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  • Organic Chemistry  (68,947)
  • Animals  (7,342)
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  • 1
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    London : Henry Stewart Talks
    Keywords: Blood pressure / Measurement ; Veterinary Medicine ; Animals ; Blood Pressure Determination / veterinary ; Blood Pressure Monitors ; Endocrine Diseases / veterinary ; Hypertension / veterinary ; Kidney Diseases / veterinary
    Description / Table of Contents: Contents: Signs that you should measure blood pressure in small animal patients -- Hypertension in small animal practice, and its association with endocrine and renal diseases -- Targets of hypertension -- The pros and cons of Doppler and Oscillometric blood pressure monitors -- The benefits of observing oscillometric tracing -- The impact of white coat effect on blood pressure and how to minimize it
    Notes: Animated audio-visual presentation with synchronized narration.
    Pages: 1 online resource (1 streaming video file (51 min.) : color, sound).
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  • 2
    Keywords: Life sciences ; Biotechnology ; Organic Chemistry ; Biochemistry ; Cell Biology ; Life sciences ; Cell Biology ; Biochemistry, general ; Biotechnology ; Organic Chemistry ; Springer eBooks
    Description / Table of Contents: 1. Trends in bioprobe research -- 2. Cell proliferation and differentiation -- 3. Epigenetics -- 4. Apoptosis and autophagy -- 5. Adaptive and innate immune Systems -- 6. Bioprobes at a glance
    Abstract: This new edition provides the most advanced research using bioprobes on the chemical control of 1) cell cycle and differentiation, 2) epigenetics, 3) apoptosis and autophagy, and 4) immune response. The “bioprobe”, first proposed in the first edition, has become an indispensable tool for chemical biology and has substantially assisted in the investigation of complex biochemical processes of cells. New areas of investigation such as stem cell research, epigenetic research, and autophagy research have rapidly advanced in the past 10 years. Including these new findings, this second edition supplies up-to-date information on the biochemical tools called bioprobes. Data on each bioprobe, such as chemical structure, origin, function, and references, are presented as one item in this volume. Readers will easily find useful information and will be able to determine the appropriate bioprobes to investigate cell functions. The information on bioprobes and their use in research makes this book a valuable source for researchers in diverse fields. Not only scientists in academia but also in the pharmaceutical industries will discover the most important information about small molecules useful for drug discovery
    Pages: VIII, 384 p. 173 illus., 10 illus. in color. : online resource.
    Edition: 2nd ed. 2017.
    ISBN: 9784431565291
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  • 3
    Publication Date: 2016-01-20
    Description: Migratory species depend on a suite of interconnected sites. Threats to unprotected links in these chains of sites are driving rapid population declines of migrants around the world, yet the extent to which different parts of the annual cycle are protected remains unknown. We show that just 9% of 1451 migratory birds are adequately covered by protected areas across all stages of their annual cycle, in comparison with 45% of nonmigratory birds. This discrepancy is driven by protected area placement that does not cover the full annual cycle of migratory species, indicating that global efforts toward coordinated conservation planning for migrants are yet to bear fruit. Better-targeted investment and enhanced coordination among countries are needed to conserve migratory species throughout their migratory cycle.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Runge, Claire A -- Watson, James E M -- Butchart, Stuart H M -- Hanson, Jeffrey O -- Possingham, Hugh P -- Fuller, Richard A -- New York, N.Y. -- Science. 2015 Dec 4;350(6265):1255-8. doi: 10.1126/science.aac9180.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Geography, Planning and Environmental Management, University of Queensland, Brisbane, QLD, 4072, Australia. National Center for Ecological Analysis and Synthesis (NCEAS), University of California, Santa Barbara, Santa Barbara, CA 93101, USA. claire.runge@uqconnect.edu.au. ; School of Geography, Planning and Environmental Management, University of Queensland, Brisbane, QLD, 4072, Australia. Global Conservation Program, Wildlife Conservation Society, New York, NY, USA. ; BirdLife International, Wellbrook Court, Cambridge CB3 0NA, UK. ; School of Biological Sciences, University of Queensland, Brisbane, QLD 4072, Australia. ; School of Biological Sciences, University of Queensland, Brisbane, QLD 4072, Australia. Department of Life Sciences, Imperial College London, Silwood Park, Ascot, Berkshire SL5 7PY, England, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26785490" target="_blank"〉PubMed〈/a〉
    Keywords: *Animal Migration ; Animals ; *Birds ; Breeding ; *Conservation of Natural Resources ; Population Dynamics ; Seasons
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    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-01-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Scheid, Johannes F -- New York, N.Y. -- Science. 2015 Dec 4;350(6265):1175. doi: 10.1126/science.aad7133.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Massachusetts General Hospital, Boston, MA 02114, USA. The Rockefeller University, New York, NY 10021, USA. fscheid@partners.org.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26785466" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/genetics/immunology/isolation & purification ; Antibodies, Neutralizing/genetics/*immunology/isolation & purification ; B-Lymphocytes/*immunology ; Cell Separation/methods ; HIV Antibodies/genetics/*immunology/isolation & purification ; HIV Infections/*blood ; Humans ; Immunologic Memory ; Mice ; env Gene Products, Human Immunodeficiency Virus/*immunology
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    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-01-20
    Description: Mitochondria generate adenosine 5'-triphosphate (ATP) and are a source of potentially toxic reactive oxygen species (ROS). It has been suggested that the gradual mitochondrial dysfunction that is observed to accompany aging could in fact be causal to the aging process. Here we review findings that suggest that age-dependent mitochondrial dysfunction is not sufficient to limit life span. Furthermore, mitochondrial ROS are not always deleterious and can even stimulate pro-longevity pathways. Thus, mitochondrial dysfunction plays a complex role in regulating longevity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Ying -- Hekimi, Siegfried -- MOP-114891/Canadian Institutes of Health Research/Canada -- MOP-123295/Canadian Institutes of Health Research/Canada -- MOP-97869/Canadian Institutes of Health Research/Canada -- New York, N.Y. -- Science. 2015 Dec 4;350(6265):1204-7. doi: 10.1126/science.aac4357.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, McGill University, Montreal, Quebec H3A 1B1, Canada. ; Department of Biology, McGill University, Montreal, Quebec H3A 1B1, Canada. siegfried.hekimi@mcgill.ca.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26785479" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/*metabolism ; Animals ; Caenorhabditis elegans Proteins/genetics ; Electron Transport/genetics ; Electron Transport Complex III/genetics ; Longevity/genetics/*physiology ; Mice ; Mice, Knockout ; Mitochondria/genetics/*metabolism ; Point Mutation ; Reactive Oxygen Species/*metabolism
