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  • 1
    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
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 2
    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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    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 3
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    Nature Publishing Group (NPG)
    Publication Date: 2016-04-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Butler, Declan -- England -- Nature. 2016 Apr 14;532(7598):155-6. doi: 10.1038/532155a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27075072" target="_blank"〉PubMed〈/a〉
    Keywords: Aedes/virology ; Angola/epidemiology ; Animals ; Asia/epidemiology ; Child ; Cities/epidemiology ; Disease Outbreaks/statistics & numerical data ; *Fear ; Haplorhini/virology ; Humans ; South America/epidemiology ; Strategic Stockpile/statistics & numerical data ; Vaccination/statistics & numerical data ; World Health Organization ; Yellow Fever/*epidemiology/*transmission/virology ; Yellow Fever Vaccine/administration & dosage/supply & distribution
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    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 4
    Publication Date: 2016-02-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wan, Zheng -- Zhu, Mo -- Chen, Shun -- Sperling, Daniel -- England -- Nature. 2016 Feb 18;530(7590):275-7. doi: 10.1038/530275a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Transportation Studies, at the University of California, Davis, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26887477" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Conservation of Natural Resources/*legislation & jurisprudence/methods/trends ; Environmental Pollution/*legislation & jurisprudence/*prevention & ; control/statistics & numerical data ; *International Cooperation ; Ships/instrumentation/*legislation & jurisprudence/methods ; Vehicle Emissions/analysis/*legislation & jurisprudence/*prevention & control
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    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
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    Nature Publishing Group (NPG)
    Publication Date: 2016-02-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Heuckeroth, Robert O -- England -- Nature. 2016 Mar 3;531(7592):44-5. doi: 10.1038/nature16877. Epub 2016 Feb 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Children's Hospital of Philadelphia Research Institute and the Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26863191" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Lineage ; *Cell- and Tissue-Based Therapy ; Drug Discovery/*methods ; Enteric Nervous System/*pathology ; Female ; Hirschsprung Disease/*drug therapy/*pathology ; Humans ; Male ; Neurons/*pathology
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    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 6
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    Nature Publishing Group (NPG)
    Publication Date: 2016-01-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Callaway, Ewen -- England -- Nature. 2016 Jan 14;529(7585):138-9. doi: 10.1038/529138a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26762436" target="_blank"〉PubMed〈/a〉
    Keywords: Africa, Western/epidemiology ; Animals ; Cats ; Chiroptera/*virology ; Disease Outbreaks/prevention & control/statistics & numerical data/veterinary ; Dogs ; Ebolavirus/*isolation & purification ; Hemorrhagic Fever, Ebola/*epidemiology/prevention & control/*veterinary/virology ; *Host Specificity ; Humans ; Livestock/virology ; Pets/virology ; Rodentia/virology ; Zoonoses/epidemiology/prevention & control/transmission/virology
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    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 7
    Publication Date: 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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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 8
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    Nature Publishing Group (NPG)
    Publication Date: 2016-01-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Callaway, Ewen -- England -- Nature. 2016 Jan 7;529(7584):10-1. doi: 10.1038/529010a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26738575" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chad/epidemiology ; Disease Eradication ; Dog Diseases/*epidemiology/parasitology/prevention & control/*transmission ; Dogs ; Dracunculiasis/*epidemiology/prevention & control/transmission/*veterinary ; Dracunculus Nematode/*isolation & purification ; Drinking Water/parasitology/standards ; Humans ; Rivers/parasitology ; Zoonoses/*epidemiology/parasitology/prevention & control/*transmission
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 9
    Publication Date: 2016-04-15
    Description: Numerous natural systems contain surfaces or threads that enable directional water transport. This behaviour is usually ascribed to hierarchical structural features at the microscale and nanoscale, with gradients in surface energy and gradients in Laplace pressure thought to be the main driving forces. Here we study the prey-trapping pitcher organs of the carnivorous plant Nepenthes alata. We find that continuous, directional water transport occurs on the surface of the 'peristome'--the rim of the pitcher--because of its multiscale structure, which optimizes and enhances capillary rise in the transport direction, and prevents backflow by pinning in place any water front that is moving in the reverse direction. This results not only in unidirectional flow despite the absence of any surface-energy gradient, but also in a transport speed that is much higher than previously thought. We anticipate that the basic 'design' principles underlying this behaviour could be used to develop artificial fluid-transport systems with practical applications.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Huawei -- Zhang, Pengfei -- Zhang, Liwen -- Liu, Hongliang -- Jiang, Ying -- Zhang, Deyuan -- Han, Zhiwu -- Jiang, Lei -- England -- Nature. 2016 Apr 7;532(7597):85-9. doi: 10.1038/nature17189.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Mechanical Engineering and Automation, Beihang University, Beijing 100191, China. ; Laboratory of Bio-inspired Smart Interface Science, Technical Institute of Physics and Chemistry, Chinese Academy of Sciences, Beijing 100190, China. ; School of Chemistry and Environment, Beihang University, Beijing 100191, China. ; Key Laboratory for Bionic Engineering, Ministry of Education, Jilin University, Changchun 130022, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27078568" target="_blank"〉PubMed〈/a〉
    Keywords: Angiosperms/*anatomy & histology/*metabolism ; Animals ; Biological Transport ; Biomimetics ; Insects ; Plant Epidermis/anatomy & histology/metabolism ; Surface Properties ; Water/*metabolism ; Water Movements
