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  • Inorganic Chemistry  (83,670)
  • Humans  (26,746)
  • Cell & Developmental Biology  (25,032)
  • Chemical Engineering  (17,980)
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  • 1
    Publication Date: 2018-04-17
    Description: © The Author(s), 2018. This article is distributed under the terms of the Creative Commons Attribution License. The definitive version was published in International Journal of Environmental Research and Public Health 15 (2018): 723, doi:10.3390/ijerph15040723.
    Description: There has been a massive increase in recent years of the use of lead (Pb) isotopes in attempts to better understand sources and pathways of Pb in the environment and in man or experimental animals. Unfortunately, there have been many cases where the quality of the isotopic data, especially that obtained by quadrupole inductively coupled plasma mass spectrometry (Q-ICP-MS), are questionable, resulting in questionable identification of potential sources, which, in turn, impacts study interpretation and conclusions. We present several cases where the isotopic data have compromised interpretation because of the use of only the major isotopes 208Pb/206Pb and 207Pb/206Pb, or their graphing in other combinations. We also present some examples comparing high precision data from thermal ionization (TIMS) or multi-collector plasma mass spectrometry (MC-ICP-MS) to illustrate the deficiency in the Q-ICP-MS data. In addition, we present cases where Pb isotopic ratios measured on Q-ICP-MS are virtually impossible for terrestrial samples. We also evaluate the Pb isotopic data for rat studies, which had concluded that Pb isotopic fractionation occurs between different organs and suggest that this notion of biological fractionation of Pb as an explanation for isotopic differences is not valid. Overall, the brief review of these case studies shows that Q-ICP-MS as commonly practiced is not a suitable technique for precise and accurate Pb isotopic analysis in the environment and health fields
    Keywords: Lead isotopes ; ICP-MS ; TIMS ; MC-ICP-MS ; Environment ; Humans ; Rats ; Fractionation
    Repository Name: Woods Hole Open Access Server
    Type: Article
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  • 2
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    American Association for the Advancement of Science (AAAS)
    In: Science
    Publication Date: 2017-01-27
    Description: Polynitrogens have the potential for ultrahigh-performing explosives or propellants because singly or doubly bonded polynitrogens can decompose to triply bonded dinitrogen (N2) with an extraordinarily large energy release. The large energy content and relatively low activation energy toward decomposition makes the synthesis of a stable polynitrogen allotrope an extraordinary challenge. Many elements exist in different forms (allotropes)—for example, carbon can exist as graphite, diamond, buckyballs, or graphene. However, no stable neutral allotropes are known for nitrogen, and only two stable homonuclear polynitrogen ions had been isolated until now—namely, the N3− anion (1) and the N5+ cation (2). On page 374 of this issue, Zhang et al. (3) report the synthesis and characterization of the first stable salt of the cyclo-N5− anion, only the third stable homonuclear polynitrogen ion ever isolated. Author: Karl O. Christe
    Keywords: Inorganic Chemistry
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    American Association for the Advancement of Science (AAAS)
    In: Science
    Publication Date: 2017-01-27
    Description: Author: Jake Yeston
    Keywords: Inorganic Chemistry
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    American Association for the Advancement of Science (AAAS)
    In: Science
    Publication Date: 2017-02-10
    Description: Author: Jake Yeston
    Keywords: Inorganic Chemistry
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
    Publication Date: 2016-01-28
    Description: Inflammasomes are intracellular protein complexes that drive the activation of inflammatory caspases. So far, four inflammasomes involving NLRP1, NLRP3, NLRC4 and AIM2 have been described that recruit the common adaptor protein ASC to activate caspase-1, leading to the secretion of mature IL-1beta and IL-18 proteins. The NLRP3 inflammasome has been implicated in the pathogenesis of several acquired inflammatory diseases as well as cryopyrin-associated periodic fever syndromes (CAPS) caused by inherited NLRP3 mutations. Potassium efflux is a common step that is essential for NLRP3 inflammasome activation induced by many stimuli. Despite extensive investigation, the molecular mechanism leading to NLRP3 activation in response to potassium efflux remains unknown. Here we report the identification of NEK7, a member of the family of mammalian NIMA-related kinases (NEK proteins), as an NLRP3-binding protein that acts downstream of potassium efflux to regulate NLRP3 oligomerization and activation. In the absence of NEK7, caspase-1 activation and IL-1beta release were abrogated in response to signals that activate NLRP3, but not NLRC4 or AIM2 inflammasomes. NLRP3-activating stimuli promoted the NLRP3-NEK7 interaction in a process that was dependent on potassium efflux. NLRP3 associated with the catalytic domain of NEK7, but the catalytic activity of NEK7 was shown to be dispensable for activation of the NLRP3 inflammasome. Activated macrophages formed a high-molecular-mass NLRP3-NEK7 complex, which, along with ASC oligomerization and ASC speck formation, was abrogated in the absence of NEK7. NEK7 was required for macrophages containing the CAPS-associated NLRP3(R258W) activating mutation to activate caspase-1. Mouse chimaeras reconstituted with wild-type, Nek7(-/-) or Nlrp3(-/-) haematopoietic cells showed that NEK7 was required for NLRP3 inflammasome activation in vivo. These studies demonstrate that NEK7 is an essential protein that acts downstream of potassium efflux to mediate NLRP3 inflammasome assembly and activation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉He, Yuan -- Zeng, Melody Y -- Yang, Dahai -- Motro, Benny -- Nunez, Gabriel -- R01AI063331/AI/NIAID NIH HHS/ -- R01DK091191/DK/NIDDK NIH HHS/ -- T32 HL007517/HL/NHLBI NIH HHS/ -- T32DK094775/DK/NIDDK NIH HHS/ -- T32HL007517/HL/NHLBI NIH HHS/ -- England -- Nature. 2016 Feb 18;530(7590):354-7. doi: 10.1038/nature16959. Epub 2016 Jan 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and Comprehensive Cancer Center, University of Michigan Medical School, Ann Arbor, Michigan 48109, USA. ; The State Key Laboratory of Bioreactor Engineering, East China University of Science and Technology, Shanghai 200237, China. ; The Mina and Everard Goodman Faculty of Life Sciences, Bar-Ilan University, Ramat-Gan 52900, Israel.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26814970" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis Regulatory Proteins/deficiency/genetics/metabolism ; Biocatalysis ; Carrier Proteins/chemistry/genetics/*metabolism ; Caspase 1/metabolism ; Catalytic Domain ; Cells, Cultured ; Cryopyrin-Associated Periodic Syndromes/genetics ; Enzyme Activation ; HEK293 Cells ; Humans ; Inflammasomes/*chemistry/*metabolism ; Interleukin-1beta/secretion ; Macrophages/metabolism ; Mice ; Mice, Inbred C57BL ; Potassium/*metabolism ; Protein Binding ; Protein Multimerization ; Protein-Serine-Threonine Kinases/chemistry/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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  • 6
    Publication Date: 2016-03-17
    Description: Lung metastasis is the lethal determinant in many cancers and a number of lines of evidence point to monocytes and macrophages having key roles in its development. Yet little is known about the immediate fate of incoming tumour cells as they colonize this tissue, and even less known about how they make first contact with the immune system. Primary tumours liberate circulating tumour cells (CTCs) into the blood and we have developed a stable intravital two-photon lung imaging model in mice for direct observation of the arrival of CTCs and subsequent host interaction. Here we show dynamic generation of tumour microparticles in shear flow in the capillaries within minutes of CTC entry. Rather than dispersing under flow, many of these microparticles remain attached to the lung vasculature or independently migrate along the inner walls of vessels. Using fluorescent lineage reporters and flow cytometry, we observed 'waves' of distinct myeloid cell subsets that load differentially and sequentially with this CTC-derived material. Many of these tumour-ingesting myeloid cells collectively accumulated in the lung interstitium along with the successful metastatic cells and, as previously understood, promote the development of successful metastases from surviving tumour cells. Although the numbers of these cells rise globally in the lung with metastatic exposure and ingesting myeloid cells undergo phenotypic changes associated with microparticle ingestion, a consistently sparse population of resident conventional dendritic cells, among the last cells to interact with CTCs, confer anti-metastatic protection. This work reveals that CTC fragmentation generates immune-interacting intermediates, and defines a competitive relationship between phagocyte populations for tumour loading during metastatic cell seeding.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Headley, Mark B -- Bins, Adriaan -- Nip, Alyssa -- Roberts, Edward W -- Looney, Mark R -- Gerard, Audrey -- Krummel, Matthew F -- P01 HL024136/HL/NHLBI NIH HHS/ -- R21 CA167601/CA/NCI NIH HHS/ -- R21CA167601/CA/NCI NIH HHS/ -- U54 CA163123/CA/NCI NIH HHS/ -- England -- Nature. 2016 Mar 24;531(7595):513-7. doi: 10.1038/nature16985. Epub 2016 Mar 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, University of California, San Francisco, 513 Parnassus Ave, HSW512, San Francisco, California 94143-0511, USA. ; Department of Medical Oncology, Academic Medical Center Amsterdam, Meibergdreef, 91105AZ Amsterdam, The Netherlands. ; Departments of Medicine and Laboratory Medicine, University of California, San Francisco, 513 Parnassus Avenue, HSW512, California 94143-0511, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26982733" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Capillaries/pathology ; Cell Line, Tumor ; Cell Lineage ; *Cell Movement ; Dendritic Cells/cytology/immunology ; Female ; Genes, Reporter/genetics ; Humans ; Lung/blood supply/cytology/*immunology/*pathology ; Lung Neoplasms/*immunology/pathology/*secondary ; Male ; Melanoma, Experimental/immunology/pathology ; Mice ; Microscopy, Confocal ; Myeloid Cells/cytology ; Neoplasm Metastasis/*immunology/*pathology ; Neoplastic Cells, Circulating/pathology