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    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
    Publication Date: 2016-01-20
    Description: In developing hearts, changes in the cardiac metabolic milieu during the perinatal period redirect mitochondrial substrate preference from carbohydrates to fatty acids. Mechanisms responsible for this mitochondrial plasticity are unknown. Here, we found that PINK1-Mfn2-Parkin-mediated mitophagy directs this metabolic transformation in mouse hearts. A mitofusin (Mfn) 2 mutant lacking PINK1 phosphorylation sites necessary for Parkin binding (Mfn2 AA) inhibited mitochondrial Parkin translocation, suppressing mitophagy without impairing mitochondrial fusion. Cardiac Parkin deletion or expression of Mfn2 AA from birth, but not after weaning, prevented postnatal mitochondrial maturation essential to survival. Five-week-old Mfn2 AA hearts retained a fetal mitochondrial transcriptional signature without normal increases in fatty acid metabolism and mitochondrial biogenesis genes. Myocardial fatty acylcarnitine levels and cardiomyocyte respiration induced by palmitoylcarnitine were concordantly depressed. Thus, instead of transcriptional reprogramming, fetal cardiomyocyte mitochondria undergo perinatal Parkin-mediated mitophagy and replacement by mature adult mitochondria. Mitophagic mitochondrial removal underlies developmental cardiomyocyte mitochondrial plasticity and metabolic transitioning of perinatal hearts.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4747105/" 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/PMC4747105/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gong, Guohua -- Song, Moshi -- Csordas, Gyorgy -- Kelly, Daniel P -- Matkovich, Scot J -- Dorn, Gerald W 2nd -- HL058493/HL/NHLBI NIH HHS/ -- HL108943/HL/NHLBI NIH HHS/ -- HL122124/HL/NHLBI NIH HHS/ -- HL128071/HL/NHLBI NIH HHS/ -- HL59888/HL/NHLBI NIH HHS/ -- R01 HL058493/HL/NHLBI NIH HHS/ -- R01 HL059888/HL/NHLBI NIH HHS/ -- R01 HL108943/HL/NHLBI NIH HHS/ -- R01 HL128071/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2015 Dec 4;350(6265):aad2459. doi: 10.1126/science.aad2459. Epub 2015 Dec 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Pharmacogenomics, Department of Internal Medicine, Washington University School of Medicine, St. Louis, MO, USA. ; Department of Pathology, Anatomy, and Cell Biology, Thomas Jefferson University, Philadelphia, PA, USA. ; Center for Metabolic Origins of Disease, Cardiovascular Metabolism Program, Sanford Burnham Prebys Medical Discovery Institute, Orlando, FL, USA. ; Center for Pharmacogenomics, Department of Internal Medicine, Washington University School of Medicine, St. Louis, MO, USA. gdorn@dom.wustl.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26785495" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cellular Reprogramming ; GTP Phosphohydrolases/genetics/metabolism ; Heart/*embryology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mitochondria, Heart/metabolism/*physiology/ultrastructure ; Mitochondrial Degradation/genetics/*physiology ; Mitochondrial Dynamics ; Myocardium/*metabolism/ultrastructure ; Myocytes, Cardiac/metabolism/ultrastructure ; Protein Kinases/metabolism ; Ubiquitin-Protein Ligases/genetics/*metabolism
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    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-01-20
    Description: Research into stem cells and aging aims to understand how stem cells maintain tissue health, what mechanisms ultimately lead to decline in stem cell function with age, and how the regenerative capacity of somatic stem cells can be enhanced to promote healthy aging. Here, we explore the effects of aging on stem cells in different tissues. Recent research has focused on the ways that genetic mutations, epigenetic changes, and the extrinsic environmental milieu influence stem cell functionality over time. We describe each of these three factors, the ways in which they interact, and how these interactions decrease stem cell health over time. We are optimistic that a better understanding of these changes will uncover potential strategies to enhance stem cell function and increase tissue resiliency into old age.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Goodell, Margaret A -- Rando, Thomas A -- P01 AG036695/AG/NIA NIH HHS/ -- R01 AG047820/AG/NIA NIH HHS/ -- R01 AR062185/AR/NIAMS NIH HHS/ -- R37 AG023806/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2015 Dec 4;350(6265):1199-204. doi: 10.1126/science.aab3388.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Stem Cells and Regenerative Medicine Center, Center for Cell and Gene Therapy, and Department of Pediatrics, Baylor College of Medicine, Houston, TX 77030, USA. goodell@bcm.edu rando@stanford.edu. ; Glenn Center for the Biology of Aging and Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA 94305, USA, and Center for Regenerative Rehabilitation, Veterans Administration Palo Alto Health Care System, Palo Alto, CA 94304, USA. goodell@bcm.edu rando@stanford.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26785478" target="_blank"〉PubMed〈/a〉
    Keywords: Adult Stem Cells/*physiology ; Aging/*physiology ; Animals ; Cell Aging ; Epigenesis, Genetic ; Genetic Drift ; *Health ; Humans ; Mice ; Mutation ; Organ Specificity ; Selection, Genetic
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-01-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grimm, David -- New York, N.Y. -- Science. 2015 Dec 4;350(6265):1182-5. doi: 10.1126/science.350.6265.1182.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26785473" target="_blank"〉PubMed〈/a〉
    Keywords: Age Factors ; Animals ; Body Weight ; Cats ; Dogs ; Humans ; *Longevity ; Pets/*physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
    Publication Date: 2016-04-02
    Description: When animals encounter conflict they initiate and escalate aggression to establish and maintain a social hierarchy. The neural mechanisms by which animals resolve fighting behaviors to determine such social hierarchies remain unknown. We identified two subregions of the dorsal habenula (dHb) in zebrafish that antagonistically regulate the outcome of conflict. The losing experience reduced neural transmission in the lateral subregion of dHb (dHbL)-dorsal/intermediate interpeduncular nucleus (d/iIPN) circuit. Silencing of the dHbL or medial subregion of dHb (dHbM) caused a stronger predisposition to lose or win a fight, respectively. These results demonstrate that the dHbL and dHbM comprise a dual control system for conflict resolution of social aggression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chou, Ming-Yi -- Amo, Ryunosuke -- Kinoshita, Masae -- Cherng, Bor-Wei -- Shimazaki, Hideaki -- Agetsuma, Masakazu -- Shiraki, Toshiyuki -- Aoki, Tazu -- Takahoko, Mikako -- Yamazaki, Masako -- Higashijima, Shin-ichi -- Okamoto, Hitoshi -- New York, N.Y. -- Science. 2016 Apr 1;352(6281):87-90. doi: 10.1126/science.aac9508.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory for Developmental Gene Regulation, RIKEN Brain Science Institute, Saitama 351-0198, Japan. ; Laboratory for Developmental Gene Regulation, RIKEN Brain Science Institute, Saitama 351-0198, Japan. Department of Life Sciences, Graduate School of Arts and Sciences, University of Tokyo, Tokyo 153-8902, Japan. ; Laboratory for Neural Computation and Adaptation, RIKEN Brain Science Institute, Saitama 351-0198, Japan. ; National Institutes of Natural Sciences, Okazaki Institute for Integrative Bioscience, National Institute for Physiological Sciences, Aichi 444-8787, Japan. ; Laboratory for Developmental Gene Regulation, RIKEN Brain Science Institute, Saitama 351-0198, Japan. Department of Life Sciences, Graduate School of Arts and Sciences, University of Tokyo, Tokyo 153-8902, Japan. Laboratory for Molecular Brain Science, Department of Life Science and Medical Bioscience, Waseda University, Tokyo 162-8430, Japan. hitoshi@brain.riken.jp.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27034372" target="_blank"〉PubMed〈/a〉