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 10
    Publication Date: 2016-03-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Norris, Dominic P -- Jackson, Peter K -- England -- Nature. 2016 Mar 31;531(7596):582-3. doi: 10.1038/nature17313. Epub 2016 Mar 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Mammalian Genetics Unit, MRC Harwell, Harwell Campus OX11 0RD, UK. ; Departments of Microbiology &Immunology and Pathology, and in the Baxter Laboratory, Stanford University School of Medicine, Stanford, California 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27007852" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/*metabolism ; Cilia/*metabolism ; Female ; Male ; *Mechanotransduction, Cellular
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 11
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    Nature Publishing Group (NPG)
    Publication Date: 2016-05-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Jihong -- Liu, Xiang -- England -- Nature. 2016 May 18;533(7603):321. doi: 10.1038/533321d.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Shanghai Maritime University, China. ; Rutgers University, Piscataway, New Jersey, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27193671" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Dissent and Disputes ; *Ecosystem ; *Environmental Monitoring ; *Models, Economic ; *Transportation
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 12
    Publication Date: 2016-03-10
    Description: The eye is a complex organ with highly specialized constituent tissues derived from different primordial cell lineages. The retina, for example, develops from neuroectoderm via the optic vesicle, the corneal epithelium is descended from surface ectoderm, while the iris and collagen-rich stroma of the cornea have a neural crest origin. Recent work with pluripotent stem cells in culture has revealed a previously under-appreciated level of intrinsic cellular self-organization, with a focus on the retina and retinal cells. Moreover, we and others have demonstrated the in vitro induction of a corneal epithelial cell phenotype from pluripotent stem cells. These studies, however, have a single, tissue-specific focus and fail to reflect the complexity of whole eye development. Here we demonstrate the generation from human induced pluripotent stem cells of a self-formed ectodermal autonomous multi-zone (SEAM) of ocular cells. In some respects the concentric SEAM mimics whole-eye development because cell location within different zones is indicative of lineage, spanning the ocular surface ectoderm, lens, neuro-retina, and retinal pigment epithelium. It thus represents a promising resource for new and ongoing studies of ocular morphogenesis. The approach also has translational potential and to illustrate this we show that cells isolated from the ocular surface ectodermal zone of the SEAM can be sorted and expanded ex vivo to form a corneal epithelium that recovers function in an experimentally induced animal model of corneal blindness.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hayashi, Ryuhei -- Ishikawa, Yuki -- Sasamoto, Yuzuru -- Katori, Ryosuke -- Nomura, Naoki -- Ichikawa, Tatsuya -- Araki, Saori -- Soma, Takeshi -- Kawasaki, Satoshi -- Sekiguchi, Kiyotoshi -- Quantock, Andrew J -- Tsujikawa, Motokazu -- Nishida, Kohji -- England -- Nature. 2016 Mar 17;531(7594):376-80. doi: 10.1038/nature17000. Epub 2016 Mar 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Stem Cells and Applied Medicine, Osaka University Graduate School of Medicine, Suita, Osaka 565-0871, Japan. ; Department of Ophthalmology, Osaka University Graduate School of Medicine, Suita, Osaka 565-0871, Japan. ; Laboratory of Extracellular Matrix Biochemistry, Institute for Protein Research, Osaka University, Suita, Osaka 565-0871, Japan. ; Structural Biophysics Group, School of Optometry and Vision Sciences, College of Biomedical and Life Sciences, Cardiff University, Cardiff CF24 4HQ, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26958835" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Lineage ; Cornea/*cytology/*growth & development/physiology ; Corneal Transplantation ; Ectoderm/cytology ; Epithelial Cells/cytology ; Epithelium, Corneal/cytology ; Female ; Humans ; Induced Pluripotent Stem Cells/*cytology ; Lens, Crystalline/cytology ; Mice ; Morphogenesis ; Phenotype ; Rabbits ; *Recovery of Function ; Retinal Pigment Epithelium/cytology
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 13
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    Nature Publishing Group (NPG)
    Publication Date: 2016-05-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wald, Chelsea -- England -- Nature. 2016 May 5;533(7601):S47. doi: 10.1038/533S47a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27144610" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Austria ; Entrepreneurship/economics/organization & administration ; Humans ; Inventions/economics ; Inventors/economics/education/psychology ; Research/*economics/*organization & administration ; Research Personnel/economics/education/psychology ; *Technology Transfer ; Uncertainty
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 14
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    Nature Publishing Group (NPG)
    Publication Date: 2016-02-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉England -- Nature. 2016 Feb 18;530(7590):254. doi: 10.1038/530254a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26887455" target="_blank"〉PubMed〈/a〉
    Keywords: Animal Feed/*analysis ; *Animal Nutritional Physiological Phenomena ; Animals ; Animals, Laboratory/*physiology ; Diet/*veterinary ; Environment ; Japan ; Longevity/*physiology ; Mice ; Models, Animal ; Reproducibility of Results ; Research Design
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 15
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    Nature Publishing Group (NPG)
    Publication Date: 2016-01-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pincus, Zachary -- England -- Nature. 2016 Feb 4;530(7588):37-8. doi: 10.1038/nature16873. Epub 2016 Jan 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departments of Developmental Biology and Genetics, Washington University School of Medicine, St. Louis, Missouri 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26814974" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/*physiology ; Animals ; Caenorhabditis elegans/*physiology ; Longevity/*physiology
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 16
    Publication Date: 2016-03-17