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 7
    Publication Date: 2016-02-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Butler, Declan -- England -- Nature. 2016 Feb 4;530(7588):13-4. doi: 10.1038/nature.2016.19259.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26842033" target="_blank"〉PubMed〈/a〉
    Keywords: Brazil/epidemiology ; Diagnostic Errors/*statistics & numerical data ; Female ; Humans ; Infectious Disease Transmission, Vertical/statistics & numerical data ; Microcephaly/*diagnosis/*epidemiology/etiology/virology ; Pregnancy ; *Uncertainty ; Zika Virus/isolation & purification/*pathogenicity ; Zika Virus Infection/*epidemiology/transmission/virology
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  • 8
    Publication Date: 2016-01-21
    Description: RNA polymerase (Pol) II produces messenger RNA during transcription of protein-coding genes in all eukaryotic cells. The Pol II structure is known at high resolution from X-ray crystallography for two yeast species. Structural studies of mammalian Pol II, however, remain limited to low-resolution electron microscopy analysis of human Pol II and its complexes with various proteins. Here we report the 3.4 A resolution cryo-electron microscopy structure of mammalian Pol II in the form of a transcribing complex comprising DNA template and RNA transcript. We use bovine Pol II, which is identical to the human enzyme except for seven amino-acid residues. The obtained atomic model closely resembles its yeast counterpart, but also reveals unknown features. Binding of nucleic acids to the polymerase involves 'induced fit' of the mobile Pol II clamp and active centre region. DNA downstream of the transcription bubble contacts a conserved 'TPSA motif' in the jaw domain of the Pol II subunit RPB5, an interaction that is apparently already established during transcription initiation. Upstream DNA emanates from the active centre cleft at an angle of approximately 105 degrees with respect to downstream DNA. This position of upstream DNA allows for binding of the general transcription elongation factor DSIF (SPT4-SPT5) that we localize over the active centre cleft in a conserved position on the clamp domain of Pol II. Our results define the structure of mammalian Pol II in its functional state, indicate that previous crystallographic analysis of yeast Pol II is relevant for understanding gene transcription in all eukaryotes, and provide a starting point for a mechanistic analysis of human transcription.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bernecky, Carrie -- Herzog, Franz -- Baumeister, Wolfgang -- Plitzko, Jurgen M -- Cramer, Patrick -- England -- Nature. 2016 Jan 28;529(7587):551-4. doi: 10.1038/nature16482. Epub 2016 Jan 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max Planck Institute for Biophysical Chemistry, Department of Molecular Biology, Am Fassberg 11, 37077 Gottingen, Germany. ; Gene Center Munich, Ludwig-Maximilians-Universitat Munchen, Feodor-Lynen-Strasse 25, 81377 Munich, Germany. ; Max Planck Institute for Biochemistry, Department of Molecular Structural Biology, Am Klopferspitz 18, 82152 Martinsried, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26789250" target="_blank"〉PubMed〈/a〉
    Keywords: Allosteric Regulation ; Amino Acid Motifs ; Animals ; Catalytic Domain ; Cattle ; *Cryoelectron Microscopy ; DNA/genetics/metabolism/ultrastructure ; Humans ; Models, Molecular ; Nucleic Acids/chemistry/metabolism ; Protein Structure, Tertiary ; Protein Subunits/chemistry/metabolism ; RNA Polymerase II/chemistry/*metabolism/*ultrastructure ; RNA, Messenger/biosynthesis/genetics/ultrastructure ; Saccharomyces cerevisiae/enzymology ; Templates, Genetic ; *Transcription Elongation, Genetic
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  • 9
    Publication Date: 2016-01-26
    Description: Intracellular aggregation of the human amyloid protein alpha-synuclein is causally linked to Parkinson's disease. While the isolated protein is intrinsically disordered, its native structure in mammalian cells is not known. Here we use nuclear magnetic resonance (NMR) and electron paramagnetic resonance (EPR) spectroscopy to derive atomic-resolution insights into the structure and dynamics of alpha-synuclein in different mammalian cell types. We show that the disordered nature of monomeric alpha-synuclein is stably preserved in non-neuronal and neuronal cells. Under physiological cell conditions, alpha-synuclein is amino-terminally acetylated and adopts conformations that are more compact than when in buffer, with residues of the aggregation-prone non-amyloid-beta component (NAC) region shielded from exposure to the cytoplasm, which presumably counteracts spontaneous aggregation. These results establish that different types of crowded intracellular environments do not inherently promote alpha-synuclein oligomerization and, more generally, that intrinsic structural disorder is sustainable in mammalian cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Theillet, Francois-Xavier -- Binolfi, Andres -- Bekei, Beata -- Martorana, Andrea -- Rose, Honor May -- Stuiver, Marchel -- Verzini, Silvia -- Lorenz, Dorothea -- van Rossum, Marleen -- Goldfarb, Daniella -- Selenko, Philipp -- England -- Nature. 2016 Feb 4;530(7588):45-50. doi: 10.1038/nature16531. Epub 2016 Jan 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉In-Cell NMR Laboratory, Department of NMR-supported Structural Biology, Leibniz Institute of Molecular Pharmacology (FMP Berlin), Robert-Rossle Strasse 10, 13125 Berlin, Germany. ; Department of Chemical Physics, Weizmann Institute of Science, Rehovot 76100, Israel. ; Department of Molecular Physiology and Cell Biology, Leibniz Institute of Molecular Pharmacology (FMP Berlin), Robert-Rossle Strasse 10, 13125 Berlin, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26808899" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Cell Line ; Cytoplasm/chemistry/metabolism ; Electron Spin Resonance Spectroscopy ; HeLa Cells ; Humans ; Intracellular Space/*chemistry/*metabolism ; Neurons/cytology/metabolism ; Nuclear Magnetic Resonance, Biomolecular ; Protein Conformation ; alpha-Synuclein/*chemistry/*metabolism
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 10
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    Nature Publishing Group (NPG)
    Publication Date: 2016-05-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bender, Eric -- England -- Nature. 2016 May 11;533(7602):S59. doi: 10.1038/533S59a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27167392" target="_blank"〉PubMed〈/a〉
    Keywords: Diffusion of Innovation ; Drug Discovery/*economics/*methods/organization & administration/trends ; Drug Industry/economics/*methods/organization & administration/*trends ; Humans ; Leadership ; Patient Advocacy
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    Electronic ISSN: 1476-4687
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  • 11
    Publication Date: 2016-01-21
    Description: The p53 pro-apoptotic tumour suppressor is mutated or functionally altered in most cancers. In epithelial tumours induced by 'high-risk' mucosal human papilloma viruses, including human cervical carcinoma and a growing number of head-and-neck cancers, p53 is degraded by the viral oncoprotein E6 (ref. 2). In this process, E6 binds to a short leucine (L)-rich LxxLL consensus sequence within the cellular ubiquitin ligase E6AP. Subsequently, the E6/E6AP heterodimer recruits and degrades p53 (ref. 4). Neither E6 nor E6AP are separately able to recruit p53 (refs 3, 5), and the precise mode of assembly of E6, E6AP and p53 is unknown. Here we solve the crystal structure of a ternary complex comprising full-length human papilloma virus type 16 (HPV-16) E6, the LxxLL motif of E6AP and the core domain of p53. The LxxLL motif of E6AP renders the conformation of E6 competent for interaction with p53 by structuring a p53-binding cleft on E6. Mutagenesis of critical positions at the E6-p53 interface disrupts p53 degradation. The E6-binding site of p53 is distal from previously described DNA- and protein-binding surfaces of the core domain. This suggests that, in principle, E6 may avoid competition with cellular factors by targeting both free and bound p53 molecules. The E6/E6AP/p53 complex represents a prototype of viral hijacking of both the ubiquitin-mediated protein degradation pathway and the p53 tumour suppressor pathway. The present structure provides a framework for the design of inhibitory therapeutic strategies against oncogenesis mediated by human papilloma virus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Martinez-Zapien, Denise -- Ruiz, Francesc Xavier -- Poirson, Juline -- Mitschler, Andre -- Ramirez, Juan -- Forster, Anne -- Cousido-Siah, Alexandra -- Masson, Murielle -- Vande Pol, Scott -- Podjarny, Alberto -- Trave, Gilles -- Zanier, Katia -- R01CA134737/CA/NCI NIH HHS/ -- England -- Nature. 2016 Jan 28;529(7587):541-5. doi: 10.1038/nature16481. Epub 2016 Jan 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Equipe labellisee Ligue, Biotechnologie et signalisation cellulaire UMR 7242, Ecole Superieure de Biotechnologie de Strasbourg, Boulevard Sebastien Brant, BP 10413, F-67412 Illkirch, France. ; Institut de Genetique et de Biologie Moleculaire et Cellulaire (IGBMC)/INSERM U964/CNRS UMR 7104/Universite de Strasbourg, 1 rue Laurent Fries, BP 10142, F-67404 Illkirch, France. ; Department of Pathology, University of Virginia, PO Box 800904, Charlottesville, Virginia 22908-0904, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26789255" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Amino Acid Sequence ; Binding Sites ; Crystallography, X-Ray ; Human papillomavirus 16/chemistry/*metabolism/pathogenicity ; Humans ; Models, Biological ; Models, Molecular ; Molecular Sequence Data ; Mutant Proteins/chemistry/metabolism ; Oncogene Proteins, Viral/*chemistry/genetics/*metabolism ; Protein Binding ; Protein Structure, Tertiary ; *Proteolysis ; Repressor Proteins/*chemistry/genetics/*metabolism ; Tumor Suppressor Protein p53/*chemistry/genetics/*metabolism ; Ubiquitin-Protein Ligases/*chemistry