    Keywords: Aggression/*physiology ; Animals ; *Conflict (Psychology) ; Habenula/*physiology ; Hierarchy, Social ; Interpeduncular Nucleus/physiology ; *Negotiating ; Synaptic Transmission ; Zebrafish
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-04-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kupferschmidt, Kai -- New York, N.Y. -- Science. 2016 Apr 22;352(6284):391-2. doi: 10.1126/science.352.6284.391. Epub 2016 Apr 21.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27102452" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Communicable Diseases/diagnosis/*epidemiology/etiology ; Echinococcosis/diagnosis/epidemiology ; Echinococcus/isolation & purification ; *Emigration and Immigration ; Europe ; Humans ; Mass Screening ; Methicillin Resistance ; Methicillin-Resistant Staphylococcus aureus/isolation & purification ; *Refugees
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 11
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-02-27
    Description: Oocytes differentiate in diverse species by receiving organelles and cytoplasm from sister germ cells while joined in germline cysts or syncytia. Mouse primordial germ cells form germline cysts, but the role of cysts in oogenesis is unknown. We find that mouse germ cells receive organelles from neighboring cyst cells and build a Balbiani body to become oocytes, whereas nurselike germ cells die. Organelle movement, Balbiani body formation, and oocyte fate determination are selectively blocked by low levels of microtubule-dependent transport inhibitors. Membrane breakdown within the cyst and an apoptosis-like process are associated with organelle transfer into the oocyte, events reminiscent of nurse cell dumping in Drosophila We propose that cytoplasmic and organelle transport plays an evolutionarily conserved and functionally important role in mammalian oocyte differentiation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lei, Lei -- Spradling, Allan C -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2016 Apr 1;352(6281):95-9. doi: 10.1126/science.aad2156. Epub 2016 Feb 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute Research Laboratories, Department of Embryology, Carnegie Institution for Science, 3520 San Martin Drive, Baltimore, MD 21218, USA. spradling@ciwemb.edu leile@med.umich.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26917595" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Biological Evolution ; Cytoplasm/physiology/ultrastructure ; Female ; Giant Cells/*cytology ; Mice ; Microtubules/drug effects/physiology ; Oocytes/*cytology ; *Oogenesis ; Organelles/*physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 12
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-01-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, Jon -- New York, N.Y. -- Science. 2016 Jan 1;351(6268):16-9. doi: 10.1126/science.351.6268.16.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26721985" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biomedical Research/*economics ; Communicable Disease Control/*economics ; Financial Management ; Humans ; National Institutes of Health (U.S.) ; United States ; Vaccines/*economics
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  • 13
    Publication Date: 2016-01-02
    Description: Several recent studies link parental environments to phenotypes in subsequent generations. In this work, we investigate the mechanism by which paternal diet affects offspring metabolism. Protein restriction in mice affects small RNA (sRNA) levels in mature sperm, with decreased let-7 levels and increased amounts of 5' fragments of glycine transfer RNAs (tRNAs). In testicular sperm, tRNA fragments are scarce but increase in abundance as sperm mature in the epididymis. Epididymosomes (vesicles that fuse with sperm during epididymal transit) carry RNA payloads matching those of mature sperm and can deliver RNAs to immature sperm in vitro. Functionally, tRNA-glycine-GCC fragments repress genes associated with the endogenous retroelement MERVL, in both embryonic stem cells and embryos. Our results shed light on sRNA biogenesis and its dietary regulation during posttesticular sperm maturation, and they also link tRNA fragments to regulation of endogenous retroelements active in the preimplantation embryo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sharma, Upasna -- Conine, Colin C -- Shea, Jeremy M -- Boskovic, Ana -- Derr, Alan G -- Bing, Xin Y -- Belleannee, Clemence -- Kucukural, Alper -- Serra, Ryan W -- Sun, Fengyun -- Song, Lina -- Carone, Benjamin R -- Ricci, Emiliano P -- Li, Xin Z -- Fauquier, Lucas -- Moore, Melissa J -- Sullivan, Robert -- Mello, Craig C -- Garber, Manuel -- Rando, Oliver J -- DP1ES025458/DP/NCCDPHP CDC HHS/ -- R01HD080224/HD/NICHD NIH HHS/ -- UL1 TR000161/TR/NCATS NIH HHS/ -- UL1 TR001453/TR/NCATS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2016 Jan 22;351(6271):391-6. doi: 10.1126/science.aad6780. Epub 2015 Dec 31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Pharmacology, University of Massachusetts Medical School, Worcester, MA 01605, USA. ; Program in Molecular Medicine, University of Massachusetts Medical School, Worcester, MA 01605, USA. Program in Bioinformatics and Integrative Biology, University of Massachusetts Medical School, Worcester, MA 01605, USA. ; Department of Obstetrics, Gynecology and Reproduction, Universite Laval, Centre Hospitalier Universitaire de Quebec Research Center, Quebec City, Quebec G1V 4G2, Canada. ; RNAi Therapeutics Institute, University of Massachusetts Medical School, Worcester, MA 01605, USA. ; Department of Biochemistry and Molecular Pharmacology, University of Massachusetts Medical School, Worcester, MA 01605, USA. RNAi Therapeutics Institute, University of Massachusetts Medical School, Worcester, MA 01605, USA. ; Department of Biochemistry and Molecular Pharmacology, University of Massachusetts Medical School, Worcester, MA 01605, USA. RNAi Therapeutics Institute, University of Massachusetts Medical School, Worcester, MA 01605, USA. Howard Hughes Medical Institute, University of Massachusetts Medical School, Worcester, MA 01605, USA. ; Program in Molecular Medicine, University of Massachusetts Medical School, Worcester, MA 01605, USA. RNAi Therapeutics Institute, University of Massachusetts Medical School, Worcester, MA 01605, USA. Howard Hughes Medical Institute, University of Massachusetts Medical School, Worcester, MA 01605, USA. ; Department of Biochemistry and Molecular Pharmacology, University of Massachusetts Medical School, Worcester, MA 01605, USA. oliver.rando@umassmed.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26721685" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blastocyst/metabolism ; Diet, Protein-Restricted ; Epididymis/metabolism ; *Fertilization ; *Gene Expression Regulation ; Male ; Mice ; MicroRNAs/metabolism ; RNA, Transfer, Gly/*metabolism/*physiology ; Retroelements/genetics ; *Sperm Maturation ; Spermatozoa/*metabolism ; Testis/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 14
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-01-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Leslie, Mitch -- New York, N.Y. -- Science. 2016 Jan 1;351(6268):13. doi: 10.1126/science.351.6268.13.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26721982" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; DNA/chemistry/genetics/metabolism ; *Epigenesis, Genetic ; Male ; Metabolism/*genetics ; Mice ; RNA, Transfer/genetics/*metabolism ; *Spermatozoa
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  • 15
