treuting, Piper -- Chinen, Takatoshi -- Zheng, Ye -- Umetsu, Dale T -- Rudensky, Alexander Y -- 1F31NS073203-01/NS/NINDS NIH HHS/ -- F31 NS073203/NS/NINDS NIH HHS/ -- GM07739/GM/NIGMS NIH HHS/ -- R37 AI034206/AI/NIAID NIH HHS/ -- T32 GM007739/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2012 Feb 8;482(7385):395-9. doi: 10.1038/nature10772.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Immunology Program, Sloan Kettering Institute, New York, New York 10021, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22318520" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Asthma/immunology/pathology ; Cell Differentiation ; Enhancer Elements, Genetic/genetics ; Female ; Forkhead Transcription Factors/genetics ; Immunity, Mucosal/*immunology ; Inflammation/*immunology/pathology ; Intestines/immunology/microbiology/pathology ; Lung/immunology/pathology ; Male ; Mice ; Organ Specificity ; Stomach/immunology/microbiology/pathology ; T-Lymphocytes, Regulatory/*cytology/*immunology ; Th2 Cells/*immunology ; Thymus Gland
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    APJ acts as a dual receptor in cardiac hypertrophy (2012)
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    Publication Date: 2012-07-20
    Description: Cardiac hypertrophy is initiated as an adaptive response to sustained overload but progresses pathologically as heart failure ensues. Here we report that genetic loss of APJ, a G-protein-coupled receptor, confers resistance to chronic pressure overload by markedly reducing myocardial hypertrophy and heart failure. In contrast, mice lacking apelin (the endogenous APJ ligand) remain sensitive, suggesting an apelin-independent function of APJ. Freshly isolated APJ-null cardiomyocytes exhibit an attenuated response to stretch, indicating that APJ is a mechanosensor. Activation of APJ by stretch increases cardiomyocyte cell size and induces molecular markers of hypertrophy. Whereas apelin stimulates APJ to activate Galphai and elicits a protective response, stretch signals in an APJ-dependent, G-protein-independent fashion to induce hypertrophy. Stretch-mediated hypertrophy is prevented by knockdown of beta-arrestins or by pharmacological doses of apelin acting through Galphai. Taken together, our data indicate that APJ is a bifunctional receptor for both mechanical stretch and the endogenous peptide apelin. By sensing the balance between these stimuli, APJ occupies a pivotal point linking sustained overload to cardiomyocyte hypertrophy.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3422434/" 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/PMC3422434/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Scimia, Maria Cecilia -- Hurtado, Cecilia -- Ray, Saugata -- Metzler, Scott -- Wei, Ke -- Wang, Jianming -- Woods, Chris E -- Purcell, Nicole H -- Catalucci, Daniele -- Akasaka, Takeshi -- Bueno, Orlando F -- Vlasuk, George P -- Kaliman, Perla -- Bodmer, Rolf -- Smith, Layton H -- Ashley, Euan -- Mercola, Mark -- Brown, Joan Heller -- Ruiz-Lozano, Pilar -- NS05422/NS/NINDS NIH HHS/ -- P01 HL085577/HL/NHLBI NIH HHS/ -- R01 HL054732/HL/NHLBI NIH HHS/ -- R01 HL086879/HL/NHLBI NIH HHS/ -- R01HL054732/HL/NHLBI NIH HHS/ -- R01HL083463/HL/NHLBI NIH HHS/ -- R01HL086879/HL/NHLBI NIH HHS/ -- R01HL28143/HL/NHLBI NIH HHS/ -- R37 HL028143/HL/NHLBI NIH HHS/ -- R37HL059502/HL/NHLBI NIH HHS/ -- England -- Nature. 2012 Aug 16;488(7411):394-8. doi: 10.1038/nature11263.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Sanford-Burnham Medical Research Institute, La Jolla, California 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22810587" target="_blank"〉PubMed〈/a〉
    Keywords: Adipokines ; Animals ; Aorta/pathology ; Arrestins/deficiency/genetics/metabolism ; Blood Pressure ; Cardiomegaly/*metabolism/pathology/physiopathology/prevention & control ; Female ; GTP-Binding Protein alpha Subunits, Gi-Go/metabolism ; Intercellular Signaling Peptides and ; Proteins/deficiency/genetics/metabolism/pharmacology ; Male ; Mechanoreceptors/metabolism ; Mechanotransduction, Cellular/drug effects/physiology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Myocytes, Cardiac/drug effects/pathology ; Receptors, G-Protein-Coupled/agonists/deficiency/genetics/*metabolism ; Signal Transduction/drug effects
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    Olfaction: Intimate neuronal whispers (2012)