    Description: CD8(+) T cells have a central role in antitumour immunity, but their activity is suppressed in the tumour microenvironment. Reactivating the cytotoxicity of CD8(+) T cells is of great clinical interest in cancer immunotherapy. Here we report a new mechanism by which the antitumour response of mouse CD8(+) T cells can be potentiated by modulating cholesterol metabolism. Inhibiting cholesterol esterification in T cells by genetic ablation or pharmacological inhibition of ACAT1, a key cholesterol esterification enzyme, led to potentiated effector function and enhanced proliferation of CD8(+) but not CD4(+) T cells. This is due to the increase in the plasma membrane cholesterol level of CD8(+) T cells, which causes enhanced T-cell receptor clustering and signalling as well as more efficient formation of the immunological synapse. ACAT1-deficient CD8(+) T cells were better than wild-type CD8(+) T cells at controlling melanoma growth and metastasis in mice. We used the ACAT inhibitor avasimibe, which was previously tested in clinical trials for treating atherosclerosis and showed a good human safety profile, to treat melanoma in mice and observed a good antitumour effect. A combined therapy of avasimibe plus an anti-PD-1 antibody showed better efficacy than monotherapies in controlling tumour progression. ACAT1, an established target for atherosclerosis, is therefore also a potential target for cancer immunotherapy.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4851431/" 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/PMC4851431/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yang, Wei -- Bai, Yibing -- Xiong, Ying -- Zhang, Jin -- Chen, Shuokai -- Zheng, Xiaojun -- Meng, Xiangbo -- Li, Lunyi -- Wang, Jing -- Xu, Chenguang -- Yan, Chengsong -- Wang, Lijuan -- Chang, Catharine C Y -- Chang, Ta-Yuan -- Zhang, Ti -- Zhou, Penghui -- Song, Bao-Liang -- Liu, Wanli -- Sun, Shao-cong -- Liu, Xiaolong -- Li, Bo-liang -- Xu, Chenqi -- HL 60306./HL/NHLBI NIH HHS/ -- R01 HL060306/HL/NHLBI NIH HHS/ -- England -- Nature. 2016 Mar 31;531(7596):651-5. doi: 10.1038/nature17412. Epub 2016 Mar 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉State Key Laboratory of Molecular Biology, National Center for Protein Science Shanghai, Shanghai Science Research Center, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China. ; State Key Laboratory of Molecular Biology, CAS Center for Excellence in Molecular Cell Science, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China. ; Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China. ; MOE Key Laboratory of Protein Science, School of Life Sciences, Collaborative Innovation Center for Infectious Diseases, Tsinghua University, Beijing 100084, China. ; Department of Biochemistry, Geisel School of Medicine at Dartmouth, Hanover, New Haven 03755, USA. ; Rheumatology and Immunology Department of ChangZheng Hospital, Second Military Medical University, Shanghai 200433, China. ; Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou 510060, China. ; College of Life Sciences, Wuhan University, Wuhan, Hubei Province 430072, China. ; Department of Immunology, The University of Texas MD Anderson Cancer Center, Houston, Texas 77054, USA. ; State Key Laboratory of Cell Biology, CAS Center for Excellence in Molecular Cell Science, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China. ; School of Life Science and Technology, ShanghaiTech University, 100 Haike Road, Shanghai 201210, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26982734" target="_blank"〉PubMed〈/a〉
    Keywords: Acetates/*pharmacology/therapeutic use ; Acetyl-CoA C-Acetyltransferase/antagonists & ; inhibitors/deficiency/genetics/metabolism ; Animals ; Atherosclerosis/drug therapy ; CD8-Positive T-Lymphocytes/*drug effects/*immunology/metabolism ; Cell Membrane/drug effects/metabolism ; Cholesterol/*metabolism ; Esterification/drug effects ; Female ; Immunological Synapses/drug effects/immunology/metabolism ; Immunotherapy/*methods ; Male ; Melanoma/*drug therapy/*immunology/metabolism/pathology ; Mice ; Programmed Cell Death 1 Receptor/antagonists & inhibitors/immunology ; Receptors, Antigen, T-Cell/immunology/metabolism ; Signal Transduction/drug effects ; Sulfonic Acids/*pharmacology/therapeutic use
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 17
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    Nature Publishing Group (NPG)
    Publication Date: 2016-03-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pollock, Kevin -- England -- Nature. 2016 Mar 17;531(7594):S64-6. doi: 10.1038/531S64a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26981733" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cities ; *City Planning ; Feedback ; Humans ; *Physics ; Plague/epidemiology ; Rats ; *Urbanization ; Vietnam/epidemiology
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  • 18
    Publication Date: 2016-03-05
    Description: How does an animal know where it is when it stops moving? Hippocampal place cells fire at discrete locations as subjects traverse space, thereby providing an explicit neural code for current location during locomotion. In contrast, during awake immobility, the hippocampus is thought to be dominated by neural firing representing past and possible future experience. The question of whether and how the hippocampus constructs a representation of current location in the absence of locomotion has been unresolved. Here we report that a distinct population of hippocampal neurons, located in the CA2 subregion, signals current location during immobility, and does so in association with a previously unidentified hippocampus-wide network pattern. In addition, signalling of location persists into brief periods of desynchronization prevalent in slow-wave sleep. The hippocampus thus generates a distinct representation of current location during immobility, pointing to mnemonic processing specific to experience occurring in the absence of locomotion.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kay, Kenneth -- Sosa, Marielena -- Chung, Jason E -- Karlsson, Mattias P -- Larkin, Margaret C -- Frank, Loren M -- R01 MH090188/MH/NIMH NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2016 Mar 10;531(7593):185-90. doi: 10.1038/nature17144. Epub 2016 Mar 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉UCSF Center for Integrative Neuroscience and Department of Physiology, University of California San Francisco, California 94158, USA. ; Howard Hughes Medical Institute, University of California San Francisco, California 94158, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26934224" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Hippocampus/anatomy & histology/*cytology/*physiology ; Male ; Models, Neurological ; Movement ; Neurons/*physiology ; Orientation/*physiology ; Rats ; Rats, Long-Evans ; Sleep/*physiology ; Space Perception/*physiology ; Spatial Memory/physiology
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 19
    Publication Date: 2016-03-24