    Publication Date: 2016-04-30
    Description: Sleep has been described in animals ranging from worms to humans. Yet the electrophysiological characteristics of brain sleep, such as slow-wave (SW) and rapid eye movement (REM) activities, are thought to be restricted to mammals and birds. Recording from the brain of a lizard, the Australian dragon Pogona vitticeps, we identified SW and REM sleep patterns, thus pushing back the probable evolution of these dynamics at least to the emergence of amniotes. The SW and REM sleep patterns that we observed in lizards oscillated continuously for 6 to 10 hours with a period of ~80 seconds. The networks controlling SW-REM antagonism in amniotes may thus originate from a common, ancient oscillator circuit. Lizard SW dynamics closely resemble those observed in rodent hippocampal CA1, yet they originate from a brain area, the dorsal ventricular ridge, that has no obvious hodological similarity with the mammalian hippocampus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shein-Idelson, Mark -- Ondracek, Janie M -- Liaw, Hua-Peng -- Reiter, Sam -- Laurent, Gilles -- New York, N.Y. -- Science. 2016 Apr 29;352(6285):590-5. doi: 10.1126/science.aaf3621.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max Planck Institute for Brain Research, Frankfurt am Main, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27126045" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Evolution ; Brain/*physiology ; CA1 Region, Hippocampal/physiology ; Lizards/*physiology ; Sleep, REM/*physiology
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  • 16
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-04-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Leslie, Mitch -- New York, N.Y. -- Science. 2016 Apr 1;352(6281):21-3. doi: 10.1126/science.352.6281.21.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27034353" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/*immunology ; Diabetes Mellitus, Type 1/immunology ; Infection/*immunology ; Inflammation/*immunology ; Lymph Nodes/cytology/*immunology ; Mice ; Pancreas/immunology ; T-Lymphocytes/*immunology
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  • 17
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-02-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stevens, Beth -- Muthukumar, Allie K -- New York, N.Y. -- Science. 2016 Feb 19;351(6275):813. doi: 10.1126/science.aaf2849.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, F. M. Kirby Neurobiology Center, Boston Children's Hospital, Boston, MA 02115, USA. beth.stevens@childrens.harvard.edu. ; Department of Neurology, F. M. Kirby Neurobiology Center, Boston Children's Hospital, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26912878" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Astrocytes/*metabolism ; Cerebellar Cortex/*cytology ; Female ; Hedgehog Proteins/*metabolism ; Male ; Neurons/*metabolism ; Receptors, G-Protein-Coupled/*metabolism
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  • 18
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-02-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ma, Eric H -- Jones, Russell G -- New York, N.Y. -- Science. 2016 Feb 12;351(6274):670-1. doi: 10.1126/science.aaf1929.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Goodman Cancer Research Centre, Department of Physiology, McGill University, Montreal, QC, H3A 1A3, Canada. Department of Physiology, McGill University, Montreal, QC, H3G 1Y6, Canada. ; Goodman Cancer Research Centre, Department of Physiology, McGill University, Montreal, QC, H3A 1A3, Canada. Department of Physiology, McGill University, Montreal, QC, H3G 1Y6, Canada. russell.jones@mcgill.ca.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26912848" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Humans ; Mitochondria/*metabolism ; Multiprotein Complexes/*metabolism ; Purines/*biosynthesis/*metabolism ; TOR Serine-Threonine Kinases/*metabolism ; Tetrahydrofolates/*metabolism
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  • 19
    Publication Date: 2016-04-23
    Description: Tissue-resident memory T (Trm) cells permanently localize to portals of pathogen entry, where they provide immediate protection against reinfection. To enforce tissue retention, Trm cells up-regulate CD69 and down-regulate molecules associated with tissue egress; however, a Trm-specific transcriptional regulator has not been identified. Here, we show that the transcription factor Hobit is specifically up-regulated in Trm cells and, together with related Blimp1, mediates the development of Trm cells in skin, gut, liver, and kidney in mice. The Hobit-Blimp1 transcriptional module is also required for other populations of tissue-resident lymphocytes, including natural killer T (NKT) cells and liver-resident NK cells, all of which share a common transcriptional program. Our results identify Hobit and Blimp1 as central regulators of this universal program that instructs tissue retention in diverse tissue-resident lymphocyte populations.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mackay, Laura K -- Minnich, Martina -- Kragten, Natasja A M -- Liao, Yang -- Nota, Benjamin -- Seillet, Cyril -- Zaid, Ali -- Man, Kevin -- Preston, Simon -- Freestone, David -- Braun, Asolina -- Wynne-Jones, Erica -- Behr, Felix M -- Stark, Regina -- Pellicci, Daniel G -- Godfrey, Dale I -- Belz, Gabrielle T -- Pellegrini, Marc -- Gebhardt, Thomas -- Busslinger, Meinrad -- Shi, Wei -- Carbone, Francis R -- van Lier, Rene A W -- Kallies, Axel -- van Gisbergen, Klaas P J M -- New York, N.Y. -- Science. 2016 Apr 22;352(6284):459-63. doi: 10.1126/science.aad2035.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, The University of Melbourne, The Peter Doherty Institute for Infection and Immunity, Melbourne, Australia. Australian Research Council (ARC) Centre of Excellence in Advanced Molecular Imaging, University of Melbourne, Melbourne, Australia. lkmackay@unimelb.edu.au kallies@wehi.edu.au k.vangisbergen@sanquin.nl. ; Research Institute of Molecular Pathology (IMP), Vienna Biocenter (VBC), Vienna, Austria. ; Department of Hematopoiesis, Sanquin Research and Landsteiner Laboratory, Academic Medical Center (AMC), University of Amsterdam, Amsterdam, Netherlands. ; The Walter and Eliza Hall Institute of Medical Research, Melbourne, Australia. Department of Medical Biology, The University of Melbourne, Melbourne, Australia. ; Department of Blood Cell Research, Sanquin Research and Landsteiner Laboratory, AMC, University of Amsterdam, Amsterdam, Netherlands. ; Department of Microbiology and Immunology, The University of Melbourne, The Peter Doherty Institute for Infection and Immunity, Melbourne, Australia. ; Department of Hematopoiesis, Sanquin Research and Landsteiner Laboratory, Academic Medical Center (AMC), University of Amsterdam, Amsterdam, Netherlands. The Walter and Eliza Hall Institute of Medical Research, Melbourne, Australia. Department of Medical Biology, The University of Melbourne, Melbourne, Australia. Department of Experimental Immunology, AMC, Amsterdam, Netherlands. ; Department of Microbiology and Immunology, The University of Melbourne, The Peter Doherty Institute for Infection and Immunity, Melbourne, Australia. Australian Research Council (ARC) Centre of Excellence in Advanced Molecular Imaging, University of Melbourne, Melbourne, Australia. ; The Walter and Eliza Hall Institute of Medical Research, Melbourne, Australia. Department of Computing and Information Systems, The University of Melbourne, Melbourne, Australia. ; The Walter and Eliza Hall Institute of Medical Research, Melbourne, Australia. Department of Medical Biology, The University of Melbourne, Melbourne, Australia. lkmackay@unimelb.edu.au kallies@wehi.edu.au k.vangisbergen@sanquin.nl. ; Department of Hematopoiesis, Sanquin Research and Landsteiner Laboratory, Academic Medical Center (AMC), University of Amsterdam, Amsterdam, Netherlands. The Walter and Eliza Hall Institute of Medical Research, Melbourne, Australia. Department of Medical Biology, The University of Melbourne, Melbourne, Australia. Department of Experimental Immunology, AMC, Amsterdam, Netherlands. lkmackay@unimelb.edu.au kallies@wehi.edu.au k.vangisbergen@sanquin.nl.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27102484" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Gastrointestinal Tract/immunology ; *Gene Expression Regulation ; Genes, Regulator/genetics/*physiology ; Immunologic Memory/*genetics ; Kidney/immunology ; Killer Cells, Natural/*immunology ; Liver/immunology ; Lymphocyte Activation ; Mice ; Mice, Knockout ; Natural Killer T-Cells/*immunology ; Skin/immunology ; Transcription Factors/genetics/*physiology ; Transcription, Genetic ; Up-Regulation
