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  • Polymer and Materials Science  (112,478)
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  • 1
    Publication Date: 2018-05-07
    Description: Niphargus is a speciose amphipod genus found in groundwater habitats across Europe. Three Niphargus species living in the sulphidic Frasassi caves in Italy harbour sulphur-oxidizing Thiothrix bacterial ectosymbionts. These three species are distantly related, implying that the ability to form ectosymbioses with Thiothrix may be common among Niphargus. Therefore, Niphargus-Thiothrix associations may also be found in sulphidic aquifers other than Frasassi. In this study, we examined this possibility by analysing niphargids of the genera Niphargus and Pontoniphargus collected from the partly sulphidic aquifers of the Southern Dobrogea region of Romania, which are accessible through springs, wells and Movile Cave. Molecular and morphological analyses revealed seven niphargid species in this region. Five of these species occurred occasionally or exclusively in sulphidic locations, whereas the remaining two were restricted to nonsulphidic areas. Thiothrix were detected by PCR on all seven Dobrogean niphargid species and observed using microscopy to be predominantly attached to their hosts' appendages. 16S rRNA gene sequences of the Thiothrix epibionts fell into two main clades, one of which (herein named T4) occurred solely on niphargids collected in sulphidic locations. The other Thiothrix clade was present on niphargids from both sulphidic and nonsulphidic areas and indistinguishable from the T3 ectosymbiont clade previously identified on Frasassi-dwelling Niphargus. Although niphargids from Frasassi and Southern Dobrogea are not closely related, the patterns of their association with Thiothrix are remarkably alike. The finding of similar Niphargus-Thiothrix associations in aquifers located 1200 km apart suggests that they may be widespread in European groundwater ecosystems.
    Keywords: amphipods; ecology; sulphide; symbiosis; systematics; taxonomy ; Amphipoda ; Animals ; DNA, Bacterial ; Ecosystem ; Groundwater ; Molecular Sequence Data ; Phylogeny ; RNA, Ribosomal, 16S ; Romania ; Sequence Analysis, DNA ; Sulfur ; Symbiosis ; Thiothrix
    Language: English , English
    Type: article , publishedVersion
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  • 2
    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
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  • 3
    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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  • 4
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    Nature Publishing Group (NPG)
    Publication Date: 2016-05-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nagata, Shigekazu -- England -- Nature. 2016 May 18;533(7604):474-6. doi: 10.1038/nature18439.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Biochemistry and Immunology, WPI Immunology Frontier Research Center, Osaka University, Osaka 565-0871, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27225115" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caspases/*metabolism ; *Cell Differentiation ; Cytochrome c Group/*metabolism ; Drosophila melanogaster/*cytology ; Male ; Spermatozoa/*cytology/*metabolism
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  • 5
    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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  • 6
    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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  • 7
    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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  • 8
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    Nature Publishing Group (NPG)
    Publication Date: 2016-05-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McGilvray, Annabel -- England -- Nature. 2016 May 11;533(7602):S65-7. doi: 10.1038/533S65a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27167395" target="_blank"〉PubMed〈/a〉
    Keywords: Access to Information ; Animals ; Anti-Bacterial Agents/*analysis/*chemistry/pharmacology ; *Crowdsourcing/economics ; Diffusion of Innovation ; Drug Evaluation, Preclinical/economics/*methods ; Drug Industry/economics/methods ; *High-Throughput Screening Assays/economics ; *Information Dissemination ; Intellectual Property ; Microbial Sensitivity Tests
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  • 9
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    Nature Publishing Group (NPG)
    Publication Date: 2016-01-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bhattacharya, Shaoni -- England -- Nature. 2016 Jan 28;529(7587):452-5. doi: 10.1038/529452a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26819027" target="_blank"〉PubMed〈/a〉
    Keywords: Animal Migration ; Animals ; Conservation of Natural Resources/*methods ; *Cooking ; Crime/legislation & jurisprudence/*prevention & control/*statistics & numerical ; data ; Cyprus ; Extinction, Biological ; Population Density ; *Songbirds/physiology
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  • 10