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  • 12
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    Nature Publishing Group (NPG)
    Publication Date: 2016-03-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gilbert, Natasha -- England -- Nature. 2016 Mar 17;531(7594):S56-7. doi: 10.1038/531S56a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26981729" target="_blank"〉PubMed〈/a〉
    Keywords: *Affect ; Health Behavior ; Humans ; Mental Health/*statistics & numerical data ; *Nature ; Parks, Recreational/*statistics & numerical data ; Urban Population
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  • 13
    Publication Date: 2016-01-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Betsholtz, Christer -- England -- Nature. 2016 Jan 14;529(7585):160-1. doi: 10.1038/nature16866. Epub 2016 Jan 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Genetics and Pathology at Uppsala University, and the Department of Medical Biochemistry and Biophysics at the Karolinska Institutet, Stockholm, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26735011" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Endothelium, Vascular/*growth & development/*metabolism ; Female ; Forkhead Transcription Factors/*metabolism ; Humans ; Male
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  • 14
    Publication Date: 2016-04-21
    Description: Our current understanding of immunology was largely defined in laboratory mice, partly because they are inbred and genetically homogeneous, can be genetically manipulated, allow kinetic tissue analyses to be carried out from the onset of disease, and permit the use of tractable disease models. Comparably reductionist experiments are neither technically nor ethically possible in humans. However, there is growing concern that laboratory mice do not reflect relevant aspects of the human immune system, which may account for failures to translate disease treatments from bench to bedside. Laboratory mice live in abnormally hygienic specific pathogen free (SPF) barrier facilities. Here we show that standard laboratory mouse husbandry has profound effects on the immune system and that environmental changes produce mice with immune systems closer to those of adult humans. Laboratory mice--like newborn, but not adult, humans--lack effector-differentiated and mucosally distributed memory T cells. These cell populations were present in free-living barn populations of feral mice and pet store mice with diverse microbial experience, and were induced in laboratory mice after co-housing with pet store mice, suggesting that the environment is involved in the induction of these cells. Altering the living conditions of mice profoundly affected the cellular composition of the innate and adaptive immune systems, resulted in global changes in blood cell gene expression to patterns that more closely reflected the immune signatures of adult humans rather than neonates, altered resistance to infection, and influenced T-cell differentiation in response to a de novo viral infection. These data highlight the effects of environment on the basal immune state and response to infection and suggest that restoring physiological microbial exposure in laboratory mice could provide a relevant tool for modelling immunological events in free-living organisms, including humans.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4871315/" 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/PMC4871315/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Beura, Lalit K -- Hamilton, Sara E -- Bi, Kevin -- Schenkel, Jason M -- Odumade, Oludare A -- Casey, Kerry A -- Thompson, Emily A -- Fraser, Kathryn A -- Rosato, Pamela C -- Filali-Mouhim, Ali -- Sekaly, Rafick P -- Jenkins, Marc K -- Vezys, Vaiva -- Haining, W Nicholas -- Jameson, Stephen C -- Masopust, David -- 1R01AI111671/AI/NIAID NIH HHS/ -- R01 AI075168/AI/NIAID NIH HHS/ -- R01 AI084913/AI/NIAID NIH HHS/ -- R01 AI111671/AI/NIAID NIH HHS/ -- R01 AI116678/AI/NIAID NIH HHS/ -- R01AI075168/AI/NIAID NIH HHS/ -- R01AI084913/AI/NIAID NIH HHS/ -- R01AI116678/AI/NIAID NIH HHS/ -- England -- Nature. 2016 Apr 28;532(7600):512-6. doi: 10.1038/nature17655. Epub 2016 Apr 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Immunology, Department of Microbiology and Immunology, University of Minnesota, Minneapolis, Minnesota 55414, USA. ; Center for Immunology, Department of Laboratory Medicine and Pathology, University of Minnesota, Minneapolis, Minnesota 55414, USA. ; Department of Pediatric Oncology, Dana-Farber Cancer Institute, and Pediatric Hematology and Oncology, Children's Hospital, Boston, Massachusetts 02115, USA. ; Department of Pathology, Case Western Reserve University, Cleveland, Ohio 44106, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27096360" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Animal Husbandry/*methods ; Animals ; Animals, Laboratory/*immunology ; Animals, Wild/*immunology ; Cell Differentiation ; *Environment ; Environmental Exposure ; Female ; Humans ; Immune System/*immunology ; Immunity/*immunology ; Immunity, Innate/immunology ; Immunologic Memory ; Infant, Newborn ; Male ; Mice ; *Models, Animal ; Phenotype ; Specific Pathogen-Free Organisms ; T-Lymphocytes/cytology/immunology ; Virus Diseases/immunology/virology
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  • 15
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    Nature Publishing Group (NPG)
    Publication Date: 2016-04-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Briggs, Adam -- England -- Nature. 2016 Mar 31;531(7596):551. doi: 10.1038/531551a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of Oxford, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27029244" target="_blank"〉PubMed〈/a〉
    Keywords: Beverages/analysis/*economics ; Child ; Dietary Sucrose/*adverse effects ; Food Industry/*economics/*legislation & jurisprudence ; Great Britain ; *Health Policy ; Humans ; *Legislation, Food ; Obesity/epidemiology/prevention & control ; Pediatric Obesity/prevention & control ; Public Health/legislation & jurisprudence ; Taxes/*legislation & jurisprudence
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  • 16
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    Nature Publishing Group (NPG)
    Publication Date: 2016-03-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McGilvray, Annabel -- England -- Nature. 2016 Mar 3;531(7592):S4-5. doi: 10.1038/531S4a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26934524" target="_blank"〉PubMed〈/a〉
    Keywords: Acetates/pharmacology/therapeutic use ; Aging/blood/drug effects/pathology/*psychology ; Alzheimer Disease/blood/therapy ; Animals ; Anti-Asthmatic Agents/pharmacology/therapeutic use ; Cognition Disorders/pathology/physiopathology/*prevention & control/*therapy ; Estrogens/pharmacology ; Female ; Hippocampus/drug effects/pathology/physiology/physiopathology ; Humans ; Inflammation Mediators/immunology ; Leukotrienes/immunology ; Macaca mulatta ; Male ; Mice ; Neuronal Plasticity/drug effects ; Parkinson Disease/therapy ; Plasma/chemistry/physiology ; Prefrontal Cortex/drug effects/pathology/physiology/physiopathology ; Quinolines/pharmacology/therapeutic use ; Rats ; Rejuvenation/*physiology/*psychology ; Synapses/drug effects/metabolism/pathology
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  • 17
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    Nature Publishing Group (NPG)
    Publication Date: 2016-05-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hodson, Richard -- England -- Nature. 2016 May 11;533(7602):S53. doi: 10.1038/533S53a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27167389" target="_blank"〉PubMed〈/a〉
    Keywords: Azepines ; *Cooperative Behavior ; *Diffusion of Innovation ; *Drug Discovery ; Drug Industry ; Humans ; *Information Dissemination ; Neglected Diseases ; *Open Access Publishing ; Triazoles ; Tropical Medicine
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  • 18
    Publication Date: 2016-05-14
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Castelvecchi, Davide -- England -- Nature. 2016 May 11;533(7602):153-4. doi: 10.1038/533153a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27172022" target="_blank"〉PubMed〈/a〉
    Keywords: *Computer Simulation/economics ; Humans ; Laboratories/*economics ; Prejudice/prevention & control/psychology ; Research/*economics/*instrumentation/trends ; Research Subjects ; Software/economics ; *User-Computer Interface
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  • 19
    Publication Date: 2016-03-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Padma, T V -- England -- Nature. 2016 Mar 3;531(7592):16-7. doi: 10.1038/531016a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26935674" target="_blank"〉PubMed〈/a〉