    Description: Endoplasmic reticulum (ER) stress is a major contributor to inflammatory diseases, such as Crohn disease and type 2 diabetes. ER stress induces the unfolded protein response, which involves activation of three transmembrane receptors, ATF6, PERK and IRE1alpha. Once activated, IRE1alpha recruits TRAF2 to the ER membrane to initiate inflammatory responses via the NF-kappaB pathway. Inflammation is commonly triggered when pattern recognition receptors (PRRs), such as Toll-like receptors or nucleotide-binding oligomerization domain (NOD)-like receptors, detect tissue damage or microbial infection. However, it is not clear which PRRs have a major role in inducing inflammation during ER stress. Here we show that NOD1 and NOD2, two members of the NOD-like receptor family of PRRs, are important mediators of ER-stress-induced inflammation in mouse and human cells. The ER stress inducers thapsigargin and dithiothreitol trigger production of the pro-inflammatory cytokine IL-6 in a NOD1/2-dependent fashion. Inflammation and IL-6 production triggered by infection with Brucella abortus, which induces ER stress by injecting the type IV secretion system effector protein VceC into host cells, is TRAF2, NOD1/2 and RIP2-dependent and can be reduced by treatment with the ER stress inhibitor tauroursodeoxycholate or an IRE1alpha kinase inhibitor. The association of NOD1 and NOD2 with pro-inflammatory responses induced by the IRE1alpha/TRAF2 signalling pathway provides a novel link between innate immunity and ER-stress-induced inflammation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4869892/" 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/PMC4869892/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Keestra-Gounder, A Marijke -- Byndloss, Mariana X -- Seyffert, Nubia -- Young, Briana M -- Chavez-Arroyo, Alfredo -- Tsai, April Y -- Cevallos, Stephanie A -- Winter, Maria G -- Pham, Oanh H -- Tiffany, Connor R -- de Jong, Maarten F -- Kerrinnes, Tobias -- Ravindran, Resmi -- Luciw, Paul A -- McSorley, Stephen J -- Baumler, Andreas J -- Tsolis, Renee M -- AI044170/AI/NIAID NIH HHS/ -- AI076246/AI/NIAID NIH HHS/ -- AI076278/AI/NIAID NIH HHS/ -- AI096528/AI/NIAID NIH HHS/ -- AI109799/AI/NIAID NIH HHS/ -- AI112258/AI/NIAID NIH HHS/ -- AI117303/AI/NIAID NIH HHS/ -- GM056765/GM/NIGMS NIH HHS/ -- R01 AI044170/AI/NIAID NIH HHS/ -- R01 AI076246/AI/NIAID NIH HHS/ -- R01 AI076278/AI/NIAID NIH HHS/ -- R01 AI096528/AI/NIAID NIH HHS/ -- R01 AI109799/AI/NIAID NIH HHS/ -- R21 AI112258/AI/NIAID NIH HHS/ -- R21 AI117303/AI/NIAID NIH HHS/ -- R25 GM056765/GM/NIGMS NIH HHS/ -- England -- Nature. 2016 Apr 21;532(7599):394-7. doi: 10.1038/nature17631. Epub 2016 Mar 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Microbiology and Immunology, School of Medicine, University of California at Davis, One Shields Ave, Davis, California 95616, USA. ; Center for Comparative Medicine, Schools of Medicine and Veterinary Medicine, University of California at Davis, One Shields Ave, Davis, California 95616, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27007849" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacterial Outer Membrane Proteins/metabolism ; Brucella abortus/immunology/pathogenicity ; Cell Line ; Dithiothreitol/pharmacology ; Endoplasmic Reticulum/drug effects/pathology ; *Endoplasmic Reticulum Stress/drug effects ; Endoribonucleases/antagonists & inhibitors ; Female ; Humans ; Immunity, Innate ; Inflammation/chemically induced/*metabolism ; Interleukin-6/biosynthesis ; Male ; Mice ; Mice, Inbred C57BL ; NF-kappa B/metabolism ; Nod1 Signaling Adaptor Protein/immunology/*metabolism ; Nod2 Signaling Adaptor Protein/immunology/*metabolism ; Protein-Serine-Threonine Kinases/antagonists & inhibitors ; Receptors, Pattern Recognition/metabolism ; *Signal Transduction/drug effects ; TNF Receptor-Associated Factor 2/metabolism ; Taurochenodeoxycholic Acid/pharmacology ; Thapsigargin/pharmacology ; Unfolded Protein Response/drug effects
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 20
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    Nature Publishing Group (NPG)
    Publication Date: 2016-01-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Popkin, Gabriel -- England -- Nature. 2016 Jan 7;529(7584):16-8. doi: 10.1038/529016a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26738578" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biophysical Phenomena ; Biophysics/*trends ; Birds/physiology ; Cytoskeleton/metabolism ; *Life ; Magnetic Phenomena ; *Models, Theoretical
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  • 21
    Publication Date: 2016-03-17
    Description: Alzheimer's disease (AD) is a neurodegenerative disorder characterized by progressive memory decline and subsequent loss of broader cognitive functions. Memory decline in the early stages of AD is mostly limited to episodic memory, for which the hippocampus has a crucial role. However, it has been uncertain whether the observed amnesia in the early stages of AD is due to disrupted encoding and consolidation of episodic information, or an impairment in the retrieval of stored memory information. Here we show that in transgenic mouse models of early AD, direct optogenetic activation of hippocampal memory engram cells results in memory retrieval despite the fact that these mice are amnesic in long-term memory tests when natural recall cues are used, revealing a retrieval, rather than a storage impairment. Before amyloid plaque deposition, the amnesia in these mice is age-dependent, which correlates with a progressive reduction in spine density of hippocampal dentate gyrus engram cells. We show that optogenetic induction of long-term potentiation at perforant path synapses of dentate gyrus engram cells restores both spine density and long-term memory. We also demonstrate that an ablation of dentate gyrus engram cells containing restored spine density prevents the rescue of long-term memory. Thus, selective rescue of spine density in engram cells may lead to an effective strategy for treating memory loss in the early stages of AD.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4847731/" 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/PMC4847731/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roy, Dheeraj S -- Arons, Autumn -- Mitchell, Teryn I -- Pignatelli, Michele -- Ryan, Tomas J -- Tonegawa, Susumu -- Howard Hughes Medical Institute/ -- England -- Nature. 2016 Mar 24;531(7595):508-12. doi: 10.1038/nature17172. Epub 2016 Mar 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉RIKEN-MIT Center for Neural Circuit Genetics at the Picower Institute for Learning and Memory, Department of Biology and Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA. ; Howard Hughes Medical Institute, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26982728" target="_blank"〉PubMed〈/a〉