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    Publication Date: 2012-11-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shimizu, Kazumichi -- Stopfer, Mark -- England -- Nature. 2012 Dec 6;492(7427):44-5. doi: 10.1038/nature11757. Epub 2012 Nov 21.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23172148" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Female ; Neural Inhibition/*physiology ; Olfactory Pathways/*physiology ; Olfactory Receptor Neurons/*metabolism ; *Synapses
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    Live-cell delamination counterbalances epithelial growth to limit tissue overcrowding (2012)
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    Publication Date: 2012-04-17
    Description: The development and maintenance of an epithelium requires finely balanced rates of growth and cell death. However, the mechanical and biochemical mechanisms that ensure proper feedback control of tissue growth, which when deregulated contribute to tumorigenesis, are poorly understood. Here we use the fly notum as a model system to identify a novel process of crowding-induced cell delamination that balances growth to ensure the development of well-ordered cell packing. In crowded regions of the tissue, a proportion of cells undergo a serial loss of cell-cell junctions and a progressive loss of apical area, before being squeezed out by their neighbours. This path of delamination is recapitulated by a simple computational model of epithelial mechanics, in which stochastic cell loss relieves overcrowding as the system tends towards equilibrium. We show that this process of delamination is mechanistically distinct from apoptosis-mediated cell extrusion and precedes the first signs of cell death. Overall, this analysis reveals a simple mechanism that buffers epithelia against variations in growth. Because live-cell delamination constitutes a mechanistic link between epithelial hyperplasia and cell invasion, this is likely to have important implications for our understanding of the early stages of cancer development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marinari, Eliana -- Mehonic, Aida -- Curran, Scott -- Gale, Jonathan -- Duke, Thomas -- Baum, Buzz -- 9786/Cancer Research UK/United Kingdom -- Cancer Research UK/United Kingdom -- England -- Nature. 2012 Apr 15;484(7395):542-5. doi: 10.1038/nature10984.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council Laboratory of Molecular Cell Biology, University College London, Gower Street, London WC1E 6BT, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22504180" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Cell Communication ; Cell Count ; Cell Death ; Cell Growth Processes ; Cell Survival ; Drosophila melanogaster/*cytology ; Epithelial Cells/*cytology ; Female ; Male ; Models, Biological ; Neoplasms/pathology ; Stochastic Processes
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    Human dorsal anterior cingulate cortex neurons mediate ongoing behavioural adaptation (2012)
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    Publication Date: 2012-06-23
    Description: The ability to optimize behavioural performance when confronted with continuously evolving environmental demands is a key element of human cognition. The dorsal anterior cingulate cortex (dACC), which lies on the medial surface of the frontal lobes, is important in regulating cognitive control. Hypotheses about its function include guiding reward-based decision making, monitoring for conflict between competing responses and predicting task difficulty. Precise mechanisms of dACC function remain unknown, however, because of the limited number of human neurophysiological studies. Here we use functional imaging and human single-neuron recordings to show that the firing of individual dACC neurons encodes current and recent cognitive load. We demonstrate that the modulation of current dACC activity by previous activity produces a behavioural adaptation that accelerates reactions to cues of similar difficulty to previous ones, and retards reactions to cues of different difficulty. Furthermore, this conflict adaptation, or Gratton effect, is abolished after surgically targeted ablation of the dACC. Our results demonstrate that the dACC provides a continuously updated prediction of expected cognitive demand to optimize future behavioural responses. In situations with stable cognitive demands, this signal promotes efficiency by hastening responses, but in situations with changing demands it engenders accuracy by delaying responses.