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  • 20
    Publication Date: 2016-02-26
    Description: The cerebrum of large mammals is convoluted, whereas that of small mammals is smooth. Mota and Herculano-Houzel (Reports, 3 July 2015, p. 74) inspired a model on an old theory that proposed a fractal geometry. I show that their model reduces to the product of gray-matter proportion times the folding index. This proportional relation describes the available data even better than the fractal model.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉de Lussanet, Marc H E -- New York, N.Y. -- Science. 2016 Feb 19;351(6275):825. doi: 10.1126/science.aad0127.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Sports Science, University of Munster, Horstmarer Landweg 62b, D-48149 Munster, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26912885" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cerebral Cortex ; Humans ; Lissencephaly/*pathology ; Neurons/*cytology
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  • 21
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-04-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Desban, Laura -- Wyart, Claire -- New York, N.Y. -- Science. 2016 Apr 1;352(6281):42-3. doi: 10.1126/science.aaf6016.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut du Cerveau et de la Moelle epiniere, GH Pitie-Salpetriere, 75013 Paris, France. ; Institut du Cerveau et de la Moelle epiniere, GH Pitie-Salpetriere, 75013 Paris, France. claire.wyart@icm-institute.org.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27034363" target="_blank"〉PubMed〈/a〉
    Keywords: Aggression/*physiology ; Animals ; *Conflict (Psychology) ; Habenula/*physiology ; *Negotiating
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  • 22
    Publication Date: 2016-04-23
    Description: Pershing et al (Science, 13 November 2015, p. 809) concluded that recent warming in the Gulf of Maine contributed to the collapse of Gulf of Maine cod. We argue that this conclusion is based on a flawed analysis of the population dynamics of this cod stock. We believe that understanding the potential role of climate change in the collapse of this stock requires more defensible analyses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Swain, Douglas P -- Benoit, Hugues P -- Cox, Sean P -- Cadigan, Noel G -- New York, N.Y. -- Science. 2016 Apr 22;352(6284):423. doi: 10.1126/science.aad9346.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Fisheries and Oceans Canada, Gulf Fisheries Centre, Moncton, NB E1C 9B6, Canada. ; Fisheries and Oceans Canada, Gulf Fisheries Centre, Moncton, NB E1C 9B6, Canada. hugues.benoit@dfo-mpo.gc.ca. ; School of Resource and Environmental Management, Simon Fraser University, Burnaby, BC V5A 1S6, Canada. ; Centre for Fisheries Ecosystems Research, Marine Institute of Memorial University of Newfoundland, St. John's, NL A1C 5R3, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27102474" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptation, Physiological ; Animals ; *Fisheries ; Gadus morhua/*physiology ; *Global Warming
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  • 23
    Publication Date: 2016-01-02
    Description: Frame-disrupting mutations in the DMD gene, encoding dystrophin, compromise myofiber integrity and drive muscle deterioration in Duchenne muscular dystrophy (DMD). Removing one or more exons from the mutated transcript can produce an in-frame mRNA and a truncated, but still functional, protein. In this study, we developed and tested a direct gene-editing approach to induce exon deletion and recover dystrophin expression in the mdx mouse model of DMD. Delivery by adeno-associated virus (AAV) of clustered regularly interspaced short palindromic repeats (CRISPR)-Cas9 endonucleases coupled with paired guide RNAs flanking the mutated Dmd exon23 resulted in excision of intervening DNA and restored the Dmd reading frame in myofibers, cardiomyocytes, and muscle stem cells after local or systemic delivery. AAV-Dmd CRISPR treatment partially recovered muscle functional deficiencies and generated a pool of endogenously corrected myogenic precursors in mdx mouse muscle.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tabebordbar, Mohammadsharif -- Zhu, Kexian -- Cheng, Jason K W -- Chew, Wei Leong -- Widrick, Jeffrey J -- Yan, Winston X -- Maesner, Claire -- Wu, Elizabeth Y -- Xiao, Ru -- Ran, F Ann -- Cong, Le -- Zhang, Feng -- Vandenberghe, Luk H -- Church, George M -- Wagers, Amy J -- 1DP2OD004345/OD/NIH HHS/ -- 5DP1-MH100706/DP/NCCDPHP CDC HHS/ -- 5PN2EY018244/EY/NEI NIH HHS/ -- 5R01DK097768-03/DK/NIDDK NIH HHS/ -- 5U01HL100402/HL/NHLBI NIH HHS/ -- P50 HG005550/HG/NHGRI NIH HHS/ -- T2GM007753/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2016 Jan 22;351(6271):407-11. doi: 10.1126/science.aad5177. Epub 2015 Dec 31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Stem Cell and Regenerative Biology, Harvard University, and Harvard Stem Cell Institute, Cambridge, MA 02138, USA. Biological and Biomedical Sciences Program, Harvard Medical School, Boston, MA 02115, USA. ; Department of Stem Cell and Regenerative Biology, Harvard University, and Harvard Stem Cell Institute, Cambridge, MA 02138, USA. Department of Molecular and Cellular Biology, Harvard University, Cambridge, MA 02138, USA. ; Department of Stem Cell and Regenerative Biology, Harvard University, and Harvard Stem Cell Institute, Cambridge, MA 02138, USA. ; Biological and Biomedical Sciences Program, Harvard Medical School, Boston, MA 02115, USA. Department of Genetics, Harvard Medical School, Boston, MA 02115, USA. ; Division of Genetics and Program in Genomics, Boston Children's Hospital, Harvard Medical School, Boston, MA 02115, USA. ; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. McGovern Institute for Brain Research, Department of Brain and Cognitive Science, and Department of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA 02139, USA. ; Grousbeck Gene Therapy Center, Schepens Eye Research Institute, and Massachusetts Eye and Ear Infirmary, 20 Staniford Street, Boston, MA 02114, USA. ; Department of Genetics, Harvard Medical School, Boston, MA 02115, USA. ; Department of Stem Cell and Regenerative Biology, Harvard University, and Harvard Stem Cell Institute, Cambridge, MA 02138, USA. amy_wagers@harvard.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26721686" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CRISPR-Cas Systems ; Clustered Regularly Interspaced Short Palindromic Repeats ; Dependovirus ; Disease Models, Animal ; Exons ; Frameshift Mutation ; Genetic Therapy/*methods ; Mice ; Mice, Inbred mdx ; Muscle, Skeletal/metabolism ; Muscular Dystrophy, Duchenne/genetics/*therapy ; Myocardium/metabolism ; RNA, Messenger/genetics ; Satellite Cells, Skeletal Muscle/*metabolism ; Sequence Deletion ; Transduction, Genetic/*methods