    Keywords: Biomedical Research/economics ; Biotechnology/economics/trends ; *Budgets ; Drug Industry/economics ; *Federal Government ; Genomics/*economics/trends ; Humans ; India ; Precision Medicine/economics ; Research Support as Topic/economics ; Technology Transfer
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  • 20
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    Nature Publishing Group (NPG)
    Publication Date: 2016-04-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Webster, Andrew -- England -- Nature. 2016 Apr 7;532(7597):7. doi: 10.1038/532007a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Director of the Science and Technology Studies Unit (SATSU) at the University of York, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27078528" target="_blank"〉PubMed〈/a〉
    Keywords: *Communication ; Great Britain ; Humans ; Lobbying ; *Public Opinion ; Public Policy ; *Research Personnel ; Social Sciences/*trends
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  • 21
    Publication Date: 2016-03-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Callaway, Ewen -- England -- Nature. 2016 Mar 17;531(7594):286. doi: 10.1038/531286a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26983523" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Nucleus/genetics ; DNA/*analysis/genetics ; DNA, Mitochondrial/analysis/genetics ; Evolution, Molecular ; Humans ; Neanderthals/*genetics ; *Phylogeny ; Sequence Analysis, DNA ; Time Factors
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  • 22
    Publication Date: 2016-04-07
    Description: Cells receive growth and survival stimuli through their attachment to an extracellular matrix (ECM). Overcoming the addiction to ECM-induced signals is required for anchorage-independent growth, a property of most malignant cells. Detachment from ECM is associated with enhanced production of reactive oxygen species (ROS) owing to altered glucose metabolism. Here we identify an unconventional pathway that supports redox homeostasis and growth during adaptation to anchorage independence. We observed that detachment from monolayer culture and growth as anchorage-independent tumour spheroids was accompanied by changes in both glucose and glutamine metabolism. Specifically, oxidation of both nutrients was suppressed in spheroids, whereas reductive formation of citrate from glutamine was enhanced. Reductive glutamine metabolism was highly dependent on cytosolic isocitrate dehydrogenase-1 (IDH1), because the activity was suppressed in cells homozygous null for IDH1 or treated with an IDH1 inhibitor. This activity occurred in absence of hypoxia, a well-known inducer of reductive metabolism. Rather, IDH1 mitigated mitochondrial ROS in spheroids, and suppressing IDH1 reduced spheroid growth through a mechanism requiring mitochondrial ROS. Isotope tracing revealed that in spheroids, isocitrate/citrate produced reductively in the cytosol could enter the mitochondria and participate in oxidative metabolism, including oxidation by IDH2. This generates NADPH in the mitochondria, enabling cells to mitigate mitochondrial ROS and maximize growth. Neither IDH1 nor IDH2 was necessary for monolayer growth, but deleting either one enhanced mitochondrial ROS and reduced spheroid size, as did deletion of the mitochondrial citrate transporter protein. Together, the data indicate that adaptation to anchorage independence requires a fundamental change in citrate metabolism, initiated by IDH1-dependent reductive carboxylation and culminating in suppression of mitochondrial ROS.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4860952/" 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/PMC4860952/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jiang, Lei -- Shestov, Alexander A -- Swain, Pamela -- Yang, Chendong -- Parker, Seth J -- Wang, Qiong A -- Terada, Lance S -- Adams, Nicholas D -- McCabe, Michael T -- Pietrak, Beth -- Schmidt, Stan -- Metallo, Christian M -- Dranka, Brian P -- Schwartz, Benjamin -- DeBerardinis, Ralph J -- R01 CA157996/CA/NCI NIH HHS/ -- R01 CA188652/CA/NCI NIH HHS/ -- R01CA157996/CA/NCI NIH HHS/ -- R01CA188652/CA/NCI NIH HHS/ -- England -- Nature. 2016 Apr 14;532(7598):255-8. doi: 10.1038/nature17393. Epub 2016 Apr 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Children's Medical Center Research Institute, UT Southwestern Medical Center, Dallas, Texas 75390-8502, USA. ; Department of Radiology, University of Pennsylvania School of Medicine, 3620 Hamilton Walk, Philadelphia, Pennsylvania 19104, USA. ; Seahorse Bioscience, 16 Esquire Road, North Billerica, Massachusetts 01862, USA. ; Department of Bioengineering, University of California, San Diego, La Jolla, California 92093, USA. ; Touchstone Diabetes Center, UT Southwestern Medical Center, Dallas, Texas 75390, USA. ; Department of Internal Medicine, UT Southwestern Medical Center, Dallas, Texas 75390, USA. ; GlaxoSmithKline, 1250 South Collegeville Road, Collegeville, Pennsylvania 19426, USA. ; Department of Pediatrics, UT Southwestern Medical Center, Dallas, Texas 75390, USA. ; McDermott Center for Human Growth and Development, UT Southwestern Medical Center, Dallas, Texas 75390, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27049945" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Adhesion ; Cell Hypoxia ; Cell Line, Tumor ; Cell Proliferation ; Citric Acid/*metabolism ; Contact Inhibition ; Cytosol/enzymology/metabolism ; Extracellular Matrix/metabolism ; Glucose/metabolism ; Glutamic Acid/metabolism ; Glutamine/metabolism ; *Homeostasis ; Humans ; Isocitrate Dehydrogenase/antagonists & inhibitors/deficiency/genetics/*metabolism ; Isocitrates/metabolism ; Mitochondria/*metabolism ; NADP/biosynthesis ; Neoplasms/enzymology/*metabolism/*pathology ; Oxidation-Reduction ; Oxidative Stress ; Reactive Oxygen Species/*metabolism ; Spheroids, Cellular/metabolism/pathology
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  • 23
    Publication Date: 2016-04-07
    Description: In bright light, cone-photoreceptors are active and colour vision derives from a comparison of signals in cones with different visual pigments. This comparison begins in the retina, where certain retinal ganglion cells have 'colour-opponent' visual responses-excited by light of one colour and suppressed by another colour. In dim light, rod-photoreceptors are active, but colour vision is impossible because they all use the same visual pigment. Instead, the rod signals are thought to splice into retinal circuits at various points, in synergy with the cone signals. Here we report a new circuit for colour vision that challenges these expectations. A genetically identified type of mouse retinal ganglion cell called JAMB (J-RGC), was found to have colour-opponent responses, OFF to ultraviolet (UV) light and ON to green light. Although the mouse retina contains a green-sensitive cone, the ON response instead originates in rods. Rods and cones both contribute to the response over several decades of light intensity. Remarkably, the rod signal in this circuit is antagonistic to that from cones. For rodents, this UV-green channel may play a role in social communication, as suggested by spectral measurements from the environment. In the human retina, all of the components for this circuit exist as well, and its function can explain certain experiences of colour in dim lights, such as a 'blue shift' in twilight. The discovery of this genetically defined pathway will enable new targeted studies of colour processing in the brain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Joesch, Maximilian -- Meister, Markus -- England -- Nature. 2016 Apr 14;532(7598):236-9. doi: 10.1038/nature17158. Epub 2016 Apr 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Harvard University, 52 Oxford Street, Cambridge, Massachusetts 02138, USA. ; Division of Biology and Biological Engineering, California Institute of Technology, Pasadena, California 91125, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27049951" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Color ; Color Perception/*physiology/radiation effects ; Color Vision/*physiology/radiation effects ; Darkness ; Female ; Humans ; Male ; Mice ; Models, Neurological ; Neural Pathways/*physiology/radiation effects ; Retinal Cone Photoreceptor Cells/*metabolism/radiation effects ; Retinal Ganglion Cells/metabolism/radiation effects ; Retinal Rod Photoreceptor Cells/*metabolism/radiation effects ; Synapses/metabolism/radiation effects ; Territoriality ; Ultraviolet Rays
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  • 24
    Publication Date: 2016-04-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Penn, Bennett H -- Cox, Jeffery S -- England -- Nature. 2016 Apr 21;532(7599):321-2. doi: 10.1038/nature17882. Epub 2016 Apr 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Division of Infectious Diseases, University of California, San Francisco, San Francisco, California 94143, USA. ; Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, California 94720-3370, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27049940" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Endoplasmic Reticulum Stress ; Female ; Humans ; Inflammation/*metabolism ; Male ; Nod1 Signaling Adaptor Protein/*metabolism ; Nod2 Signaling Adaptor Protein/*metabolism ; *Signal Transduction
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  • 25
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    Nature Publishing Group (NPG)
    Publication Date: 2016-04-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chi, Kelly Rae -- England -- Nature. 2016 Apr 14;532(7598):269-71. doi: 10.1038/532269a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27075102" target="_blank"〉PubMed〈/a〉