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3416924/" 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/PMC3416924/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sheth, Sameer A -- Mian, Matthew K -- Patel, Shaun R -- Asaad, Wael F -- Williams, Ziv M -- Dougherty, Darin D -- Bush, George -- Eskandar, Emad N -- 1R01EY017658-01A/EY/NEI NIH HHS/ -- 1R01NS063249/NS/NINDS NIH HHS/ -- 5R01DP000339/DP/NCCDPHP CDC HHS/ -- MH086400/MH/NIMH NIH HHS/ -- P41RR14075/RR/NCRR NIH HHS/ -- R01 DA026297/DA/NIDA NIH HHS/ -- R01 EY017658/EY/NEI NIH HHS/ -- R25 NS065743/NS/NINDS NIH HHS/ -- R25NS065743/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2012 Aug 9;488(7410):218-21. doi: 10.1038/nature11239.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Nayef Al-Rodhan Laboratories, Department of Neurosurgery, Massachusetts General Hospital, Boston, Massachusetts 02114, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22722841" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptation, Physiological/*physiology ; Adult ; Cognition/*physiology ; Cues ; Decision Making/physiology ; Female ; Functional Neuroimaging ; Gyrus Cinguli/*cytology/*physiology/surgery ; Humans ; Magnetic Resonance Imaging ; Male ; Microelectrodes ; Neurons/*physiology ; Photic Stimulation ; Reaction Time ; Reward ; Single-Cell Analysis
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    Ice-sheet collapse and sea-level rise at the Bolling warming 14,600 years ago (2012)
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    Publication Date: 2012-03-31
    Description: Past sea-level records provide invaluable information about the response of ice sheets to climate forcing. Some such records suggest that the last deglaciation was punctuated by a dramatic period of sea-level rise, of about 20 metres, in less than 500 years. Controversy about the amplitude and timing of this meltwater pulse (MWP-1A) has, however, led to uncertainty about the source of the melt water and its temporal and causal relationships with the abrupt climate changes of the deglaciation. Here we show that MWP-1A started no earlier than 14,650 years ago and ended before 14,310 years ago, making it coeval with the Bolling warming. Our results, based on corals drilled offshore from Tahiti during Integrated Ocean Drilling Project Expedition 310, reveal that the increase in sea level at Tahiti was between 12 and 22 metres, with a most probable value between 14 and 18 metres, establishing a significant meltwater contribution from the Southern Hemisphere. This implies that the rate of eustatic sea-level rise exceeded 40 millimetres per year during MWP-1A.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Deschamps, Pierre -- Durand, Nicolas -- Bard, Edouard -- Hamelin, Bruno -- Camoin, Gilbert -- Thomas, Alexander L -- Henderson, Gideon M -- Okuno, Jun'ichi -- Yokoyama, Yusuke -- England -- Nature. 2012 Mar 28;483(7391):559-64. doi: 10.1038/nature10902.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉CEREGE, UMR Aix-Marseille Universite - CNRS - IRD - College de France, Technopole de l'Arbois, BP 80, 13545 Aix-en-Provence Cedex 4, France. deschamps@cerege.fr〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22460900" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anthozoa ; Coral Reefs ; Freezing ; Global Warming/*history ; History, Ancient ; *Ice Cover ; Oceans and Seas ; Polynesia ; Seawater/*analysis ; Time Factors ; Uncertainty
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    Genomics: the breast cancer landscape (2012)
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    Publication Date: 2012-06-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gray, Joe -- Druker, Brian -- U54 CA112970/CA/NCI NIH HHS/ -- England -- Nature. 2012 Jun 20;486(7403):328-9. doi: 10.1038/486328a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Knight Cancer Institute, Oregon Health and Science University, Portland, Oregon 97239, USA. grayjo@ohsu.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22722187" target="_blank"〉PubMed〈/a〉
    Keywords: Aromatase/*metabolism ; Aromatase Inhibitors/*therapeutic use ; Breast Neoplasms/*classification/*drug therapy/*genetics/*pathology ; Cell Transformation, Neoplastic/*genetics ; DNA Copy Number Variations/*genetics ; *Evolution, Molecular ; Female ; *Gene Expression Profiling ; *Gene Expression Regulation, Neoplastic ; Genome, Human/*genetics ; Humans ; Mutagenesis/*genetics ; Mutation/*genetics ; Oncogenes/*genetics ; Translocation, Genetic/*genetics
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    Ethics: Two faces of marine ecology research (2012)