    Keywords: Aging ; Alzheimer Disease/*pathology/*physiopathology ; Amnesia/pathology/physiopathology ; Amyloid beta-Protein Precursor/genetics ; Animals ; Dendritic Spines/pathology/physiology ; Dentate Gyrus/*cytology/pathology/*physiology/physiopathology ; *Disease Models, Animal ; Early Medical Intervention ; Humans ; Long-Term Potentiation ; Male ; Memory, Episodic ; Memory, Long-Term/*physiology ; Mice ; Mice, Transgenic ; Optogenetics ; Plaque, Amyloid ; Presenilin-1/genetics ; Synapses/metabolism ; Transgenes/genetics ; tau Proteins/genetics
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 22
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    Nature Publishing Group (NPG)
    Publication Date: 2016-02-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roy, Helen -- England -- Nature. 2016 Feb 18;530(7590):281. doi: 10.1038/530281d.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉NERC Centre for Ecology and Hydrology, Wallingford, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26887485" target="_blank"〉PubMed〈/a〉
    Keywords: Animal Diseases/epidemiology/*microbiology ; Animals ; Animals, Wild/*microbiology ; Biodiversity ; Biological Evolution ; Endangered Species/statistics & numerical data ; Host Specificity ; Humans ; Introduced Species/*statistics & numerical data
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  • 23
    Publication Date: 2016-03-31
    Description: Colonic epithelial cells are covered by thick inner and outer mucus layers. The inner mucus layer is free of commensal microbiota, which contributes to the maintenance of gut homeostasis. In the small intestine, molecules critical for prevention of bacterial invasion into epithelia such as Paneth-cell-derived anti-microbial peptides and regenerating islet-derived 3 (RegIII) family proteins have been identified. Although there are mucus layers providing physical barriers against the large number of microbiota present in the large intestine, the mechanisms that separate bacteria and colonic epithelia are not fully elucidated. Here we show that Ly6/PLAUR domain containing 8 (Lypd8) protein prevents flagellated microbiota invading the colonic epithelia in mice. Lypd8, selectively expressed in epithelial cells at the uppermost layer of the large intestinal gland, was secreted into the lumen and bound flagellated bacteria including Proteus mirabilis. In the absence of Lypd8, bacteria were present in the inner mucus layer and many flagellated bacteria invaded epithelia. Lypd8(-/-) mice were highly sensitive to intestinal inflammation induced by dextran sulfate sodium (DSS). Antibiotic elimination of Gram-negative flagellated bacteria restored the bacterial-free state of the inner mucus layer and ameliorated DSS-induced intestinal inflammation in Lypd8(-/-) mice. Lypd8 bound to flagella and suppressed motility of flagellated bacteria. Thus, Lypd8 mediates segregation of intestinal bacteria and epithelial cells in the colon to preserve intestinal homeostasis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Okumura, Ryu -- Kurakawa, Takashi -- Nakano, Takashi -- Kayama, Hisako -- Kinoshita, Makoto -- Motooka, Daisuke -- Gotoh, Kazuyoshi -- Kimura, Taishi -- Kamiyama, Naganori -- Kusu, Takashi -- Ueda, Yoshiyasu -- Wu, Hong -- Iijima, Hideki -- Barman, Soumik -- Osawa, Hideki -- Matsuno, Hiroshi -- Nishimura, Junichi -- Ohba, Yusuke -- Nakamura, Shota -- Iida, Tetsuya -- Yamamoto, Masahiro -- Umemoto, Eiji -- Sano, Koichi -- Takeda, Kiyoshi -- England -- Nature. 2016 Apr 7;532(7597):117-21. doi: 10.1038/nature17406. Epub 2016 Mar 30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Immune Regulation, Department of Microbiology and Immunology, Graduate School of Medicine, WPI Immunology Frontier Research Center, Osaka University, Suita, Osaka 565-0871, Japan. ; Core Research for Evolutional Science and Technology, Japan Agency for Medical Research and Development, Tokyo 100-0004, Japan. ; Department of Microbiology and Infection Control, Osaka Medical College, Takatsuki, Osaka 569-8686, Japan. ; Department of Infection Metagenomics, Genome Information Research Center, Research Institute for Microbial Diseases, Osaka University, Suita, Osaka 565-0871, Japan. ; Department of Bacteriology, Okayama University Graduate School of Medicine, Okayama 700-8558, Japan. ; Department of Gastroenterology and Hepatology, Graduate School of Medicine, Osaka University, Osaka 565-0871, Japan. ; Department of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, Osaka 565-0871, Japan. ; Department of Cell Physiology, Hokkaido University Graduate School of Medicine, Sapporo 060-8638, Japan. ; Department of Bacterial Infections, Research Institute for Microbial Diseases, Osaka University, Suita, Osaka 565-0871, Japan. ; Laboratory of Immunoparasitology, Research Institute for Microbial Diseases, WPI Immunology Frontier Research Center, Osaka University, Suita, Osaka 565-0871, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27027293" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacterial Adhesion ; Caco-2 Cells ; Cell Line ; Colitis/chemically induced/drug therapy/genetics ; Colon/*microbiology ; Dextran Sulfate ; Epithelium/*microbiology ; Female ; *Flagella ; GPI-Linked Proteins/deficiency/genetics/*metabolism/secretion ; Gram-Negative Bacteria/drug effects/metabolism/pathogenicity/*physiology ; Homeostasis ; Humans ; Inflammation/chemically induced/drug therapy/genetics ; Intestinal Mucosa/cytology/metabolism/*microbiology/secretion ; Male ; Mice ; Proteus mirabilis/drug effects/metabolism/pathogenicity ; Symbiosis
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  • 24
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    Nature Publishing Group (NPG)
    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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  • 25
    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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  • 26
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    Nature Publishing Group (NPG)
    Publication Date: 2016-03-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kirk, Edwin P -- England -- Nature. 2016 Mar 10;531(7593):173. doi: 10.1038/531173b.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Sydney Children's Hospital; University of New South Wales; and SEALS Laboratories, Randwick, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26961646" target="_blank"〉PubMed〈/a〉
    Keywords: Aedes/*virology ; Animals ; Female ; Humans ; Mosquito Control/*methods ; Pregnancy ; Virology/*trends ; Zika Virus/*pathogenicity ; Zika Virus Infection/*epidemiology
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  • 27
    Publication Date: 2016-03-31