    Keywords: Aged, 80 and over ; Biopsy/economics/*methods ; Blood Platelets/cytology ; DNA Mutational Analysis/economics/methods ; DNA, Neoplasm/*blood/genetics ; Drug Resistance, Neoplasm/genetics ; Exosomes/genetics ; Female ; Humans ; Neoplasm Metastasis/diagnosis/genetics ; Neoplasm Recurrence, Local/blood/diagnosis/genetics ; Neoplasms/*blood/*diagnosis/drug therapy/genetics ; Neoplastic Cells, Circulating/metabolism ; Phagocytosis ; Polymerase Chain Reaction ; Reproducibility of Results ; Sensitivity and Specificity
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  • 26
    Publication Date: 2016-02-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Check Hayden, Erika -- England -- Nature. 2016 Feb 11;530(7589):142-3. doi: 10.1038/530142a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26863963" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Viral/analysis/immunology ; Biomedical Research/*trends ; Brazil/epidemiology ; Case-Control Studies ; Disease Models, Animal ; *Evidence-Based Medicine ; Female ; Fetal Diseases/epidemiology/etiology/virology ; Humans ; Infant, Newborn ; Infant, Newborn, Diseases/epidemiology/etiology/virology ; Infectious Disease Transmission, Vertical ; Microcephaly/epidemiology/*etiology/pathology/*virology ; Pregnancy ; Time Factors ; Zika Virus/genetics/immunology/isolation & purification/*pathogenicity ; Zika Virus Infection/*complications/diagnosis/epidemiology/*virology
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  • 27
    Publication Date: 2016-03-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kamoun, Sophien -- Zipfel, Cyril -- England -- Nature. 2016 Mar 10;531(7593):173. doi: 10.1038/531173e.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Sainsbury Laboratory, Norwich, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26961649" target="_blank"〉PubMed〈/a〉
    Keywords: *Editorial Policies ; Humans ; Peer Review, Research/*methods/*standards ; Periodicals as Topic/*standards ; Research Design/*statistics & numerical data ; *Retraction of Publication as Topic
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  • 28
    Publication Date: 2016-05-14
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Check Hayden, Erika -- England -- Nature. 2016 May 11;533(7602):154-5. doi: 10.1038/533154a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27172023" target="_blank"〉PubMed〈/a〉
    Keywords: Cognition ; *Educational Status ; European Continental Ancestry Group/genetics ; Gene-Environment Interaction ; Genetic Markers/genetics ; Genetic Variation/*genetics ; Humans ; Intelligence/genetics ; Multifactorial Inheritance/*genetics ; Socioeconomic Factors ; Students/*psychology
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  • 29
    Publication Date: 2016-02-26
    Description: Thalidomide and its derivatives, lenalidomide and pomalidomide, are immune modulatory drugs (IMiDs) used in the treatment of haematologic malignancies. IMiDs bind CRBN, the substrate receptor of the CUL4-RBX1-DDB1-CRBN (also known as CRL4(CRBN)) E3 ubiquitin ligase, and inhibit ubiquitination of endogenous CRL4(CRBN) substrates. Unexpectedly, IMiDs also repurpose the ligase to target new proteins for degradation. Lenalidomide induces degradation of the lymphoid transcription factors Ikaros and Aiolos (also known as IKZF1 and IKZF3), and casein kinase 1alpha (CK1alpha), which contributes to its clinical efficacy in the treatment of multiple myeloma and 5q-deletion associated myelodysplastic syndrome (del(5q) MDS), respectively. How lenalidomide alters the specificity of the ligase to degrade these proteins remains elusive. Here we present the 2.45 A crystal structure of DDB1-CRBN bound to lenalidomide and CK1alpha. CRBN and lenalidomide jointly provide the binding interface for a CK1alpha beta-hairpin-loop located in the kinase N-lobe. We show that CK1alpha binding to CRL4(CRBN) is strictly dependent on the presence of an IMiD. Binding of IKZF1 to CRBN similarly requires the compound and both, IKZF1 and CK1alpha, use a related binding mode. Our study provides a mechanistic explanation for the selective efficacy of lenalidomide in del(5q) MDS therapy. We anticipate that high-affinity protein-protein interactions induced by small molecules will provide opportunities for drug development, particularly for targeted protein degradation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Petzold, Georg -- Fischer, Eric S -- Thoma, Nicolas H -- England -- Nature. 2016 Apr 7;532(7597):127-30. doi: 10.1038/nature16979. Epub 2016 Feb 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Friedrich Miescher Institute for Biomedical Research, Maulbeerstrasse 66, CH-4058 Basel, Switzerland. ; University of Basel, Petersplatz 10, CH-4003 Basel, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26909574" target="_blank"〉PubMed〈/a〉
    Keywords: Binding Sites/drug effects ; Casein Kinase Ialpha/chemistry/*metabolism ; Catalytic Domain ; Crystallography, X-Ray ; Humans ; Ikaros Transcription Factor/chemistry/metabolism ; Models, Molecular ; Protein Binding/drug effects ; Proteolysis/drug effects ; Structure-Activity Relationship ; Substrate Specificity/drug effects ; Thalidomide/*analogs & derivatives/chemistry/metabolism/pharmacology ; Ubiquitin-Protein Ligases/chemistry/*metabolism ; Ubiquitination/drug effects
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  • 30
    Publication Date: 2016-03-24
    Description: A marked bias towards risk aversion has been observed in nearly every species tested. A minority of individuals, however, instead seem to prefer risk (repeatedly choosing uncertain large rewards over certain but smaller rewards), and even risk-averse individuals sometimes opt for riskier alternatives. It is not known how neural activity underlies such important shifts in decision-making--either as a stable trait across individuals or at the level of variability within individuals. Here we describe a model of risk-preference in rats, in which stable individual differences, trial-by-trial choices, and responses to pharmacological agents all parallel human behaviour. By combining new genetic targeting strategies with optical recording of neural activity during behaviour in this model, we identify relevant temporally specific signals from a genetically and anatomically defined population of neurons. This activity occurred within dopamine receptor type-2 (D2R)-expressing cells in the nucleus accumbens (NAc), signalled unfavourable outcomes from the recent past at a time appropriate for influencing subsequent decisions, and also predicted subsequent choices made. Having uncovered this naturally occurring neural correlate of risk selection, we then mimicked the temporally specific signal with optogenetic control during decision-making and demonstrated its causal effect in driving risk-preference. Specifically, risk-preferring rats could be instantaneously converted to risk-averse rats with precisely timed phasic stimulation of NAc D2R cells. These findings suggest that individual differences in risk-preference, as well as real-time risky decision-making, can be largely explained by the encoding in D2R-expressing NAc cells of prior unfavourable outcomes during decision-making.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zalocusky, Kelly A -- Ramakrishnan, Charu -- Lerner, Talia N -- Davidson, Thomas J -- Knutson, Brian -- Deisseroth, Karl -- 1F31MH105151-01/MH/NIMH NIH HHS/ -- 1F32MH105053-01/MH/NIMH NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2016 Mar 31;531(7596):642-6. doi: 10.1038/nature17400. Epub 2016 Mar 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Bioengineering Department, Stanford University, Stanford, California 94305, USA. ; Neurosciences Program, Stanford University, Stanford, California 94305, USA. ; CNC Program, Stanford University, Stanford, California 94305, USA. ; Psychology Department, Stanford University, Stanford, California 94305, USA. ; Howard Hughes Medical Institute, Stanford University, Stanford, California 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27007845" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Choice Behavior ; *Decision Making ; Humans ; Individuality ; Male ; Models, Animal ; Models, Neurological ; Models, Psychological ; Neurons/*metabolism ; Nucleus Accumbens/*cytology/*metabolism ; Rats ; Rats, Long-Evans ; Receptors, Dopamine D2/*metabolism ; Reward ; *Risk Management ; Signal Transduction ; Uncertainty
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  • 31
    Publication Date: 2016-04-14
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chu, Derrick M -- Aagaard, Kjersti M -- England -- Nature. 2016 Apr 21;532(7599):316-7. doi: 10.1038/nature17887. Epub 2016 Apr 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Obstetrics and Gynecology, Baylor College of Medicine, Houston, Texas 77030, USA. ; Departments of Molecular and Human Genetics, Molecular and Cell Biology, and Molecular Physiology and Biophysics, Baylor College of Medicine.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27074514" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Child, Preschool ; Chronic Disease ; Clostridium symbiosum/isolation & purification/physiology ; Diet/adverse effects/methods ; Feces/microbiology ; Female ; Germ-Free Life ; Growth Disorders/*diet therapy/etiology/*microbiology ; Healthy Volunteers ; Humans ; Infant ; Intestines/drug effects/*microbiology ; Liver/metabolism ; Malawi ; Malnutrition/complications/*diet therapy/*microbiology ; Mice ; Microbiota/drug effects/genetics/*physiology ; Milk, Human/chemistry/microbiology ; Mothers ; Oligosaccharides/analysis/pharmacology/therapeutic use ; Ruminococcus/isolation & purification/physiology ; Somatomedins/biosynthesis ; Weight Gain/drug effects
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  • 32
    Publication Date: 2016-03-31