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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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  • 11
    Publication Date: 2016-03-05
    Description: Observing marine mammal (MM) populations continuously in time and space over the immense ocean areas they inhabit is challenging but essential for gathering an unambiguous record of their distribution, as well as understanding their behaviour and interaction with prey species. Here we use passive ocean acoustic waveguide remote sensing (POAWRS) in an important North Atlantic feeding ground to instantaneously detect, localize and classify MM vocalizations from diverse species over an approximately 100,000 km(2) region. More than eight species of vocal MMs are found to spatially converge on fish spawning areas containing massive densely populated herring shoals at night-time and diffuse herring distributions during daytime. We find the vocal MMs divide the enormous fish prey field into species-specific foraging areas with varying degrees of spatial overlap, maintained for at least two weeks of the herring spawning period. The recorded vocalization rates are diel (24 h)-dependent for all MM species, with some significantly more vocal at night and others more vocal during the day. The four key baleen whale species of the region: fin, humpback, blue and minke have vocalization rate trends that are highly correlated to trends in fish shoaling density and to each other over the diel cycle. These results reveal the temporospatial dynamics of combined multi-species MM foraging activities in the vicinity of an extensive fish prey field that forms a massive ecological hotspot, and would be unattainable with conventional methodologies. Understanding MM behaviour and distributions is essential for management of marine ecosystems and for accessing anthropogenic impacts on these protected marine species.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Delin -- Garcia, Heriberto -- Huang, Wei -- Tran, Duong D -- Jain, Ankita D -- Yi, Dong Hoon -- Gong, Zheng -- Jech, J Michael -- Godo, Olav Rune -- Makris, Nicholas C -- Ratilal, Purnima -- England -- Nature. 2016 Mar 17;531(7594):366-70. doi: 10.1038/nature16960. Epub 2016 Mar 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory for Ocean Acoustics and Ecosystem Sensing, Northeastern University, 360 Huntington Avenue, Boston, Massachusetts 02115, USA. ; Laboratory for Undersea Remote Sensing, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, Massachusetts 02139, USA. ; Northeast Fisheries Science Center, 166 Water Street, Woods Hole, Massachusetts 02543, USA. ; Institute of Marine Research, Post Office Box 1870, Nordnes, N-5817 Bergen, Norway.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26934221" target="_blank"〉PubMed〈/a〉
    Keywords: Acoustics ; Animals ; Aquatic Organisms/*physiology ; Atlantic Ocean ; Diet/veterinary ; Ecosystem ; *Feeding Behavior ; Fishes/*physiology ; Male ; Mammals/*physiology ; *Predatory Behavior ; Time Factors ; *Vocalization, Animal ; Whales/physiology
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  • 12
    Publication Date: 2016-04-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pendse, Mihir -- Hooper, Lora V -- England -- Nature. 2016 May 5;533(7601):42-3. doi: 10.1038/nature17895. Epub 2016 Apr 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA. ; Howard Hughes Medical Institute, University of Texas Southwestern Medical Center.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27120165" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Female ; Gastrointestinal Microbiome/*immunology ; Immune System/*growth & development/*microbiology ; Immunity, Innate/*immunology ; Immunity, Maternally-Acquired/*immunology ; Intestines/*immunology ; Pregnancy
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  • 13
    Publication Date: 2016-03-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Callaway, Ewen -- England -- Nature. 2016 Mar 24;531(7595):426-7. doi: 10.1038/531426a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27008948" target="_blank"〉PubMed〈/a〉
    Keywords: Animal Husbandry ; Animal Welfare ; Animals ; Animals, Wild/physiology ; Animals, Zoo/*physiology ; Bias (Epidemiology) ; *Dissent and Disputes ; Longevity/*physiology ; Research Personnel ; Survival Rate ; Uncertainty ; Whale, Killer/*physiology
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  • 14
    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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  • 15
    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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  • 16
    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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  • 17
    Publication Date: 2016-02-26