    Description: Cerebral cavernous malformations (CCMs) are common inherited and sporadic vascular malformations that cause strokes and seizures in younger individuals. CCMs arise from endothelial cell loss of KRIT1, CCM2 or PDCD10, non-homologous proteins that form an adaptor complex. How disruption of the CCM complex results in disease remains controversial, with numerous signalling pathways (including Rho, SMAD and Wnt/beta-catenin) and processes such as endothelial-mesenchymal transition (EndMT) proposed to have causal roles. CCM2 binds to MEKK3 (refs 7, 8, 9, 10, 11), and we have recently shown that CCM complex regulation of MEKK3 is essential during vertebrate heart development. Here we investigate this mechanism in CCM disease pathogenesis. Using a neonatal mouse model of CCM disease, we show that expression of the MEKK3 target genes Klf2 and Klf4, as well as Rho and ADAMTS protease activity, are increased in the endothelial cells of early CCM lesions. By contrast, we find no evidence of EndMT or increased SMAD or Wnt signalling during early CCM formation. Endothelial-specific loss of Map3k3 (also known as Mekk3), Klf2 or Klf4 markedly prevents lesion formation, reverses the increase in Rho activity, and rescues lethality. Consistent with these findings in mice, we show that endothelial expression of KLF2 and KLF4 is increased in human familial and sporadic CCM lesions, and that a disease-causing human CCM2 mutation abrogates the MEKK3 interaction without affecting CCM complex formation. These studies identify gain of MEKK3 signalling and KLF2/4 function as causal mechanisms for CCM pathogenesis that may be targeted to develop new CCM therapeutics.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4864035/" 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/PMC4864035/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhou, Zinan -- Tang, Alan T -- Wong, Weng-Yew -- Bamezai, Sharika -- Goddard, Lauren M -- Shenkar, Robert -- Zhou, Su -- Yang, Jisheng -- Wright, Alexander C -- Foley, Matthew -- Arthur, J Simon C -- Whitehead, Kevin J -- Awad, Issam A -- Li, Dean Y -- Zheng, Xiangjian -- Kahn, Mark L -- P01 HL075215/HL/NHLBI NIH HHS/ -- P01 HL120846/HL/NHLBI NIH HHS/ -- P01 NS092521/NS/NINDS NIH HHS/ -- P01NS092521/NS/NINDS NIH HHS/ -- R01 HL094326/HL/NHLBI NIH HHS/ -- R01HL-084516/HL/NHLBI NIH HHS/ -- R01HL094326/HL/NHLBI NIH HHS/ -- R01NS075168/NS/NINDS NIH HHS/ -- T32HL07439/HL/NHLBI NIH HHS/ -- England -- Nature. 2016 Apr 7;532(7597):122-6. doi: 10.1038/nature17178. Epub 2016 Mar 30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine and Cardiovascular Institute, University of Pennsylvania, 3400 Civic Center Blvd, Philadelphia, Pennsylvania 19104, USA. ; Laboratory of Cardiovascular Signaling, Centenary Institute, Sydney, New South Wales 2050, Australia. ; Neurovascular Surgery Program, Section of Neurosurgery, Department of Surgery, The University of Chicago Medicine and Biological Sciences, Chicago, Illinois 60637, USA. ; Department of Radiology, University of Pennsylvania Medical Center, 3400 Spruce Street, Philadelphia, Pennsylvania 19104, USA. ; Sydney Microscopy &Microanalysis, University of Sydney, Sydney, New South Wales 2050, Australia. ; Division of Cell Signaling and Immunology, University of Dundee, Dundee DD1 5EH, UK. ; Division of Cardiovascular Medicine and the Program in Molecular Medicine, University of Utah, Salt Lake City, Utah 84112, USA. ; The Key Laboratory for Human Disease Gene Study of Sichuan Province, Institute of Laboratory Medicine, Sichuan Academy of Medical Sciences &Sichuan Provincial People's Hospital, Chengdu, Sichuan 610072, China. ; Faculty of Medicine, Sydney Medical School, University of Sydney, Sydney, New South Wales 2050, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27027284" target="_blank"〉PubMed〈/a〉
    Keywords: ADAM Proteins/metabolism ; Animals ; Animals, Newborn ; Carrier Proteins/genetics/metabolism ; Disease Models, Animal ; Endothelial Cells/enzymology/*metabolism ; Female ; Hemangioma, Cavernous, Central Nervous System/etiology/*metabolism/pathology ; Humans ; Kruppel-Like Transcription Factors/deficiency/*metabolism ; MAP Kinase Kinase Kinase 3/deficiency/*metabolism ; *MAP Kinase Signaling System ; Male ; Mice ; Protein Binding ; rho GTP-Binding Proteins/metabolism
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  • 28
    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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  • 29
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    Nature Publishing Group (NPG)
    Publication Date: 2016-01-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉England -- Nature. 2016 Jan 7;529(7584):5. doi: 10.1038/529005a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26738571" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bibliometrics ; *Cooperative Behavior ; Developed Countries ; Developing Countries ; *Group Processes ; Humans ; *International Cooperation ; Research/manpower/*organization & administration
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  • 30
    Publication Date: 2016-02-04
    Description: Chronic opiate use induces opiate dependence, which is characterized by extremely unpleasant physical and emotional feelings after drug use is terminated. Both the rewarding effects of a drug and the desire to avoid withdrawal symptoms motivate continued drug use, and the nucleus accumbens is important for orchestrating both processes. While multiple inputs to the nucleus accumbens regulate reward, little is known about the nucleus accumbens circuitry underlying withdrawal. Here we identify the paraventricular nucleus of the thalamus as a prominent input to the nucleus accumbens mediating the expression of opiate-withdrawal-induced physical signs and aversive memory. Activity in the paraventricular nucleus of the thalamus to nucleus accumbens pathway is necessary and sufficient to mediate behavioural aversion. Selectively silencing this pathway abolishes aversive symptoms in two different mouse models of opiate withdrawal. Chronic morphine exposure selectively potentiates excitatory transmission between the paraventricular nucleus of the thalamus and D2-receptor-expressing medium spiny neurons via synaptic insertion of GluA2-lacking AMPA receptors. Notably, in vivo optogenetic depotentiation restores normal transmission at these synapses and robustly suppresses morphine withdrawal symptoms. This links morphine-evoked pathway- and cell-type-specific plasticity in the paraventricular nucleus of the thalamus to nucleus accumbens circuit to opiate dependence, and suggests that reprogramming this circuit holds promise for treating opiate addiction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhu, Yingjie -- Wienecke, Carl F R -- Nachtrab, Gregory -- Chen, Xiaoke -- 5T32DA035165-02/DA/NIDA NIH HHS/ -- T32 DA035165/DA/NIDA NIH HHS/ -- England -- Nature. 2016 Feb 11;530(7589):219-22. doi: 10.1038/nature16954. Epub 2016 Feb 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Stanford University, Stanford, California 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26840481" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Avoidance Learning ; Disease Models, Animal ; Long-Term Synaptic Depression ; Male ; Mice ; Mice, Inbred C57BL ; Morphine/administration & dosage/pharmacology ; *Neural Pathways/drug effects ; Neuronal Plasticity ; Neurons/drug effects/metabolism ; Nucleus Accumbens/drug effects/*physiopathology ; Opioid-Related Disorders/*physiopathology/therapy ; Optogenetics ; Rats, Sprague-Dawley ; Receptors, AMPA/metabolism ; Receptors, Dopamine D2/metabolism ; Reward ; Substance Withdrawal Syndrome/*physiopathology/therapy ; Synaptic Transmission/drug effects ; Thalamus/drug effects/pathology/*physiopathology