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  • 24
    Publication Date: 2016-02-26
    Description: Astrocytes are specialized and heterogeneous cells that contribute to central nervous system function and homeostasis. However, the mechanisms that create and maintain differences among astrocytes and allow them to fulfill particular physiological roles remain poorly defined. We reveal that neurons actively determine the features of astrocytes in the healthy adult brain and define a role for neuron-derived sonic hedgehog (Shh) in regulating the molecular and functional profile of astrocytes. Thus, the molecular and physiological program of astrocytes is not hardwired during development but, rather, depends on cues from neurons that drive and sustain their specialized properties.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Farmer, W Todd -- Abrahamsson, Therese -- Chierzi, Sabrina -- Lui, Christopher -- Zaelzer, Cristian -- Jones, Emma V -- Bally, Blandine Ponroy -- Chen, Gary G -- Theroux, Jean-Francois -- Peng, Jimmy -- Bourque, Charles W -- Charron, Frederic -- Ernst, Carl -- Sjostrom, P Jesper -- Murai, Keith K -- FDN 143337/Canadian Institutes of Health Research/Canada -- MOP 111152/Canadian Institutes of Health Research/Canada -- MOP 123390/Canadian Institutes of Health Research/Canada -- MOP 126137/Canadian Institutes of Health Research/Canada -- NIA 288936/Canadian Institutes of Health Research/Canada -- New York, N.Y. -- Science. 2016 Feb 19;351(6275):849-54. doi: 10.1126/science.aab3103.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre for Research in Neuroscience, Department of Neurology and Neurosurgery, Brain Repair and Integrative Neuroscience Program, The Research Institute of the McGill University Health Centre, Montreal General Hospital, Montreal, Quebec, Canada. ; Department of Psychiatry, McGill University, Montreal, Quebec, Canada. McGill Group for Suicide Studies, Douglas Hospital, Montreal, Quebec, Canada. ; Molecular Biology of Neural Development, Institut de Recherches Cliniques de Montreal, Department of Medicine, University of Montreal, Montreal, Quebec, Canada. Department of Biology, McGill University, Montreal, Quebec, Canada. ; Department of Psychiatry, McGill University, Montreal, Quebec, Canada. McGill Group for Suicide Studies, Douglas Hospital, Montreal, Quebec, Canada. Department of Human Genetics, McGill University, Montreal, Quebec, Canada. Douglas Hospital Research Institute, Verdun, Quebec, Canada. ; Centre for Research in Neuroscience, Department of Neurology and Neurosurgery, Brain Repair and Integrative Neuroscience Program, The Research Institute of the McGill University Health Centre, Montreal General Hospital, Montreal, Quebec, Canada. keith.murai@mcgill.ca.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26912893" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Astrocytes/*metabolism ; Cerebellar Cortex/*cytology ; Female ; Gene Deletion ; Hedgehog Proteins/genetics/*metabolism ; Male ; Mice ; Mice, Mutant Strains ; Neurons/*metabolism ; Receptors, G-Protein-Coupled/genetics/*metabolism ; Signal Transduction
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  • 25
    Publication Date: 2016-03-26
    Description: Brazil has experienced an unprecedented epidemic of Zika virus (ZIKV), with ~30,000 cases reported to date. ZIKV was first detected in Brazil in May 2015, and cases of microcephaly potentially associated with ZIKV infection were identified in November 2015. We performed next-generation sequencing to generate seven Brazilian ZIKV genomes sampled from four self-limited cases, one blood donor, one fatal adult case, and one newborn with microcephaly and congenital malformations. Results of phylogenetic and molecular clock analyses show a single introduction of ZIKV into the Americas, which we estimated to have occurred between May and December 2013, more than 12 months before the detection of ZIKV in Brazil. The estimated date of origin coincides with an increase in air passengers to Brazil from ZIKV-endemic areas, as well as with reported outbreaks in the Pacific Islands. ZIKV genomes from Brazil are phylogenetically interspersed with those from other South American and Caribbean countries. Mapping mutations onto existing structural models revealed the context of viral amino acid changes present in the outbreak lineage; however, no shared amino acid changes were found among the three currently available virus genomes from microcephaly cases. Municipality-level incidence data indicate that reports of suspected microcephaly in Brazil best correlate with ZIKV incidence around week 17 of pregnancy, although this correlation does not demonstrate causation. Our genetic description and analysis of ZIKV isolates in Brazil provide a baseline for future studies of the evolution and molecular epidemiology of this emerging virus in the Americas.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Faria, Nuno Rodrigues -- Azevedo, Raimunda do Socorro da Silva -- Kraemer, Moritz U G -- Souza, Renato -- Cunha, Mariana Sequetin -- Hill, Sarah C -- Theze, Julien -- Bonsall, Michael B -- Bowden, Thomas A -- Rissanen, Ilona -- Rocco, Iray Maria -- Nogueira, Juliana Silva -- Maeda, Adriana Yurika -- Vasami, Fernanda Giseli da Silva -- Macedo, Fernando Luiz de Lima -- Suzuki, Akemi -- Rodrigues, Sueli Guerreiro -- Cruz, Ana Cecilia Ribeiro -- Nunes, Bruno Tardeli -- Medeiros, Daniele Barbosa de Almeida -- Rodrigues, Daniela Sueli Guerreiro -- Nunes Queiroz, Alice Louize -- da Silva, Eliana Vieira Pinto -- Henriques, Daniele Freitas -- Travassos da Rosa, Elisabeth Salbe -- de Oliveira, Consuelo Silva -- Martins, Livia Caricio -- Vasconcelos, Helena Baldez -- Casseb, Livia Medeiros Neves -- Simith, Darlene de Brito -- Messina, Jane P -- Abade, Leandro -- Lourenco, Jose -- Carlos Junior Alcantara, Luiz -- de Lima, Maricelia Maia -- Giovanetti, Marta -- Hay, Simon I -- de Oliveira, Rodrigo Santos -- Lemos, Poliana da Silva -- de Oliveira, Layanna Freitas -- de Lima, Clayton Pereira Silva -- da Silva, Sandro Patroca -- de Vasconcelos, Janaina Mota -- Franco, Luciano -- Cardoso, Jedson Ferreira -- Vianez-Junior, Joao Lidio da Silva Goncalves -- Mir, Daiana -- Bello, Gonzalo -- Delatorre, Edson -- Khan, Kamran -- Creatore, Marisa -- Coelho, Giovanini Evelim -- de Oliveira, Wanderson Kleber -- Tesh, Robert -- Pybus, Oliver G -- Nunes, Marcio R T -- Vasconcelos, Pedro F C -- 090532/Z/09/Z/Wellcome Trust/United Kingdom -- 095066/Wellcome Trust/United Kingdom -- 102427/Wellcome Trust/United Kingdom -- MR/L009528/1/Medical Research Council/United Kingdom -- R24 AT 120942/AT/NCCIH NIH HHS/ -- New York, N.Y. -- Science. 2016 Apr 15;352(6283):345-9. doi: 10.1126/science.aaf5036. Epub 2016 Mar 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Technological Innovation, Evandro Chagas Institute, Ministry of Health, Ananindeua, PA 67030-000, Brazil. Department of Zoology, University of Oxford, South Parks Road, Oxford OX1 3PS, UK. ; Department of Arbovirology and Hemorrhagic Fevers, Evandro Chagas Institute, Ministry of Health, Ananindeua, Para State, Brazil. ; Department of Zoology, University of Oxford, South Parks Road, Oxford OX1 3PS, UK. ; Instituto Adolfo Lutz, University of Sao Paulo, Sao Paulo, Brazil. ; Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford, UK. ; Department of Zoology, University of Oxford, South Parks Road, Oxford OX1 3PS, UK. Metabiota, San Francisco, CA 94104, USA. ; Oswaldo Cruz Foundation (FIOCRUZ), Salvador, Bahia, Brazil. ; Centre of Post Graduation in Collective Health, Department of Health, Universidade Estadual de Feira de Santana, Feira de Santana, Bahia, Brazil. ; Institute for Health Metrics and Evaluation, University of Washington, Seattle, WA 98121, USA. Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford, UK. ; Center for Technological Innovation, Evandro Chagas Institute, Ministry of Health, Ananindeua, PA 67030-000, Brazil. ; Laboratorio de AIDS and Imunologia Molecular, Instituto Oswaldo Cruz, FIOCRUZ, Rio de Janeiro, Brazil. ; Li Ka Shing Knowledge Institute, St. Michael's Hospital, Toronto, Ontario, Canada. Department of Medicine, Division of Infectious Diseases, University of Toronto, Toronto, Ontario, Canada. ; Dalla Lana School of Public Health, University of Toronto, Toronto, Ontario, Canada. ; Brazilian Ministry of Health, Brasilia, Brazil. ; Department of Pathology, University of Texas Medical Branch, Galveston, TX 77555, USA. ; Department of Zoology, University of Oxford, South Parks Road, Oxford OX1 3PS, UK. Metabiota, San Francisco, CA 94104, USA. oliver.pybus@zoo.ox.ac.uk marcionunesbrasil@yahoo.com.br pedrovasconcelos@iec.pa.gov.br. ; Center for Technological Innovation, Evandro Chagas Institute, Ministry of Health, Ananindeua, PA 67030-000, Brazil. Department of Pathology, University of Texas Medical Branch, Galveston, TX 77555, USA. oliver.pybus@zoo.ox.ac.uk marcionunesbrasil@yahoo.com.br pedrovasconcelos@iec.pa.gov.br. ; Department of Arbovirology and Hemorrhagic Fevers, Evandro Chagas Institute, Ministry of Health, Ananindeua, Para State, Brazil. oliver.pybus@zoo.ox.ac.uk marcionunesbrasil@yahoo.com.br pedrovasconcelos@iec.pa.gov.br.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27013429" target="_blank"〉PubMed〈/a〉
    Keywords: Aedes/virology ; Americas/epidemiology ; Animals ; *Disease Outbreaks ; Female ; Genome, Viral/genetics ; Humans ; Incidence ; Insect Vectors/virology ; Microcephaly/*epidemiology/virology ; Molecular Epidemiology ; Molecular Sequence Data ; Mutation ; Pacific Islands/epidemiology ; Phylogeny ; Pregnancy ; RNA, Viral/genetics ; Sequence Analysis, RNA ; Travel ; Zika Virus/classification/*genetics/isolation & purification ; Zika Virus Infection/*epidemiology/transmission/*virology
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  • 26
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-02-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Underwood, Emily -- New York, N.Y. -- Science. 2016 Feb 19;351(6275):799-800. doi: 10.1126/science.351.6275.799.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26912871" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*physiology ; Brain Mapping/economics/*methods ; DNA/*analysis ; Financing, Organized ; Fluorescence ; Mice ; Nerve Net/physiology ; Neurons/*chemistry ; Neurosciences/economics/trends ; RNA/*analysis ; Synapses/*physiology
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  • 27
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-01-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Farrell, Anthony P -- Franklin, Craig E -- New York, N.Y. -- Science. 2016 Jan 8;351(6269):132-3. doi: 10.1126/science.351.6269.132-b.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Zoology, University of British Columbia, Vancouver, BC V6T1Z4, Canada. farrellt@mail.ubc.ca. ; School of Biological Sciences, The University of Queensland, St. Lucia, QLD 4072, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26744399" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Birds/*classification ; *Climate Change ; *Endangered Species ; Fishes/*classification ; Mammals/*classification ; Turtles/*classification
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  • 28
    Publication Date: 2016-01-28
    Description: Vocal imitation involves incorporating instructive auditory information into relevant motor circuits through processes that are poorly understood. In zebra finches, we found that exposure to a tutor's song drives spiking activity within premotor neurons in the juvenile, whereas inhibition suppresses such responses upon learning in adulthood. We measured inhibitory currents evoked by the tutor song throughout development while simultaneously quantifying each bird's learning trajectory. Surprisingly, we found that the maturation of synaptic inhibition onto premotor neurons is correlated with learning but not age. We used synthetic tutoring to demonstrate that inhibition is selective for specific song elements that have already been learned and not those still in refinement. Our results suggest that structured inhibition plays a crucial role during song acquisition, enabling a piece-by-piece mastery of complex tasks.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vallentin, Daniela -- Kosche, Georg -- Lipkind, Dina -- Long, Michael A -- R01NS075044/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2016 Jan 15;351(6270):267-71. doi: 10.1126/science.aad3023.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉NYU Neuroscience Institute and Department of Otolaryngology, New York University Langone Medical Center, New York, NY 10016, USA. Center for Neural Science, New York University, New York, NY 10003, USA. ; Laboratory of Vocal Learning, Department of Psychology, Hunter College, New York, NY 10065, USA. ; NYU Neuroscience Institute and Department of Otolaryngology, New York University Langone Medical Center, New York, NY 10016, USA. Center for Neural Science, New York University, New York, NY 10003, USA. mlong@med.nyu.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26816377" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Finches/*physiology ; High Vocal Center/*physiology ; *Learning ; Male ; Motor Neurons/physiology ; Music ; *Neural Inhibition ; Neural Pathways/*physiology ; Prosencephalon/physiology ; Synapses/physiology ; *Vocalization, Animal
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  • 29
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-03-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gibbons, Ann -- New York, N.Y. -- Science. 2016 Mar 18;351(6279):1250-1. doi: 10.1126/science.351.6279.1250. Epub 2016 Mar 17.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26989228" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Asia ; Biological Evolution ; Bone and Bones ; DNA/genetics ; Europe ; Female ; Fossils ; Humans ; Male ; *Mating Preference, Animal ; Neanderthals/*genetics/*psychology ; *Sexual Behavior
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  • 30
    Publication Date: 2016-04-02
    Description: Until recently, programmed cell death was conceived of as a single set of molecular pathways. We now know of several distinct sets of death-inducing mechanisms that lead to differing cell-death processes. In one of them--apoptosis--the dying cell affects others minimally. In contrast, programmed necrotic cell death causes release of immunostimulatory intracellular components after cell-membrane rupture. Defining the in vivo relevance of necrotic death is hampered because the molecules initiating it [such as receptor-interacting protein kinase-1 (RIPK1), RIPK3, or caspase-1] also serve other functions. Proteins that participate in late events in two forms of programmed necrosis [mixed lineage kinase domain-like protein (MLKL) in necroptosis and gasdermin-D in pyroptosis] were recently discovered, bringing us closer to identifying molecules that strictly serve in death mediation, thereby providing probes for better assessing its role in inflammation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wallach, David -- Kang, Tae-Bong -- Dillon, Christopher P -- Green, Douglas R -- New York, N.Y. -- Science. 2016 Apr 1;352(6281):aaf2154. doi: 10.1126/science.aaf2154.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biomolecular Sciences, The Weizmann Institute of Science, 76100 Rehovot, Israel. d.wallach@weizmann.ac.il douglas.green@stjude.org. ; Department of Biotechnology, College of Biomedical and Health Science, Konkuk University, Chung-Ju 380-701, Korea. ; Department of Immunology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA. ; Department of Immunology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA. d.wallach@weizmann.ac.il douglas.green@stjude.org.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27034377" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Caspase 1/metabolism ; Cytokines/metabolism ; Humans ; Inflammation/*metabolism/*pathology ; Necrosis/pathology ; Neoplasm Proteins/metabolism ; Protein Kinases/metabolism ; Receptor-Interacting Protein Serine-Threonine Kinases/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 31