    Description: The RAS/MAPK (mitogen-activated protein kinase) signalling pathway is frequently deregulated in non-small-cell lung cancer, often through KRAS activating mutations. A single endogenous mutant Kras allele is sufficient to promote lung tumour formation in mice but malignant progression requires additional genetic alterations. We recently showed that advanced lung tumours from Kras(G12D/+);p53-null mice frequently exhibit Kras(G12D) allelic enrichment (Kras(G12D)/Kras(wild-type) 〉 1) (ref. 7), implying that mutant Kras copy gains are positively selected during progression. Here we show, through a comprehensive analysis of mutant Kras homozygous and heterozygous mouse embryonic fibroblasts and lung cancer cells, that these genotypes are phenotypically distinct. In particular, Kras(G12D/G12D) cells exhibit a glycolytic switch coupled to increased channelling of glucose-derived metabolites into the tricarboxylic acid cycle and glutathione biosynthesis, resulting in enhanced glutathione-mediated detoxification. This metabolic rewiring is recapitulated in mutant KRAS homozygous non-small-cell lung cancer cells and in vivo, in spontaneous advanced murine lung tumours (which display a high frequency of Kras(G12D) copy gain), but not in the corresponding early tumours (Kras(G12D) heterozygous). Finally, we demonstrate that mutant Kras copy gain creates unique metabolic dependences that can be exploited to selectively target these aggressive mutant Kras tumours. Our data demonstrate that mutant Kras lung tumours are not a single disease but rather a heterogeneous group comprising two classes of tumours with distinct metabolic profiles, prognosis and therapeutic susceptibility, which can be discriminated on the basis of their relative mutant allelic content. We also provide the first, to our knowledge, in vivo evidence of metabolic rewiring during lung cancer malignant progression.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4780242/" 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/PMC4780242/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kerr, Emma M -- Gaude, Edoardo -- Turrell, Frances K -- Frezza, Christian -- Martins, Carla P -- MC_UU_12022/4/Medical Research Council/United Kingdom -- MC_UU_12022/6/Medical Research Council/United Kingdom -- Medical Research Council/United Kingdom -- England -- Nature. 2016 Mar 3;531(7592):110-3. doi: 10.1038/nature16967. Epub 2016 Feb 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉MRC Cancer Unit, University of Cambridge, Box 197, Cambridge Biomedical Campus, Cambridge CB2 0XZ, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26909577" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Carcinoma, Non-Small-Cell Lung/drug therapy/genetics/metabolism/pathology ; Cell Line, Tumor ; Cell Transformation, Neoplastic/drug effects/genetics/metabolism/pathology ; Citric Acid Cycle ; DNA Copy Number Variations/*genetics ; Disease Progression ; Female ; Fibroblasts/metabolism ; Genes, ras/*genetics ; Genotype ; Glucose/*metabolism ; Glutathione/biosynthesis/metabolism ; *Glycolysis ; Lung Neoplasms/*drug therapy/genetics/*metabolism/pathology ; Male ; Mice ; Mutation/*genetics ; Oxidation-Reduction ; Phenotype ; Prognosis
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  • 18
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    Nature Publishing Group (NPG)
    Publication Date: 2016-05-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Perkel, Jeffrey M -- England -- Nature. 2016 May 5;533(7601):131-2. doi: 10.1038/533131a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27147030" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Databases, Factual/supply & distribution/utilization ; Datasets as Topic/*supply & distribution/utilization ; Information Dissemination/*methods ; Information Storage and Retrieval/*methods/standards ; Molecular Imaging ; Video Recording
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  • 19
    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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  • 20
    Publication Date: 2016-04-07
    Description: How tissue regeneration programs are triggered by injury has received limited research attention. Here we investigate the existence of enhancer regulatory elements that are activated in regenerating tissue. Transcriptomic analyses reveal that leptin b (lepb) is highly induced in regenerating hearts and fins of zebrafish. Epigenetic profiling identified a short DNA sequence element upstream and distal to lepb that acquires open chromatin marks during regeneration and enables injury-dependent expression from minimal promoters. This element could activate expression in injured neonatal mouse tissues and was divisible into tissue-specific modules sufficient for expression in regenerating zebrafish fins or hearts. Simple enhancer-effector transgenes employing lepb-linked sequences upstream of pro- or anti-regenerative factors controlled the efficacy of regeneration in zebrafish. Our findings provide evidence for 'tissue regeneration enhancer elements' (TREEs) that trigger gene expression in injury sites and can be engineered to modulate the regenerative potential of vertebrate organs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4844022/" 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/PMC4844022/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kang, Junsu -- Hu, Jianxin -- Karra, Ravi -- Dickson, Amy L -- Tornini, Valerie A -- Nachtrab, Gregory -- Gemberling, Matthew -- Goldman, Joseph A -- Black, Brian L -- Poss, Kenneth D -- F32 HL120494/HL/NHLBI NIH HHS/ -- K08 HL116485/HL/NHLBI NIH HHS/ -- P01 HL089707/HL/NHLBI NIH HHS/ -- R01 GM074057/GM/NIGMS NIH HHS/ -- R01 HL064658/HL/NHLBI NIH HHS/ -- R01 HL081674/HL/NHLBI NIH HHS/ -- R01 HL089707/HL/NHLBI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2016 Apr 14;532(7598):201-6. doi: 10.1038/nature17644. Epub 2016 Apr 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Duke University Medical Center, Durham, North Carolina 27710, USA. ; Cardiovascular Research Institute, University of California, San Francisco, San Francisco, California 94143, USA. ; Department of Medicine, Duke University Medical Center, Durham, North Carolina 27710, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27049946" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Animal Fins/injuries/metabolism ; Animals ; Animals, Newborn ; Cell Proliferation ; Chromatin Assembly and Disassembly/genetics ; Enhancer Elements, Genetic/*genetics ; Epigenesis, Genetic/genetics ; Female ; Gene Expression Profiling ; Gene Expression Regulation/genetics ; Heart ; Histones/chemistry/metabolism ; Leptin/biosynthesis/genetics ; Lysine/metabolism ; Male ; Mice ; Myocytes, Cardiac/cytology ; Organ Specificity/*genetics ; Promoter Regions, Genetic/genetics ; Regeneration/*genetics/*physiology ; Transgenes/genetics ; Wound Healing/*genetics ; Zebrafish/*genetics/*physiology ; Zebrafish Proteins/genetics
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  • 21
    Publication Date: 2016-03-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pfeifer, Gerd P -- England -- Nature. 2016 Apr 21;532(7599):319-20. doi: 10.1038/nature17315. Epub 2016 Mar 30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Epigenetics, Van Andel Research Institute, Grand Rapids, Michigan 49503, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27027294" target="_blank"〉PubMed〈/a〉
    Keywords: Adenine/*analogs & derivatives ; Animals ; *DNA Methylation ; Epigenesis, Genetic/*genetics ; Mouse Embryonic Stem Cells/*metabolism
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  • 22
    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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  • 23
    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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  • 24
    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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  • 25
    Publication Date: 2016-03-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Price, Nicholas -- Bourne, James -- Rosa, Marcello -- England -- Nature. 2016 Mar 3;531(7592):35. doi: 10.1038/531035c.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Monash University, Melbourne, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26935690" target="_blank"〉PubMed〈/a〉
    Keywords: Animal Experimentation/legislation & jurisprudence ; Animal Welfare ; Animals ; *Animals, Laboratory ; Australia ; Commerce/*legislation & jurisprudence ; *Federal Government ; *Primates ; Research Personnel/psychology
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  • 26
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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):437-8. doi: 10.1038/529437b.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26819007" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; China ; Cities ; Congo ; Conservation of Natural Resources/*legislation & jurisprudence ; Ecosystem ; Great Britain ; *Parks, Recreational/legislation & jurisprudence ; Pleasure ; Uganda ; United States ; *Wilderness
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  • 27
    Publication Date: 2016-04-14
    Description: Tullimonstrum gregarium is an iconic soft-bodied fossil from the Carboniferous Mazon Creek Lagerstatte (Illinois, USA). Despite a large number of specimens and distinct anatomy, various analyses over the past five decades have failed to determine the phylogenetic affinities of the 'Tully monster', and although it has been allied to such disparate phyla as the Mollusca, Annelida or Chordata, it remains enigmatic. The nature and phylogenetic affinities of Tullimonstrum have defied confident systematic placement because none of its preserved anatomy provides unequivocal evidence of homology, without which comparative analysis fails. Here we show that the eyes of Tullimonstrum possess ultrastructural details indicating homology with vertebrate eyes. Anatomical analysis using scanning electron microscopy reveals that the eyes of Tullimonstrum preserve a retina defined by a thick sheet comprising distinct layers of spheroidal and cylindrical melanosomes. Time-of-flight secondary ion mass spectrometry and multivariate statistics provide further evidence that these microbodies are melanosomes. A range of animals have melanin in their eyes, but the possession of melanosomes of two distinct morphologies arranged in layers, forming retinal pigment epithelium, is a synapomorphy of vertebrates. Our analysis indicates that in addition to evidence of colour patterning, ecology and thermoregulation, fossil melanosomes can also carry a phylogenetic signal. Identification in Tullimonstrum of spheroidal and cylindrical melanosomes forming the remains of retinal pigment epithelium indicates that it is a vertebrate; considering its body parts in this new light suggests it was an anatomically unusual member of total group Vertebrata.