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 31
    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 ; Female ; Humans ; Inflammasomes/*antagonists & inhibitors/metabolism ; Inflammation/etiology/*metabolism/pathology/prevention & control ; Interleukin-1beta/immunology ; Intestines/*metabolism/*pathology ; Male ; Mice ; Microtubule-Associated Proteins/deficiency/metabolism ; Protein-Serine-Threonine Kinases/deficiency/genetics/*metabolism ; Reactive Oxygen Species/metabolism ; Stress, Physiological ; Th17 Cells/immunology ; Ubiquitin-Activating Enzymes/deficiency/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 32
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    Nature Publishing Group (NPG)
    Publication Date: 2016-02-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Reardon, Sara -- England -- Nature. 2016 Feb 18;530(7590):264. doi: 10.1038/nature.2016.19335.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26887470" target="_blank"〉PubMed〈/a〉
    Keywords: Animal Feed/*analysis/standards ; Animal Nutritional Physiological Phenomena ; Animals ; *Animals, Laboratory/genetics/microbiology ; Confounding Factors (Epidemiology) ; Diet/standards/veterinary ; *Environment ; Female ; Gastrointestinal Microbiome ; *Housing, Animal ; Humans ; Lighting ; Male ; Mice ; Mice, Inbred Strains ; Models, Animal ; Reproducibility of Results ; *Research Design/standards
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  • 33
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    Nature Publishing Group (NPG)
    Publication Date: 2016-04-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cressey, Daniel -- England -- Nature. 2016 Apr 7;532(7597):18-9. doi: 10.1038/532018a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27078545" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aquatic Organisms/genetics/isolation & purification ; *Biodiversity ; Conservation of Natural Resources/*legislation & jurisprudence ; International Cooperation/*legislation & jurisprudence ; *Negotiating ; Oceans and Seas ; United Nations/legislation & jurisprudence
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  • 34
    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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  • 35
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    Nature Publishing Group (NPG)
    Publication Date: 2016-03-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dance, Amber -- England -- Nature. 2016 Mar 3;531(7592):S2-3. doi: 10.1038/531S2a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26934523" target="_blank"〉PubMed〈/a〉
    Keywords: Aging ; Amphetamines/adverse effects/pharmacology ; Animals ; Benzhydryl Compounds/pharmacology ; Biomedical Enhancement/ethics/*methods ; Caffeine/pharmacology ; Child ; Cognition/drug effects ; Dopamine/metabolism ; Healthy Volunteers ; Humans ; Intelligence/*drug effects ; Intelligence Tests ; Methylphenidate/adverse effects/pharmacology ; Neurotransmitter Agents/metabolism ; Nicotine/adverse effects/pharmacology ; Norepinephrine/metabolism ; Off-Label Use ; Performance-Enhancing Substances/adverse effects/*pharmacology ; Prefrontal Cortex/drug effects/physiology ; Rats ; Substance-Related Disorders/etiology ; Video Games/psychology
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  • 36
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    Nature Publishing Group (NPG)
    Publication Date: 2016-05-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉de Bruyn, P J Nico -- England -- Nature. 2016 May 5;533(7601):36. doi: 10.1038/533036c.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of Pretoria, South Africa.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27147024" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Zoo/*physiology ; *Dissent and Disputes ; Longevity/*physiology ; Whale, Killer/*physiology
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  • 37
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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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  • 38
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    Nature Publishing Group (NPG)
    Publication Date: 2016-04-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Santarem, Frederico -- England -- Nature. 2016 Apr 14;532(7598):177. doi: 10.1038/532177b.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Research Centre in Biodiversity and Genetic Resources (CIBIO/InBIO), Porto, Portugal.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27075086" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Beekeeping/economics ; Bees/physiology ; Ecosystem ; Europe ; Humans ; *Introduced Species/economics ; *Pollination ; Predatory Behavior/physiology ; Wasps/pathogenicity/*physiology
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  • 39
    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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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 40
    Publication Date: 2016-03-24
    Description: Arrestins are cytosolic proteins that regulate G-protein-coupled receptor (GPCR) desensitization, internalization, trafficking and signalling. Arrestin recruitment uncouples GPCRs from heterotrimeric G proteins, and targets the proteins for internalization via clathrin-coated pits. Arrestins also function as ligand-regulated scaffolds that recruit multiple non-G-protein effectors into GPCR-based 'signalsomes'. Although the dominant function(s) of arrestins vary between receptors, the mechanism whereby different GPCRs specify these divergent functions is unclear. Using a panel of intramolecular fluorescein arsenical hairpin (FlAsH) bioluminescence resonance energy transfer (BRET) reporters to monitor conformational changes in beta-arrestin2, here we show that GPCRs impose distinctive arrestin 'conformational signatures' that reflect the stability of the receptor-arrestin complex and role of beta-arrestin2 in activating or dampening downstream signalling events. The predictive value of these signatures extends to structurally distinct ligands activating the same GPCR, such that the innate properties of the ligand are reflected as changes in beta-arrestin2 conformation. Our findings demonstrate that information about ligand-receptor conformation is encoded within the population average beta-arrestin2 conformation, and provide insight into how different GPCRs can use a common effector for different purposes. This approach may have application in the characterization and development of functionally selective GPCR ligands and in identifying factors that dictate arrestin conformation and function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, Mi-Hye -- Appleton, Kathryn M -- Strungs, Erik G -- Kwon, Joshua Y -- Morinelli, Thomas A -- Peterson, Yuri K -- Laporte, Stephane A -- Luttrell, Louis M -- DK055524/DK/NIDDK NIH HHS/ -- GM095497/GM/NIGMS NIH HHS/ -- MOP-74603/Canadian Institutes of Health Research/Canada -- R01 DK055524/DK/NIDDK NIH HHS/ -- R01 GM095497/GM/NIGMS NIH HHS/ -- RR027777/RR/NCRR NIH HHS/ -- S10 RR027777/RR/NCRR NIH HHS/ -- England -- Nature. 