    Description: Brown and beige adipose tissues can dissipate chemical energy as heat through thermogenic respiration, which requires uncoupling protein 1 (UCP1). Thermogenesis from these adipocytes can combat obesity and diabetes, encouraging investigation of factors that control UCP1-dependent respiration in vivo. Here we show that acutely activated thermogenesis in brown adipose tissue is defined by a substantial increase in levels of mitochondrial reactive oxygen species (ROS). Remarkably, this process supports in vivo thermogenesis, as pharmacological depletion of mitochondrial ROS results in hypothermia upon cold exposure, and inhibits UCP1-dependent increases in whole-body energy expenditure. We further establish that thermogenic ROS alter the redox status of cysteine thiols in brown adipose tissue to drive increased respiration, and that Cys253 of UCP1 is a key target. UCP1 Cys253 is sulfenylated during thermogenesis, while mutation of this site desensitizes the purine-nucleotide-inhibited state of the carrier to adrenergic activation and uncoupling. These studies identify mitochondrial ROS induction in brown adipose tissue as a mechanism that supports UCP1-dependent thermogenesis and whole-body energy expenditure, which opens the way to improved therapeutic strategies for combating metabolic disorders.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chouchani, Edward T -- Kazak, Lawrence -- Jedrychowski, Mark P -- Lu, Gina Z -- Erickson, Brian K -- Szpyt, John -- Pierce, Kerry A -- Laznik-Bogoslavski, Dina -- Vetrivelan, Ramalingam -- Clish, Clary B -- Robinson, Alan J -- Gygi, Steve P -- Spiegelman, Bruce M -- DK31405/DK/NIDDK NIH HHS/ -- Canadian Institutes of Health Research/Canada -- England -- Nature. 2016 Apr 7;532(7597):112-6. doi: 10.1038/nature17399. Epub 2016 Mar 30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA. ; Department of Cell Biology, Harvard Medical School, Boston, Massachusetts 02115, USA. ; Broad Institute of Harvard and MIT, Cambridge, Massachusetts 02142, USA. ; Department of Neurology, Harvard Medical School, Boston, Massachusetts 02215, USA. ; MRC Mitochondrial Biology Unit, Hills Road, Cambridge CB2 0XY, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27027295" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue, Brown/chemistry/cytology/metabolism ; Animals ; Cell Respiration ; Cysteine/*chemistry/genetics/metabolism ; *Energy Metabolism/drug effects ; Female ; Humans ; Ion Channels/*chemistry/deficiency/genetics/*metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mitochondria/drug effects/*metabolism ; Mitochondrial Proteins/*chemistry/deficiency/genetics/*metabolism ; Mutant Proteins/chemistry/genetics/metabolism ; Oxidation-Reduction ; Reactive Oxygen Species/*metabolism ; Sulfhydryl Compounds/metabolism ; *Thermogenesis/drug effects
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  • 33
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    Nature Publishing Group (NPG)
    Publication Date: 2016-01-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉England -- Nature. 2016 Jan 28;529(7587):438. doi: 10.1038/529438a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26819008" target="_blank"〉PubMed〈/a〉
    Keywords: *Anxiety ; Humans ; Professional Competence ; Research Personnel/*psychology ; *Self Concept ; Syndrome ; Wit and Humor as Topic
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  • 34
    Publication Date: 2016-02-11
    Description: Since the origins of agriculture, the scale of human cooperation and societal complexity has dramatically expanded. This fact challenges standard evolutionary explanations of prosociality because well-studied mechanisms of cooperation based on genetic relatedness, reciprocity and partner choice falter as people increasingly engage in fleeting transactions with genetically unrelated strangers in large anonymous groups. To explain this rapid expansion of prosociality, researchers have proposed several mechanisms. Here we focus on one key hypothesis: cognitive representations of gods as increasingly knowledgeable and punitive, and who sanction violators of interpersonal social norms, foster and sustain the expansion of cooperation, trust and fairness towards co-religionist strangers. We tested this hypothesis using extensive ethnographic interviews and two behavioural games designed to measure impartial rule-following among people (n = 591, observations = 35,400) from eight diverse communities from around the world: (1) inland Tanna, Vanuatu; (2) coastal Tanna, Vanuatu; (3) Yasawa, Fiji; (4) Lovu, Fiji; (5) Pesqueiro, Brazil; (6) Pointe aux Piments, Mauritius; (7) the Tyva Republic (Siberia), Russia; and (8) Hadzaland, Tanzania. Participants reported adherence to a wide array of world religious traditions including Christianity, Hinduism and Buddhism, as well as notably diverse local traditions, including animism and ancestor worship. Holding a range of relevant variables constant, the higher participants rated their moralistic gods as punitive and knowledgeable about human thoughts and actions, the more coins they allocated to geographically distant co-religionist strangers relative to both themselves and local co-religionists. Our results support the hypothesis that beliefs in moralistic, punitive and knowing gods increase impartial behaviour towards distant co-religionists, and therefore can contribute to the expansion of prosociality.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Purzycki, Benjamin Grant -- Apicella, Coren -- Atkinson, Quentin D -- Cohen, Emma -- McNamara, Rita Anne -- Willard, Aiyana K -- Xygalatas, Dimitris -- Norenzayan, Ara -- Henrich, Joseph -- England -- Nature. 2016 Feb 18;530(7590):327-30. doi: 10.1038/nature16980. Epub 2016 Feb 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre for Human Evolution, Cognition, and Culture, University of British Columbia, 1871 West Mall, Vancouver, British Columbia V6T 1Z2, Canada. ; Department of Psychology, University of Pennsylvania, Solomon Laboratories, 3720 Walnut Street, Philadelphia, Pennsylvania 19104-6241, USA. ; Department of Psychology, University of Auckland, Human Sciences Building, 10 Symonds Street, Auckland 1010, New Zealand. ; Max Planck Institute for the Science of Human History, Kahlaische Strasse 10, D-07745 Jena, Germany. ; Institute of Cognitive and Evolutionary Anthropology, University of Oxford, 64 Banbury Road, Oxford OX2 6PN, UK. ; Wadham College, University of Oxford, Parks Road, Oxford, OX1 3PN, UK. ; Department of Psychology, University of British Columbia, 2136 West Mall, Vancouver, British Columbia V6T 1Z4, Canada. ; Culture, and Development Laboratory, Department of Psychology, The University of Texas at Austin, 1 University Station #A8000, Austin, Texas 78712-0187, USA. ; Department of Anthropology, University of Connecticut, 354 Mansfield Road, Unit 1176, Storrs, Connecticut 06029, USA. ; Interacting Minds Centre, Aarhus University, Jens Chr. Skous Vej 4, building 1483, DK-8000, Aarhus, Denmark. ; LEVYNA, Masaryk University, Brno 60200, Czech Republic. ; Department of Economics, University of British Columbia, 2136 West Mall, Vancouver, British Columbia V6T 1Z4, Canada. ; Department of Human Evolutionary Biology, Harvard University, 11 Divinity Ave, Cambridge, Massachusetts 02138, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26863190" target="_blank"〉PubMed〈/a〉
    Keywords: Altruism ; *Cooperative Behavior ; Ethnic Groups/psychology ; Female ; Games, Experimental ; Humans ; Internationality ; *Interpersonal Relations ; Interviews as Topic ; Logistic Models ; Male ; *Morals ; Odds Ratio ; Punishment/*psychology ; Random Allocation ; *Religion and Psychology ; Trust
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  • 35
    Publication Date: 2016-04-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Qiu, Jane -- England -- Nature. 2016 Apr 28;532(7600):428-31. doi: 10.1038/532428a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27121822" target="_blank"〉PubMed〈/a〉
    Keywords: Altitude ; Disasters/*prevention & control/*statistics & numerical data ; Earthquakes/mortality/*statistics & numerical data ; *Forecasting ; Humans ; Landslides/mortality/*statistics & numerical data ; Nepal ; Rain
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  • 36
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    Nature Publishing Group (NPG)
    Publication Date: 2016-01-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉England -- Nature. 2016 Jan 28;529(7587):437. doi: 10.1038/529437a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26819006" target="_blank"〉PubMed〈/a〉
    Keywords: *Artificial Intelligence ; Games, Recreational ; Humans ; *Intuition ; Neural Networks (Computer) ; *Software
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  • 37
    Publication Date: 2016-04-05