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    Publication Date: 2012-06-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brunnschweiler, Juerg -- England -- Nature. 2012 Jun 6;486(7401):34. doi: 10.1038/486034b.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22678272" target="_blank"〉PubMed〈/a〉
    Keywords: *Communication ; *Ethics, Research ; Female ; Humans ; Pregnancy ; *Research ; *Research Personnel ; *Security Measures
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    Deglacial rapid sea level rises caused by ice-sheet saddle collapses (2012)
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    Publication Date: 2012-07-13
    Description: The last deglaciation (21 to 7 thousand years ago) was punctuated by several abrupt meltwater pulses, which sometimes caused noticeable climate change. Around 14 thousand years ago, meltwater pulse 1A (MWP-1A), the largest of these events, produced a sea level rise of 14-18 metres over 350 years. Although this enormous surge of water certainly originated from retreating ice sheets, there is no consensus on the geographical source or underlying physical mechanisms governing the rapid sea level rise. Here we present an ice-sheet modelling simulation in which the separation of the Laurentide and Cordilleran ice sheets in North America produces a meltwater pulse corresponding to MWP-1A. Another meltwater pulse is produced when the Labrador and Baffin ice domes around Hudson Bay separate, which could be associated with the '8,200-year' event, the most pronounced abrupt climate event of the past nine thousand years. For both modelled pulses, the saddle between the two ice domes becomes subject to surface melting because of a general surface lowering caused by climate warming. The melting then rapidly accelerates as the saddle between the two domes gets lower, producing nine metres of sea level rise over 500 years. This mechanism of an ice 'saddle collapse' probably explains MWP-1A and the 8,200-year event and sheds light on the consequences of these events on climate.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gregoire, Lauren J -- Payne, Antony J -- Valdes, Paul J -- England -- Nature. 2012 Jul 11;487(7406):219-22. doi: 10.1038/nature11257.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Geographical Sciences, University of Bristol, University Road, Bristol BS8 1SS, UK. lauren.gregoire@bristol.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22785319" target="_blank"〉PubMed〈/a〉
    Keywords: Computer Simulation ; *Global Warming ; *Ice Cover ; North America ; Oceans and Seas ; Time Factors
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    HVEM signalling at mucosal barriers provides host defence against pathogenic bacteria (2012)
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    Publication Date: 2012-07-18
    Description: The herpes virus entry mediator (HVEM), a member of the tumour-necrosis factor receptor family, has diverse functions, augmenting or inhibiting the immune response. HVEM was recently reported as a colitis risk locus in patients, and in a mouse model of colitis we demonstrated an anti-inflammatory role for HVEM, but its mechanism of action in the mucosal immune system was unknown. Here we report an important role for epithelial HVEM in innate mucosal defence against pathogenic bacteria. HVEM enhances immune responses by NF-kappaB-inducing kinase-dependent Stat3 activation, which promotes the epithelial expression of genes important for immunity. During intestinal Citrobacter rodentium infection, a mouse model for enteropathogenic Escherichia coli infection, Hvem-/- mice showed decreased Stat3 activation, impaired responses in the colon, higher bacterial burdens and increased mortality. We identified the immunoglobulin superfamily molecule CD160 (refs 7 and 8), expressed predominantly by innate-like intraepithelial lymphocytes, as the ligand engaging epithelial HVEM for host protection. Likewise, in pulmonary Streptococcus pneumoniae infection, HVEM is also required for host defence. Our results pinpoint HVEM as an important orchestrator of mucosal immunity, integrating signals from innate lymphocytes to induce optimal epithelial Stat3 activation, which indicates that targeting HVEM with agonists could improve host defence.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3477500/" 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/PMC3477500/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shui, Jr-Wen -- Larange, Alexandre -- Kim, Gisen -- Vela, Jose Luis -- Zahner, Sonja -- Cheroutre, Hilde -- Kronenberg, Mitchell -- F32 AI083029/AI/NIAID NIH HHS/ -- F32 DK082249/DK/NIDDK NIH HHS/ -- F32-AI083029/AI/NIAID NIH HHS/ -- F32-DK082249/DK/NIDDK NIH HHS/ -- P01 DK046763/DK/NIDDK NIH HHS/ -- P01 DK46763/DK/NIDDK NIH HHS/ -- R01 AI050265/AI/NIAID NIH HHS/ -- R01 AI061516/AI/NIAID NIH HHS/ -- R01 AI064584/AI/NIAID NIH HHS/ -- R01-AI061516/AI/NIAID NIH HHS/ -- England -- Nature. 