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Clements, Thomas -- Dolocan, Andrei -- Martin, Peter -- Purnell, Mark A -- Vinther, Jakob -- Gabbott, Sarah E -- England -- Nature. 2016 Apr 28;532(7600):500-3. doi: 10.1038/nature17647. Epub 2016 Apr 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Geology, University of Leicester, Leicester LE1 7RH, UK. ; Texas Materials Institute, The University of Texas at Austin, Austin, Texas 78712, USA. ; School of Earth Sciences, University of Bristol, Bristol BS8 1RJ, UK. ; Interface Analysis Centre, HH Wills Physics Laboratory, University of Bristol, Bristol BS8 1TQ, UK. ; School of Biological Sciences, University of Bristol, Bristol BS8 1TQ, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27074512" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Eye/chemistry/cytology/ultrastructure ; *Fossils ; Illinois ; Melanosomes/ultrastructure ; Microscopy, Electron, Scanning ; *Phylogeny ; Retinal Pigment Epithelium/chemistry/ultrastructure ; Vertebrates/anatomy & histology/*classification
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  • 28
    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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  • 29
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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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  • 30
    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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  • 31
    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
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  • 32
    Publication Date: 2016-03-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cyranoski, David -- England -- Nature. 2016 Mar 24;531(7595):424-5. doi: 10.1038/nature.2016.19590.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27008970" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain Mapping/trends ; China ; Conservation of Natural Resources/trends ; Environmental Pollution/prevention & control ; Humans ; Neurosciences/trends ; Oceanography/trends ; Science/*trends ; Stem Cell Research
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  • 33
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    Nature Publishing Group (NPG)
    Publication Date: 2016-02-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉England -- Nature. 2016 Feb 11;530(7589):129-30. doi: 10.1038/530130a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26863944" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Disease Eradication/economics/*statistics & numerical data/*trends ; Dog Diseases/epidemiology/parasitology ; Dogs ; Dracunculiasis/*epidemiology/*parasitology/prevention & control/transmission ; *Dracunculus Nematode/isolation & purification ; Drinking Water/parasitology/standards ; Female ; Ghana/epidemiology ; Goals ; Malaria/epidemiology/parasitology/prevention & control/transmission ; Male ; Mosquito Control/methods ; Poliomyelitis/epidemiology ; Time Factors
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  • 34
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    Unknown
    Nature Publishing Group (NPG)
    Publication Date: 2016-04-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cyranoski, David -- England -- Nature. 2016 Apr 21;532(7599):300-2. doi: 10.1038/532300a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Nature from Shanghai, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27111614" target="_blank"〉PubMed〈/a〉
    Keywords: Animal Husbandry ; Animal Welfare/economics/legislation & jurisprudence/standards ; Animals ; *Animals, Laboratory/genetics ; Biological Evolution ; Biomedical Research/economics/legislation & jurisprudence/*methods/*trends ; CRISPR-Cas Systems/genetics ; Callithrix ; China ; Cooperative Behavior ; Disease Models, Animal ; Genetic Engineering ; *Haplorhini/genetics ; Humans ; International Cooperation ; Japan ; Neurosciences/methods/trends ; Research Personnel/organization & administration
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 35
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    Nature Publishing Group (NPG)
    Publication Date: 2016-04-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rodriguez, Barbra -- England -- Nature. 2016 Apr 21;532(7599):403-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27127819" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptation, Physiological ; Animal Migration ; Animals ; Biodiversity ; Climate Change/economics/*statistics & numerical data ; Ecology/economics/manpower/*methods/*trends ; *Ecosystem ; Plants ; Research/economics/manpower/*trends ; *Research Design ; Research Personnel ; *Uncertainty ; Ursidae ; *Weather