    Description: Cancer is a disease of ageing. Clinically, aged cancer patients tend to have a poorer prognosis than young. This may be due to accumulated cellular damage, decreases in adaptive immunity, and chronic inflammation. However, the effects of the aged microenvironment on tumour progression have been largely unexplored. Since dermal fibroblasts can have profound impacts on melanoma progression, we examined whether age-related changes in dermal fibroblasts could drive melanoma metastasis and response to targeted therapy. Here we find that aged fibroblasts secrete a Wnt antagonist, sFRP2, which activates a multi-step signalling cascade in melanoma cells that results in a decrease in beta-catenin and microphthalmia-associated transcription factor (MITF), and ultimately the loss of a key redox effector, APE1. Loss of APE1 attenuates the response of melanoma cells to DNA damage induced by reactive oxygen species, rendering the cells more resistant to targeted therapy (vemurafenib). Age-related increases in sFRP2 also augment both angiogenesis and metastasis of melanoma cells. These data provide an integrated view of how fibroblasts in the aged microenvironment contribute to tumour progression, offering new possibilities for the design of therapy for the elderly.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4833579/" 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/PMC4833579/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaur, Amanpreet -- Webster, Marie R -- Marchbank, Katie -- Behera, Reeti -- Ndoye, Abibatou -- Kugel, Curtis H 3rd -- Dang, Vanessa M -- Appleton, Jessica -- O'Connell, Michael P -- Cheng, Phil -- Valiga, Alexander A -- Morissette, Rachel -- McDonnell, Nazli B -- Ferrucci, Luigi -- Kossenkov, Andrew V -- Meeth, Katrina -- Tang, Hsin-Yao -- Yin, Xiangfan -- Wood, William H 3rd -- Lehrmann, Elin -- Becker, Kevin G -- Flaherty, Keith T -- Frederick, Dennie T -- Wargo, Jennifer A -- Cooper, Zachary A -- Tetzlaff, Michael T -- Hudgens, Courtney -- Aird, Katherine M -- Zhang, Rugang -- Xu, Xiaowei -- Liu, Qin -- Bartlett, Edmund -- Karakousis, Giorgos -- Eroglu, Zeynep -- Lo, Roger S -- Chan, Matthew -- Menzies, Alexander M -- Long, Georgina V -- Johnson, Douglas B -- Sosman, Jeffrey -- Schilling, Bastian -- Schadendorf, Dirk -- Speicher, David W -- Bosenberg, Marcus -- Ribas, Antoni -- Weeraratna, Ashani T -- P01 CA 114046-06/CA/NCI NIH HHS/ -- P01 CA114046/CA/NCI NIH HHS/ -- P30 CA010815/CA/NCI NIH HHS/ -- P50 CA093372/CA/NCI NIH HHS/ -- R01 CA174746/CA/NCI NIH HHS/ -- R01 CA174746-01/CA/NCI NIH HHS/ -- T32 CA009171/CA/NCI NIH HHS/ -- T32 CA9171-36/CA/NCI NIH HHS/ -- Intramural NIH HHS/ -- England -- Nature. 2016 Apr 14;532(7598):250-4. doi: 10.1038/nature17392. Epub 2016 Apr 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Wistar Institute, Philadelphia, Pennsylvania 19104, USA. ; University of the Sciences, Philadelphia, Pennsylvania 19104, USA. ; Department of Dermatology, University of Zurich, Zurich CH-8006, Switzerland. ; The National Institute on Aging, National Institutes of Health, Baltimore, Maryland 21224, USA. ; Department of Dermatology and Pathology, Yale University, New Haven, Connecticut 06511, USA. ; Massachusetts General Hospital Cancer Center, Developmental Therapeutics, Boston 02114, Massachusetts, USA. ; Department of Surgical Oncology, MD Anderson Cancer Center, Houston, Texas 77030, USA. ; Departments of Surgery and Pathology, Abramson Cancer Center, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA. ; Department of Medical Oncology, City of Hope Medical Center, Duarte, California 91010, USA. ; Department of Medicine, Division of Hematology-Oncology, University of California Los Angeles, Los Angeles, California 90095, USA. ; Crown Princess Mary Cancer Centre, Westmead Hospital, Westmead 2145, Australia. ; Melanoma Institute Australia and The University of Sydney, Sydney 2000, Australia. ; Department of Medicine, Vanderbilt University Medical Center, Nashville Tennessee 37232, USA. ; Department of Dermatology, University Hospital, West German Cancer Center, University Duesburg-Essen, Essen, Germany. ; German Cancer Consortium (DKTK), Heidelberg 45127, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27042933" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aging/*metabolism ; Animals ; Cell Line, Tumor ; Culture Media, Conditioned/pharmacology ; DNA Damage ; DNA-(Apurinic or Apyrimidinic Site) Lyase/metabolism ; Disease Progression ; *Drug Resistance, Neoplasm ; Fibroblasts/secretion ; Humans ; Indoles/pharmacology/therapeutic use ; Male ; Melanoma/blood supply/*drug therapy/genetics/*pathology ; Membrane Proteins/*metabolism/secretion ; Mice ; Microphthalmia-Associated Transcription Factor/metabolism ; Middle Aged ; Molecular Targeted Therapy ; *Neoplasm Metastasis ; Neovascularization, Pathologic ; Oxidative Stress ; Phenotype ; Reactive Oxygen Species/metabolism ; Sulfonamides/pharmacology/therapeutic use ; *Tumor Microenvironment ; Wnt Signaling Pathway ; Wnt1 Protein/antagonists & inhibitors ; beta Catenin/metabolism
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  • 38
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    Nature Publishing Group (NPG)
    Publication Date: 2016-03-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉King, Anthony -- England -- Nature. 2016 Mar 3;531(7592):S18-9. doi: 10.1038/531S18a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26934522" target="_blank"〉PubMed〈/a〉
    Keywords: Amygdala/metabolism ; Animals ; Brain/*physiology ; Bullying ; DNA Methylation ; Depression/complications/prevention & control/therapy ; Emotional Adjustment ; Epigenesis, Genetic/genetics ; Female ; Hippocampus/metabolism ; Humans ; Hydrocortisone/metabolism ; Maternal Behavior ; Memory/physiology ; Mice ; Models, Animal ; Oxytocin/metabolism ; Pregnancy ; Prenatal Exposure Delayed Effects/genetics ; Psychological Trauma/complications/genetics/metabolism ; Rats ; *Resilience, Psychological ; Social Isolation/psychology ; Stress, Psychological/complications/genetics/metabolism/therapy
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  • 39
    Publication Date: 2016-02-04
    Description: The Ebola virus disease epidemic in West Africa is the largest on record, responsible for over 28,599 cases and more than 11,299 deaths. Genome sequencing in viral outbreaks is desirable to characterize the infectious agent and determine its evolutionary rate. Genome sequencing also allows the identification of signatures of host adaptation, identification and monitoring of diagnostic targets, and characterization of responses to vaccines and treatments. The Ebola virus (EBOV) genome substitution rate in the Makona strain has been estimated at between 0.87 x 10(-3) and 1.42 x 10(-3) mutations per site per year. This is equivalent to 16-27 mutations in each genome, meaning that sequences diverge rapidly enough to identify distinct sub-lineages during a prolonged epidemic. Genome sequencing provides a high-resolution view of pathogen evolution and is increasingly sought after for outbreak surveillance. Sequence data may be used to guide control measures, but only if the results are generated quickly enough to inform interventions. Genomic surveillance during the epidemic has been sporadic owing to a lack of local sequencing capacity coupled with practical difficulties transporting samples to remote sequencing facilities. To address this problem, here we devise a genomic surveillance system that utilizes a novel nanopore DNA sequencing instrument. In April 2015 this system was transported in standard airline luggage to Guinea and used for real-time genomic surveillance of the ongoing epidemic. We present sequence data and analysis of 142 EBOV samples collected during the period March to October 2015. We were able to generate results less than 24 h after receiving an Ebola-positive sample, with the sequencing process taking as little as 15-60 min. We show that real-time genomic surveillance is possible in resource-limited settings and can be established rapidly to monitor outbreaks.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Quick, Joshua -- Loman, Nicholas J -- Duraffour, Sophie -- Simpson, Jared T -- Severi, Ettore -- Cowley, Lauren -- Bore, Joseph Akoi -- Koundouno, Raymond -- Dudas, Gytis -- Mikhail, Amy -- Ouedraogo, Nobila -- Afrough, Babak -- Bah, Amadou -- Baum, Jonathan H J -- Becker-Ziaja, Beate -- Boettcher, Jan Peter -- Cabeza-Cabrerizo, Mar -- Camino-Sanchez, Alvaro -- Carter, Lisa L -- Doerrbecker, Juliane -- Enkirch, Theresa -- Garcia-Dorival, Isabel -- Hetzelt, Nicole -- Hinzmann, Julia -- Holm, Tobias -- Kafetzopoulou, Liana Eleni -- Koropogui, Michel -- Kosgey, Abigael -- Kuisma, Eeva -- Logue, Christopher H -- Mazzarelli, Antonio -- Meisel, Sarah -- Mertens, Marc -- Michel, Janine -- Ngabo, Didier -- Nitzsche, Katja -- Pallasch, Elisa -- Patrono, Livia Victoria -- Portmann, Jasmine -- Repits, Johanna Gabriella -- Rickett, Natasha Y -- Sachse, Andreas -- Singethan, Katrin -- Vitoriano, Ines -- Yemanaberhan, Rahel L -- Zekeng, Elsa G -- Racine, Trina -- Bello, Alexander -- Sall, Amadou Alpha -- Faye, Ousmane -- Faye, Oumar -- Magassouba, N'Faly -- Williams, Cecelia V -- Amburgey, Victoria -- Winona, Linda -- Davis, Emily -- Gerlach, Jon -- Washington, Frank -- Monteil, Vanessa -- Jourdain, Marine -- Bererd, Marion -- Camara, Alimou -- Somlare, Hermann -- Camara, Abdoulaye -- Gerard, Marianne -- Bado, Guillaume -- Baillet, Bernard -- Delaune, Deborah -- Nebie, Koumpingnin Yacouba -- Diarra, Abdoulaye -- Savane, Yacouba -- Pallawo, Raymond Bernard -- Gutierrez, Giovanna Jaramillo -- Milhano, Natacha -- Roger, Isabelle -- Williams, Christopher J -- Yattara, Facinet -- Lewandowski, Kuiama -- Taylor, James -- Rachwal, Phillip -- Turner, Daniel J -- Pollakis, Georgios -- Hiscox, Julian A -- Matthews, David A -- O'Shea, Matthew K -- Johnston, Andrew McD -- Wilson, Duncan -- Hutley, Emma -- Smit, Erasmus -- Di Caro, Antonino -- Wolfel, Roman -- Stoecker, Kilian -- Fleischmann, Erna -- Gabriel, Martin -- Weller, Simon A -- Koivogui, Lamine -- Diallo, Boubacar -- Keita, Sakoba -- Rambaut, Andrew -- Formenty, Pierre -- Gunther, Stephan -- Carroll, Miles W -- Medical Research Council/United Kingdom -- England -- Nature. 