2012 Aug 9;488(7410):222-5. doi: 10.1038/nature11242.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Developmental Immunology, La Jolla Institute for Allergy and Immunology, 9420 Athena Circle, La Jolla, California 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22801499" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD/immunology/metabolism ; Bacterial Load ; Cell Line ; Citrobacter rodentium/*immunology/*pathogenicity ; Disease Models, Animal ; Enterobacteriaceae Infections/immunology/microbiology ; Enteropathogenic Escherichia coli ; Epithelial Cells/immunology/metabolism ; Escherichia coli Infections ; GPI-Linked Proteins/immunology/metabolism ; Immunity, Mucosal/*immunology ; Intestines/immunology/microbiology ; Ligands ; Lung/immunology/microbiology ; Lymphocytes/immunology/metabolism ; Mice ; Mice, Inbred C57BL ; Mucous Membrane/*immunology/metabolism/*microbiology ; Pneumococcal Infections/immunology/microbiology ; Protein-Serine-Threonine Kinases/metabolism ; Receptors, Immunologic/immunology/metabolism ; Receptors, Tumor Necrosis Factor, Member ; 14/deficiency/genetics/immunology/*metabolism ; STAT3 Transcription Factor/metabolism ; *Signal Transduction ; Streptococcus pneumoniae/immunology ; Survival Rate
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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    A novel sensor to map auxin response and distribution at high spatio-temporal resolution (2012)
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    Publication Date: 2012-01-17
    Description: Auxin is a key plant morphogenetic signal but tools to analyse dynamically its distribution and signalling during development are still limited. Auxin perception directly triggers the degradation of Aux/IAA repressor proteins. Here we describe a novel Aux/IAA-based auxin signalling sensor termed DII-VENUS that was engineered in the model plant Arabidopsis thaliana. The VENUS fast maturing form of yellow fluorescent protein was fused in-frame to the Aux/IAA auxin-interaction domain (termed domain II; DII) and expressed under a constitutive promoter. We initially show that DII-VENUS abundance is dependent on auxin, its TIR1/AFBs co-receptors and proteasome activities. Next, we demonstrate that DII-VENUS provides a map of relative auxin distribution at cellular resolution in different tissues. DII-VENUS is also rapidly degraded in response to auxin and we used it to visualize dynamic changes in cellular auxin distribution successfully during two developmental responses, the root gravitropic response and lateral organ production at the shoot apex. Our results illustrate the value of developing response input sensors such as DII-VENUS to provide high-resolution spatio-temporal information about hormone distribution and response during plant growth and development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brunoud, Geraldine -- Wells, Darren M -- Oliva, Marina -- Larrieu, Antoine -- Mirabet, Vincent -- Burrow, Amy H -- Beeckman, Tom -- Kepinski, Stefan -- Traas, Jan -- Bennett, Malcolm J -- Vernoux, Teva -- BB/F007418/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/F013981/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- England -- Nature. 2012 Jan 15;482(7383):103-6. doi: 10.1038/nature10791.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratoire de Reproduction et Developpement des Plantes, CNRS, INRA, ENS Lyon, UCBL, Universite de Lyon, 69364 Lyon, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22246322" target="_blank"〉PubMed〈/a〉
    Keywords: Arabidopsis/*drug effects/growth & development/*metabolism ; Bacterial Proteins/genetics/metabolism ; *Gene Expression Regulation, Plant ; Gravitropism/drug effects ; Indoleacetic Acids/analysis/*metabolism/*pharmacology ; Luminescent Proteins/genetics/metabolism ; Organ Specificity ; Plant Shoots/drug effects/growth & development/metabolism ; Plants, Genetically Modified ; Proteasome Endopeptidase Complex/metabolism ; Protein Structure, Tertiary/genetics/physiology ; Time Factors
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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    Lab-animal flights squeezed (2012)
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    Publication Date: 2012-09-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wadman, Meredith -- England -- Nature. 2012 Sep 20;489(7416):344-5. doi: 10.1038/489344a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22996523" target="_blank"〉PubMed〈/a〉