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  • 36
    Publication Date: 2016-04-28
    Description: The primary visual cortex contains a detailed map of the visual scene, which is represented according to multiple stimulus dimensions including spatial location, ocular dominance and stimulus orientation. The maps for spatial location and ocular dominance arise from the spatial arrangement of thalamic afferent axons in the cortex. However, the origins of the other maps remain unclear. Here we show that the cortical maps for orientation, direction and retinal disparity in the cat (Felis catus) are all strongly related to the organization of the map for spatial location of light (ON) and dark (OFF) stimuli, an organization that we show is OFF-dominated, OFF-centric and runs orthogonal to ocular dominance columns. Because this ON-OFF organization originates from the clustering of ON and OFF thalamic afferents in the visual cortex, we conclude that all main features of visual cortical topography, including orientation, direction and retinal disparity, follow a common organizing principle that arranges thalamic axons with similar retinotopy and ON-OFF polarity in neighbouring cortical regions.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4860131/" 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/PMC4860131/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kremkow, Jens -- Jin, Jianzhong -- Wang, Yushi -- Alonso, Jose M -- EY005253/EY/NEI NIH HHS/ -- R01 EY005253/EY/NEI NIH HHS/ -- R01 EY020679/EY/NEI NIH HHS/ -- England -- Nature. 2016 May 5;533(7601):52-7. doi: 10.1038/nature17936. Epub 2016 Apr 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Graduate Center for Vision Research, State University of New York, College of Optometry, 33 West 42nd Street, New York, New York 10036, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27120164" target="_blank"〉PubMed〈/a〉
    Keywords: Afferent Pathways/radiation effects ; Animals ; Axons/physiology ; *Brain Mapping ; Cats ; Darkness ; Dominance, Ocular/physiology ; Light ; Macaca mulatta ; Male ; Models, Neurological ; Orientation/physiology/radiation effects ; Photic Stimulation ; Retina/physiology/radiation effects ; Space Perception/*physiology/radiation effects ; Thalamus/physiology/radiation effects ; Visual Cortex/*physiology/radiation effects ; Visual Fields/*physiology
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  • 37
    Publication Date: 2016-04-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ransohoff, Richard M -- England -- Nature. 2016 Apr 14;532(7598):185-6. doi: 10.1038/nature17881. Epub 2016 Apr 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neuroimmunology group, Biogen, Cambridge, Massachusetts 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27049948" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*metabolism ; Female ; Male ; Microglia/*physiology ; Proto-Oncogene Proteins/*metabolism ; Receptor Protein-Tyrosine Kinases/*metabolism
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  • 38
    Publication Date: 2016-03-10
    Description: The origins of the genus Homo are murky, but by H. erectus, bigger brains and bodies had evolved that, along with larger foraging ranges, would have increased the daily energetic requirements of hominins. Yet H. erectus differs from earlier hominins in having relatively smaller teeth, reduced chewing muscles, weaker maximum bite force capabilities, and a relatively smaller gut. This paradoxical combination of increased energy demands along with decreased masticatory and digestive capacities is hypothesized to have been made possible by adding meat to the diet, by mechanically processing food using stone tools, or by cooking. Cooking, however, was apparently uncommon until 500,000 years ago, and the effects of carnivory and Palaeolithic processing techniques on mastication are unknown. Here we report experiments that tested how Lower Palaeolithic processing technologies affect chewing force production and efficacy in humans consuming meat and underground storage organs (USOs). We find that if meat comprised one-third of the diet, the number of chewing cycles per year would have declined by nearly 2 million (a 13% reduction) and total masticatory force required would have declined by 15%. Furthermore, by simply slicing meat and pounding USOs, hominins would have improved their ability to chew meat into smaller particles by 41%, reduced the number of chews per year by another 5%, and decreased masticatory force requirements by an additional 12%. Although cooking has important benefits, it appears that selection for smaller masticatory features in Homo would have been initially made possible by the combination of using stone tools and eating meat.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zink, Katherine D -- Lieberman, Daniel E -- England -- Nature. 2016 Mar 24;531(7595):500-3. doi: 10.1038/nature16990. Epub 2016 Mar 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Human Evolutionary Biology, Harvard University, 11 Divinity Avenue, Cambridge, Massachusetts 02138, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26958832" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Animals ; Bite Force ; Carnivory ; Diet/*history ; Female ; Food Handling/*history ; Goats ; History, Ancient ; Hominidae ; Humans ; Male ; Mastication/*physiology ; Meat/*history ; Particle Size ; Plants ; Tool Use Behavior ; Tooth/physiology