2016 Feb 11;530(7589):228-32. doi: 10.1038/nature16996. Epub 2016 Feb 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Microbiology and Infection, University of Birmingham, Birmingham B15 2TT, UK. ; The European Mobile Laboratory Consortium, Bernhard-Nocht-Institute for Tropical Medicine, D-20359 Hamburg, Germany. ; Bernhard-Nocht-Institute for Tropical Medicine, D-20359 Hamburg, Germany. ; Ontario Institute for Cancer Research, Toronto M5G 0A3, Canada. ; Department of Computer Science, University of Toronto, Toronto M5S 3G4, Canada. ; European Centre for Disease Prevention and Control (ECDC), 171 65 Solna, Sweden. ; National Infection Service, Public Health England, London NW9 5EQ, UK. ; Institute of Evolutionary Biology, University of Edinburgh, Edinburgh EH9 2FL, UK. ; Postgraduate Training for Applied Epidemiology (PAE, German FETP), Robert Koch Institute, D-13302 Berlin, Germany. ; National Infection Service, Public Health England, Porton Down, Wiltshire SP4 0JG, UK. ; Swiss Tropical and Public Health Institute, 4002 Basel, Switzerland. ; Robert Koch Institute, D-13302 Berlin, Germany. ; University College London, London WC1E 6BT, UK. ; Paul-Ehrlich-Institut, Division of Veterinary Medicine, D-63225 Langen, Germany. ; Institute of Infection and Global Health, University of Liverpool, Liverpool L69 7BE, UK. ; Laboratory for Clinical and Epidemiological Virology, Department of Microbiology and Immunology, KU Leuven, Leuven B-3000, Belgium. ; Ministry of Health Guinea, Conakry BP 585, Guinea. ; Kenya Medical Research Institute, Nairobi P.O. BOX 54840 - 00200, Kenya. ; National Institute for Infectious Diseases L. Spallanzani, 00149 Rome, Italy. ; Friedrich-Loeffler-Institute, D-17493 Greifswald, Germany. ; Federal Office for Civil Protection, Spiez Laboratory, 3700 Spiez, Switzerland. ; Janssen-Cilag, Stockholm, Box 7073 - 19207, Sweden. ; NIHR Health Protection Research Unit in Emerging and Zoonotic Infections, University of Liverpool, Liverpool L69 7BE, UK. ; Institute of Virology, Technische Universitat Munchen, D-81675 Munich, Germany. ; Public Health Agency of Canada, Winnipeg, Manitoba R3E 3R2, Canada. ; Institut Pasteur Dakar, Dakar, DP 220 Senegal. ; Laboratoire de Fievres Hemorragiques de Guinee, Conakry BP 5680, Guinea. ; Sandia National Laboratories, PO Box 5800 MS1363, Albuquerque, New Mexico 87185-1363, USA. ; Ratoma Ebola Diagnostic Center, Conakry, Guinea. ; MRIGlobal, Kansas City, Missouri 64110-2241, USA. ; Expertise France, Laboratoire K-plan de Forecariah en Guinee, 75006 Paris, France. ; Federation des Laboratoires - HIA Begin, 94163 Saint-Mande cedex, France. ; Laboratoire de Biologie - Centre de Traitement des Soignants, Conakry, Guinea. ; World Health Organization, Conakry BP 817, Guinea. ; London School of Hygiene and Tropical Medicine, London EC1E 7HT, UK. ; Norwegian Institute of Public Health, PO Box 4404 Nydalen, 0403 Oslo, Norway. ; Public Health Wales, Cardiff CF11 9LJ, UK. ; Defence Science and Technology Laboratory (Dstl) Porton Down, Salisbury SP4 0JQ, UK. ; Oxford Nanopore Technologies, Oxford OX4 4GA, UK. ; Department of Cellular and Molecular Medicine, School of Medical Sciences, University of Bristol, Bristol BS8 1TD, UK. ; Academic Department of Military Medicine, Royal Centre for Defence Medicine, Birmingham B15 2TH, UK. ; Centre of Defence Pathology, Royal Centre for Defence Medicine, Birmingham B15 2TH, UK. ; Queen Elizabeth Hospital, Birmingham B12 2TH, UK. ; Bundeswehr Institute of Microbiology, D-80937 Munich, Germany. ; Institut National de Sante Publique, Conakry BP 1147, Guinea. ; Fogarty International Center, National Institutes of Health, Bethesda, MD 20892-2220, USA. ; Centre for Immunology, Infection and Evolution, University of Edinburgh, Edinburgh EH9 2FL, UK. ; University of Southampton, South General Hospital, Southampton SO16 6YD, UK. ; NIHR Health Protection Research Unit in Emerging and Zoonotic Infections, PHE Porton Down, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26840485" target="_blank"〉PubMed〈/a〉
    Keywords: Aircraft ; Disease Outbreaks/statistics & numerical data ; Ebolavirus/classification/*genetics/pathogenicity ; *Epidemiological Monitoring ; Genome, Viral/*genetics ; Guinea/epidemiology ; Hemorrhagic Fever, Ebola/*epidemiology/*virology ; Humans ; Mutagenesis/genetics ; Mutation Rate ; Sequence Analysis, DNA/*instrumentation/*methods ; Time Factors
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  • 40
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    Publication Date: 2016-02-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉England -- Nature. 2016 Feb 18;530(7590):253-4. doi: 10.1038/530253b.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26887453" target="_blank"〉PubMed〈/a〉
    Keywords: Biomedical Research/*economics/*trends ; Child ; *Federal Government ; *Goals ; Humans ; Immunotherapy ; Information Dissemination ; Neoplasms/*therapy ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/drug therapy ; United States
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  • 41
    Publication Date: 2016-01-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cyranoski, David -- England -- Nature. 2016 Jan 14;529(7585):136-7. doi: 10.1038/529136a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26762435" target="_blank"〉PubMed〈/a〉
    Keywords: Diffusion of Innovation ; *Federal Government ; History, 21st Century ; Humans ; Severe Acute Respiratory Syndrome/diagnosis/*epidemiology/prevention & control ; Taiwan/epidemiology
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  • 42
    Publication Date: 2016-01-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cyranoski, David -- England -- Nature. 2016 Jan 28;529(7587):449. doi: 10.1038/529449a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26819024" target="_blank"〉PubMed〈/a〉
    Keywords: Animal Experimentation ; Animals ; Animals, Laboratory ; Autistic Disorder/*genetics/physiopathology/psychology ; CRISPR-Cas Systems ; China ; DNA Copy Number Variations/genetics ; Deep Brain Stimulation ; *Disease Models, Animal ; Female ; *Genetic Engineering ; Humans ; Japan ; Macaca fascicularis/*genetics/psychology ; Male ; Methyl-CpG-Binding Protein 2/genetics ; Monkey Diseases/*genetics/physiopathology/psychology ; Neuroimaging
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  • 43
    Publication Date: 2016-01-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cyranoski, David -- England -- Nature. 2016 Jan 7;529(7584):9-10. doi: 10.1038/529009a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26738574" target="_blank"〉PubMed〈/a〉
    Keywords: China ; *Federal Government ; Genome, Human/genetics ; Genomics/economics/manpower/trends ; Humans ; Physicians/supply & distribution ; Population Density ; Precision Medicine/economics/*trends ; Reproducibility of Results
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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    Publication Date: 2016-04-29
    Description: Umbilical cord blood-derived haematopoietic stem cells (HSCs) are essential for many life-saving regenerative therapies. However, despite their advantages for transplantation, their clinical use is restricted because HSCs in cord blood are found only in small numbers. Small molecules that enhance haematopoietic stem and progenitor cell (HSPC) expansion in culture have been identified, but in many cases their mechanisms of action or the nature of the pathways they impinge on are poorly understood. A greater understanding of the molecular circuitry that underpins the self-renewal of human HSCs will facilitate the development of targeted strategies that expand HSCs for regenerative therapies. Whereas transcription factor networks have been shown to influence the self-renewal and lineage decisions of human HSCs, the post-transcriptional mechanisms that guide HSC fate have not been closely investigated. Here we show that overexpression of the RNA-binding protein Musashi-2 (MSI2) induces multiple pro-self-renewal phenotypes, including a 17-fold increase in short-term repopulating cells and a net 23-fold ex vivo expansion of long-term repopulating HSCs. By performing a global analysis of MSI2-RNA interactions, we show that MSI2 directly attenuates aryl hydrocarbon receptor (AHR) signalling through post-transcriptional downregulation of canonical AHR pathway components in cord blood HSPCs. Our study gives mechanistic insight into RNA networks controlled by RNA-binding proteins that underlie self-renewal and provides evidence that manipulating such networks ex vivo can enhance the regenerative potential of human HSCs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4880456/" 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/PMC4880456/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rentas, Stefan -- Holzapfel, Nicholas T -- Belew, Muluken S -- Pratt, Gabriel A -- Voisin, Veronique -- Wilhelm, Brian T -- Bader, Gary D -- Yeo, Gene W -- Hope, Kristin J -- HG004659/HG/NHGRI NIH HHS/ -- MOP-126030/Canadian Institutes of Health Research/Canada -- NS075449/NS/NINDS NIH HHS/ -- England -- Nature. 2016 Apr 28;532(7600):508-11. doi: 10.1038/nature17665.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Biomedical Sciences, Stem Cell and Cancer Research Institute, McMaster University, Hamilton, Ontario L8S 4K1, Canada. ; Department of Cellular and Molecular Medicine, Institute for Genomic Medicine, University of California, San Diego, La Jolla, California 92037, USA. ; Bioinformatics Graduate Program, University of California, San Diego, La Jolla, California 92037, USA. ; The Donnelly Centre, University of Toronto, Toronto, Ontario M5S 3E1, Canada. ; Institute for Research in Immunology and Cancer, University of Montreal, Montreal, Quebec H3C 3J7, Canada. ; Department of Physiology, National University of Singapore and Molecular Engineering Laboratory, A*STAR, Singapore 138632, Singapore.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27121842" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Basic Helix-Loop-Helix Transcription Factors/genetics/*metabolism ; Cell Count ; *Cell Self Renewal/genetics ; Down-Regulation/genetics ; Female ; Fetal Blood/cytology ; Gene Knockdown Techniques ; Hematopoietic Stem Cells/*cytology/*metabolism ; Humans ; Male ; Mice ; Protein Binding ; RNA, Messenger/genetics/metabolism ; RNA-Binding Proteins/genetics/*metabolism ; Receptors, Aryl Hydrocarbon/genetics/*metabolism ; *Signal Transduction/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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