    Keywords: *Aircraft ; Animal Rights/*legislation & jurisprudence ; Animals ; *Animals, Laboratory ; Biomedical Research/ethics/methods ; Disease Models, Animal ; Female ; Humans ; Mice ; Persuasive Communication ; Transportation/*methods/*statistics & numerical data ; Xenopus laevis
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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    The clonal and mutational evolution spectrum of primary triple-negative breast cancers (2012)
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    Publication Date: 2012-04-13
    Description: Primary triple-negative breast cancers (TNBCs), a tumour type defined by lack of oestrogen receptor, progesterone receptor and ERBB2 gene amplification, represent approximately 16% of all breast cancers. Here we show in 104 TNBC cases that at the time of diagnosis these cancers exhibit a wide and continuous spectrum of genomic evolution, with some having only a handful of coding somatic aberrations in a few pathways, whereas others contain hundreds of coding somatic mutations. High-throughput RNA sequencing (RNA-seq) revealed that only approximately 36% of mutations are expressed. Using deep re-sequencing measurements of allelic abundance for 2,414 somatic mutations, we determine for the first time-to our knowledge-in an epithelial tumour subtype, the relative abundance of clonal frequencies among cases representative of the population. We show that TNBCs vary widely in their clonal frequencies at the time of diagnosis, with the basal subtype of TNBC showing more variation than non-basal TNBC. Although p53 (also known as TP53), PIK3CA and PTEN somatic mutations seem to be clonally dominant compared to other genes, in some tumours their clonal frequencies are incompatible with founder status. Mutations in cytoskeletal, cell shape and motility proteins occurred at lower clonal frequencies, suggesting that they occurred later during tumour progression. Taken together, our results show that understanding the biology and therapeutic responses of patients with TNBC will require the determination of individual tumour clonal genotypes.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3863681/" 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/PMC3863681/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shah, Sohrab P -- Roth, Andrew -- Goya, Rodrigo -- Oloumi, Arusha -- Ha, Gavin -- Zhao, Yongjun -- Turashvili, Gulisa -- Ding, Jiarui -- Tse, Kane -- Haffari, Gholamreza -- Bashashati, Ali -- Prentice, Leah M -- Khattra, Jaswinder -- Burleigh, Angela -- Yap, Damian -- Bernard, Virginie -- McPherson, Andrew -- Shumansky, Karey -- Crisan, Anamaria -- Giuliany, Ryan -- Heravi-Moussavi, Alireza -- Rosner, Jamie -- Lai, Daniel -- Birol, Inanc -- Varhol, Richard -- Tam, Angela -- Dhalla, Noreen -- Zeng, Thomas -- Ma, Kevin -- Chan, Simon K -- Griffith, Malachi -- Moradian, Annie -- Cheng, S-W Grace -- Morin, Gregg B -- Watson, Peter -- Gelmon, Karen -- Chia, Stephen -- Chin, Suet-Feung -- Curtis, Christina -- Rueda, Oscar M -- Pharoah, Paul D -- Damaraju, Sambasivarao -- Mackey, John -- Hoon, Kelly -- Harkins, Timothy -- Tadigotla, Vasisht -- Sigaroudinia, Mahvash -- Gascard, Philippe -- Tlsty, Thea -- Costello, Joseph F -- Meyer, Irmtraud M -- Eaves, Connie J -- Wasserman, Wyeth W -- Jones, Steven -- Huntsman, David -- Hirst, Martin -- Caldas, Carlos -- Marra, Marco A -- Aparicio, Samuel -- 5U01ES017154-02/ES/NIEHS NIH HHS/ -- R01 GM084875/GM/NIGMS NIH HHS/ -- R01GM084875/GM/NIGMS NIH HHS/ -- Cancer Research UK/United Kingdom -- England -- Nature. 2012 Apr 4;486(7403):395-9. doi: 10.1038/nature10933.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, British Columbia V6T 2B5, Canada. sshah@bccrc.ca〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22495314" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Breast Neoplasms/diagnosis/*genetics/*pathology ; Clone Cells/metabolism/pathology ; DNA Copy Number Variations/genetics ; DNA Mutational Analysis ; Disease Progression ; *Evolution, Molecular ; Female ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic/genetics ; Genotype ; High-Throughput Nucleotide Sequencing ; Humans ; INDEL Mutation/genetics ; Mutation/*genetics ; Point Mutation/genetics ; Precision Medicine ; Reproducibility of Results ; Sequence Analysis, RNA
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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