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  • 39
    Publication Date: 2016-03-18
    Description: Chronic hepatitis B virus infection is a leading cause of cirrhosis and liver cancer. Hepatitis B virus encodes the regulatory HBx protein whose primary role is to promote transcription of the viral genome, which persists as an extrachromosomal DNA circle in infected cells. HBx accomplishes this task by an unusual mechanism, enhancing transcription only from extrachromosomal DNA templates. Here we show that HBx achieves this by hijacking the cellular DDB1-containing E3 ubiquitin ligase to target the 'structural maintenance of chromosomes' (Smc) complex Smc5/6 for degradation. Blocking this event inhibits the stimulatory effect of HBx both on extrachromosomal reporter genes and on hepatitis B virus transcription. Conversely, silencing the Smc5/6 complex enhances extrachromosomal reporter gene transcription in the absence of HBx, restores replication of an HBx-deficient hepatitis B virus, and rescues wild-type hepatitis B virus in a DDB1-knockdown background. The Smc5/6 complex associates with extrachromosomal reporters and the hepatitis B virus genome, suggesting a direct mechanism of transcriptional inhibition. These results uncover a novel role for the Smc5/6 complex as a restriction factor selectively blocking extrachromosomal DNA transcription. By destroying this complex, HBx relieves the inhibition to allow productive hepatitis B virus gene expression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Decorsiere, Adrien -- Mueller, Henrik -- van Breugel, Pieter C -- Abdul, Fabien -- Gerossier, Laetitia -- Beran, Rudolf K -- Livingston, Christine M -- Niu, Congrong -- Fletcher, Simon P -- Hantz, Olivier -- Strubin, Michel -- England -- Nature. 2016 Mar 17;531(7594):386-9. doi: 10.1038/nature17170.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Molecular Medicine, University Medical Centre (C.M.U.), Rue Michel-Servet 1, 1211 Geneva 4, Switzerland. ; CRCL, INSERM U1052, CNRS 5286, Universite de Lyon, 151, Cours A Thomas, 69424 Lyon Cedex, France. ; Gilead Sciences, Inc., 333 Lakeside Drive, Foster City, California 94404, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26983541" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Cycle Proteins/*metabolism ; Cell Line, Tumor ; DNA, Viral/genetics/metabolism ; Genes, Reporter ; Genome, Viral/genetics ; Hepatitis B/virology ; Hepatitis B virus/genetics/*physiology ; Hepatocytes/virology ; *Host Specificity ; Humans ; Liver/metabolism/virology ; Male ; Mice ; Plasmids/genetics/metabolism ; Protein Binding ; Proteolysis ; Trans-Activators/*metabolism ; Transcription, Genetic ; Ubiquitin/metabolism ; Ubiquitin-Protein Ligases/metabolism ; Virus Replication
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  • 40
    Publication Date: 2016-03-24
    Description: Primary cilia are solitary, generally non-motile, hair-like protrusions that extend from the surface of cells between cell divisions. Their antenna-like structure leads naturally to the assumption that they sense the surrounding environment, the most common hypothesis being sensation of mechanical force through calcium-permeable ion channels within the cilium. This Ca(2+)-responsive mechanosensor hypothesis for primary cilia has been invoked to explain a large range of biological responses, from control of left-right axis determination in embryonic development to adult progression of polycystic kidney disease and some cancers. Here we report the complete lack of mechanically induced calcium increases in primary cilia, in tissues upon which this hypothesis has been based. We developed a transgenic mouse, Arl13b-mCherry-GECO1.2, expressing a ratiometric genetically encoded calcium indicator in all primary cilia. We then measured responses to flow in primary cilia of cultured kidney epithelial cells, kidney thick ascending tubules, crown cells of the embryonic node, kinocilia of inner ear hair cells, and several cell lines. Cilia-specific Ca(2+) influxes were not observed in physiological or even highly supraphysiological levels of fluid flow. We conclude that mechanosensation, if it originates in primary cilia, is not via calcium signalling.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4851444/" 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/PMC4851444/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Delling, M -- Indzhykulian, A A -- Liu, X -- Li, Y -- Xie, T -- Corey, D P -- Clapham, D E -- 5R01 DC000304/DC/NIDCD NIH HHS/ -- P30-HD 18655/HD/NICHD NIH HHS/ -- R01 DC000304/DC/NIDCD NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2016 Mar 31;531(7596):656-60. doi: 10.1038/nature17426. Epub 2016 Mar 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cardiology, Howard Hughes Medical Institute, Boston Children's Hospital, Boston, Massachusetts 02115, USA. ; Department of Neurobiology, Howard Hughes Medical Institute, Harvard Medical School, Boston, Massachusetts 02115, USA. ; Image and Data Analysis Core (IDAC), Harvard Medical School, Boston, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27007841" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/analysis/*metabolism ; Calcium Signaling ; Cilia/*metabolism ; Embryo, Mammalian/cytology ; Epithelial Cells/cytology ; Female ; Hair Cells, Auditory, Inner/cytology ; Kidney/cytology ; Male ; *Mechanotransduction, Cellular ; Mice ; Mice, Transgenic ; Models, Biological