2016 Mar 31;531(7596):665-8. doi: 10.1038/nature17154. Epub 2016 Mar 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Medical University of South Carolina, Charleston, South Carolina 29425, USA. ; Department of Pharmaceutical &Biomedical Sciences, College of Pharmacy, Medical University of South Carolina, Charleston, South Carolina 29425, USA. ; Department of Medicine, McGill University Health Center Research Institute, McGill University, Quebec H4A 3J1, Canada. ; Pharmacology and Therapeutics, McGill University, Quebec H3G 1Y6, Canada. ; Anatomy and Cell Biology, McGill University, Quebec H3A 0C7, Canada. ; Research Service of the Ralph H. Johnson Veterans Affairs Medical Center, Charleston, South Carolina 29401, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27007854" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arrestins/*chemistry/*metabolism ; Enzyme Activation ; HEK293 Cells ; Humans ; Ligands ; Mitogen-Activated Protein Kinase 1/metabolism ; Mitogen-Activated Protein Kinase 3/metabolism ; Protein Conformation ; Protein Transport ; Rats ; Receptors, G-Protein-Coupled/chemistry/*metabolism ; *Signal Transduction
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 41
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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
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 42
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    Nature Publishing Group (NPG)
    Publication Date: 2016-03-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Eisenstein, Michael -- England -- Nature. 2016 Mar 17;531(7594):S61-3. doi: 10.1038/531S61a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26981732" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chagas Disease/epidemiology/transmission ; Cholera/epidemiology/transmission ; Cities/*statistics & numerical data ; Communicable Diseases/*epidemiology/*transmission ; Crowding ; Disease Vectors ; Hemorrhagic Fever, Ebola/epidemiology/transmission ; Humans ; *Poverty Areas ; Sanitation/statistics & numerical data ; Urbanization
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 43
    Publication Date: 2016-04-07
    Description: Neoplastic pancreatic epithelial cells are believed to die through caspase 8-dependent apoptotic cell death, and chemotherapy is thought to promote tumour apoptosis. Conversely, cancer cells often disrupt apoptosis to survive. Another type of programmed cell death is necroptosis (programmed necrosis), but its role in pancreatic ductal adenocarcinoma (PDA) is unclear. There are many potential inducers of necroptosis in PDA, including ligation of tumour necrosis factor receptor 1 (TNFR1), CD95, TNF-related apoptosis-inducing ligand (TRAIL) receptors, Toll-like receptors, reactive oxygen species, and chemotherapeutic drugs. Here we report that the principal components of the necrosome, receptor-interacting protein (RIP)1 and RIP3, are highly expressed in PDA and are further upregulated by the chemotherapy drug gemcitabine. Blockade of the necrosome in vitro promoted cancer cell proliferation and induced an aggressive oncogenic phenotype. By contrast, in vivo deletion of RIP3 or inhibition of RIP1 protected against oncogenic progression in mice and was associated with the development of a highly immunogenic myeloid and T cell infiltrate. The immune-suppressive tumour microenvironment associated with intact RIP1/RIP3 signalling depended in part on necroptosis-induced expression of the chemokine attractant CXCL1, and CXCL1 blockade protected against PDA. Moreover, cytoplasmic SAP130 (a subunit of the histone deacetylase complex) was expressed in PDA in a RIP1/RIP3-dependent manner, and Mincle--its cognate receptor--was upregulated in tumour-infiltrating myeloid cells. Ligation of Mincle by SAP130 promoted oncogenesis, whereas deletion of Mincle protected against oncogenesis and phenocopied the immunogenic reprogramming of the tumour microenvironment that was induced by RIP3 deletion. Cellular depletion suggested that whereas inhibitory macrophages promote tumorigenesis in PDA, they lose their immune-suppressive effects when RIP3 or Mincle is deleted. Accordingly, T cells, which are not protective against PDA progression in mice with intact RIP3 or Mincle signalling, are reprogrammed into indispensable mediators of anti-tumour immunity in the absence of RIP3 or Mincle. Our work describes parallel networks of necroptosis-induced CXCL1 and Mincle signalling that promote macrophage-induced adaptive immune suppression and thereby enable PDA progression.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4833566/" 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/PMC4833566/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Seifert, Lena -- Werba, Gregor -- Tiwari, Shaun -- Giao Ly, Nancy Ngoc -- Alothman, Sara -- Alqunaibit, Dalia -- Avanzi, Antonina -- Barilla, Rocky -- Daley, Donnele -- Greco, Stephanie H -- Torres-Hernandez, Alejandro -- Pergamo, Matthew -- Ochi, Atsuo -- Zambirinis, Constantinos P -- Pansari, Mridul -- Rendon, Mauricio -- Tippens, Daniel -- Hundeyin, Mautin -- Mani, Vishnu R -- Hajdu, Cristina -- Engle, Dannielle -- Miller, George -- CA155649/CA/NCI NIH HHS/ -- CA168611/CA/NCI NIH HHS/ -- CA193111/CA/NCI NIH HHS/ -- P30CA016087/CA/NCI NIH HHS/ -- R01 CA168611/CA/NCI NIH HHS/ -- T32 CA193111/CA/NCI NIH HHS/ -- UL1 TR000038/TR/NCATS NIH HHS/ -- England -- Nature. 2016 Apr 14;532(7598):245-9. doi: 10.1038/nature17403. Epub 2016 Apr 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉S. Arthur Localio Laboratory, Department of Surgery, New York University School of Medicine, 550 First Avenue, New York, New York 10016, USA. ; Department of Cell Biology, New York University School of Medicine, 550 First Avenue, New York, New York 10016, USA. ; Department of Pathology, New York University School of Medicine, 550 First Avenue, New York, New York 10016, USA. ; Cold Spring Harbor Laboratories, Cold Spring Harbor, New York 11724, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27049944" target="_blank"〉PubMed〈/a〉
    Keywords: Adenocarcinoma/immunology/metabolism/pathology ; Animals ; Apoptosis/drug effects ; *Carcinogenesis/drug effects ; Carcinoma, Pancreatic Ductal/immunology/metabolism/pathology ; Cell Line, Tumor ; Cell Proliferation/drug effects ;