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 41
    Publication Date: 2016-02-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Reardon, Sara -- England -- Nature. 2016 Feb 11;530(7589):142. doi: 10.1038/nature.2016.19290.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26863962" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Embryo Research/*legislation & jurisprudence ; Extrachromosomal Inheritance/genetics ; Female ; Follow-Up Studies ; Genetic Therapy/*legislation & jurisprudence/*methods ; Great Britain ; Haplorhini/genetics ; Heredity/genetics/physiology ; Humans ; Male ; Mitochondrial Diseases/genetics/*prevention & control ; Mitochondrial Replacement Therapy/adverse effects/*legislation & ; jurisprudence/*methods ; Mutation/genetics ; *Patient Safety ; Sex Factors ; United States ; United States Food and Drug Administration/legislation & jurisprudence
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 42
    Publication Date: 2016-03-17
    Description: The integrated stress response (ISR) is a homeostatic mechanism by which eukaryotic cells sense and respond to stress-inducing signals, such as amino acid starvation. General controlled non-repressed (GCN2) kinase is a key orchestrator of the ISR, and modulates protein synthesis in response to amino acid starvation. Here we demonstrate in mice that GCN2 controls intestinal inflammation by suppressing inflammasome activation. Enhanced activation of ISR was observed in intestinal antigen presenting cells (APCs) and epithelial cells during amino acid starvation, or intestinal inflammation. Genetic deletion of Gcn2 (also known as Eif2ka4) in CD11c(+) APCs or intestinal epithelial cells resulted in enhanced intestinal inflammation and T helper 17 cell (TH17) responses, owing to enhanced inflammasome activation and interleukin (IL)-1beta production. This was caused by reduced autophagy in Gcn2(-/-) intestinal APCs and epithelial cells, leading to increased reactive oxygen species (ROS), a potent activator of inflammasomes. Thus, conditional ablation of Atg5 or Atg7 in intestinal APCs resulted in enhanced ROS and TH17 responses. Furthermore, in vivo blockade of ROS and IL-1beta resulted in inhibition of TH17 responses and reduced inflammation in Gcn2(-/-) mice. Importantly, acute amino acid starvation suppressed intestinal inflammation via a mechanism dependent on GCN2. These results reveal a mechanism that couples amino acid sensing with control of intestinal inflammation via GCN2.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4854628/" 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/PMC4854628/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ravindran, Rajesh -- Loebbermann, Jens -- Nakaya, Helder I -- Khan, Nooruddin -- Ma, Hualing -- Gama, Leonardo -- Machiah, Deepa K -- Lawson, Benton -- Hakimpour, Paul -- Wang, Yi-chong -- Li, Shuzhao -- Sharma, Prachi -- Kaufman, Randal J -- Martinez, Jennifer -- Pulendran, Bali -- R01 DK088227/DK/NIDDK NIH HHS/ -- R01 DK103185/DK/NIDDK NIH HHS/ -- R37 AI048638/AI/NIAID NIH HHS/ -- R37 DK042394/DK/NIDDK NIH HHS/ -- R37 DK057665/DK/NIDDK NIH HHS/ -- U19 AI057266/AI/NIAID NIH HHS/ -- U19 AI090023/AI/NIAID NIH HHS/ -- ZIA ES103286-01/Intramural NIH HHS/ -- England -- Nature. 2016 Mar 24;531(7595):523-7. doi: 10.1038/nature17186. Epub 2016 Mar 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Emory Vaccine Center, Yerkes National Primate Research Center, 954 Gatewood Road, Atlanta, Georgia 30329, USA. ; School of Pharmaceutical Sciences, University of Sao Paulo, Sao Paulo 05508, Brazil. ; Department of Biotechnology and Bioinformatics, School of Life Sciences, University of Hyderabad, Hyderabad 500 046, India. ; Division of Pathology, Yerkes National Primate Research Center, 954 Gatewood Road, Atlanta, Georgia 30329, USA. ; Virology Core, Emory Vaccine Center and Yerkes National Primate Research Center, 954 Gatewood Road, Atlanta, Georgia 30329, USA. ; Degenerative Disease Program, Sanford Burnham Prebys Medical Discovery Institute, 10901 North Torrey Pines Road, La Jolla, California 92037 USA. ; National Institute of Environmental Health Sciences, Mail Drop D2-01 Research Triangle Park, North Carolina 27709, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26982722" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acids/administration & dosage/deficiency/*metabolism/pharmacology ; Animals ; Antigen-Presenting Cells/immunology/metabolism ; Autophagy ; Colitis/etiology/*metabolism/pathology/prevention & control ; Disease Models, Animal ; Epithelial Cells/metabolism