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-04-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Monahan, Patrick -- New York, N.Y. -- Science. 2016 Apr 22;352(6284):395. doi: 10.1126/science.352.6284.395. Epub 2016 Apr 21.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27102456" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Bone Development ; Bone and Bones/*anatomy & histology ; Dinosaurs/*anatomy & histology/*growth & development
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 32
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-04-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wade, Lizzie -- New York, N.Y. -- Science. 2016 Apr 8;352(6282):129-30. doi: 10.1126/science.352.6282.129. Epub 2016 Apr 7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27124429" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Anthozoa ; Biodiversity ; Colombia ; Conservation of Natural Resources/*methods ; *Coral Reefs ; *Ships
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 33
    Publication Date: 2016-04-23
    Description: Progression through the stages of lymphocyte development requires coordination of the cell cycle. Such coordination ensures genomic integrity while cells somatically rearrange their antigen receptor genes [in a process called variable-diversity-joining (VDJ) recombination] and, upon successful rearrangement, expands the pools of progenitor lymphocytes. Here we show that in developing B lymphocytes, the RNA-binding proteins (RBPs) ZFP36L1 and ZFP36L2 are critical for maintaining quiescence before precursor B cell receptor (pre-BCR) expression and for reestablishing quiescence after pre-BCR-induced expansion. These RBPs suppress an evolutionarily conserved posttranscriptional regulon consisting of messenger RNAs whose protein products cooperatively promote transition into the S phase of the cell cycle. This mechanism promotes VDJ recombination and effective selection of cells expressing immunoglobulin-mu at the pre-BCR checkpoint.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Galloway, Alison -- Saveliev, Alexander -- Lukasiak, Sebastian -- Hodson, Daniel J -- Bolland, Daniel -- Balmanno, Kathryn -- Ahlfors, Helena -- Monzon-Casanova, Elisa -- Mannurita, Sara Ciullini -- Bell, Lewis S -- Andrews, Simon -- Diaz-Munoz, Manuel D -- Cook, Simon J -- Corcoran, Anne -- Turner, Martin -- Medical Research Council/United Kingdom -- Biotechnology and Biological Sciences Research Council/United Kingdom -- New York, N.Y. -- Science. 2016 Apr 22;352(6284):453-9. doi: 10.1126/science.aad5978.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Lymphocyte Signalling and Development, The Babraham Institute, Cambridge CB22 3AT, UK. ; Laboratory of Lymphocyte Signalling and Development, The Babraham Institute, Cambridge CB22 3AT, UK. Department of Haematology, University of Cambridge, The Clifford Allbutt Building, Cambridge Biomedical Campus, Hills Road, Cambridge CB2 0AH, UK. ; Laboratory of Nuclear Dynamics, The Babraham Institute, Cambridge CB22 3AT, UK. ; Laboratory of Signalling, The Babraham Institute, Cambridge CB22 3AT, UK. ; Laboratory of Lymphocyte Signalling and Development, The Babraham Institute, Cambridge CB22 3AT, UK. Department of Biochemistry, University of Cambridge, Tennis Court Road, Cambridge CB2 1QW, UK. ; Bioinformatics Group, The Babraham Institute, Cambridge CB22 3AT, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27102483" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/*cytology ; Conserved Sequence ; Cyclins/metabolism ; G0 Phase/genetics/physiology ; G1 Phase/genetics/physiology ; Gene Expression Regulation ; Immunoglobulin mu-Chains/genetics ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Nuclear Proteins/genetics/*physiology ; Pre-B Cell Receptors ; RNA, Messenger/metabolism ; RNA-Binding Proteins/genetics/*physiology ; S Phase/genetics/*physiology ; Selection, Genetic ; Transcription, Genetic ; Tristetraprolin/genetics/*physiology ; V(D)J Recombination
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  • 34
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-02-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gibbons, Ann -- New York, N.Y. -- Science. 2016 Feb 12;351(6274):648-9. doi: 10.1126/science.351.6274.648.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26912836" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Disease/*genetics ; Humans ; Neanderthals/*genetics
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  • 35
    Publication Date: 2016-03-26
    Description: Cell assembly sequences during learning are "replayed" during hippocampal ripples and contribute to the consolidation of episodic memories. However, neuronal sequences may also reflect preexisting dynamics. We report that sequences of place-cell firing in a novel environment are formed from a combination of the contributions of a rigid, predominantly fast-firing subset of pyramidal neurons with low spatial specificity and limited change across sleep-experience-sleep and a slow-firing plastic subset. Slow-firing cells, rather than fast-firing cells, gained high place specificity during exploration, elevated their association with ripples, and showed increased bursting and temporal coactivation during postexperience sleep. Thus, slow- and fast-firing neurons, although forming a continuous distribution, have different coding and plastic properties.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grosmark, Andres D -- Buzsaki, Gyorgy -- MH102840/MH/NIMH NIH HHS/ -- MH54671/MH/NIMH NIH HHS/ -- NS075015/NS/NINDS NIH HHS/ -- R01 MH107396/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2016 Mar 25;351(6280):1440-3. doi: 10.1126/science.aad1935.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, Columbia University Medical Center, New York, NY 10019, USA. The Neuroscience Institute, School of Medicine, New York University, New York, NY 10016, USA. ; The Neuroscience Institute, School of Medicine, New York University, New York, NY 10016, USA. Center for Neural Science, New York University, New York, NY 10016, USA. gyorgy.buzsaki@nyumc.org.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27013730" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Hippocampus/cytology/*physiopathology ; Learning/*physiology ; Male ; Maze Learning ; Neuronal Plasticity ; Pyramidal Cells/*physiology ; Rats ; Rats, Inbred LEC ; Sleep/physiology
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  • 36
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-04-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉O'Neill, Scott L -- New York, N.Y. -- Science. 2016 Apr 29;352(6285):526. doi: 10.1126/science.352.6285.526-a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Eliminate Dengue Program, School of Biological Sciences, Monash University, Clayton, Victoria 3800, Australia. scott.oneill@monash.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27126028" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Culicidae/*microbiology ; Dengue/*prevention & control ; Mosquito Control/*methods ; *Wolbachia
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  • 37
    Publication Date: 2016-03-19
    Description: Postnatal colonization of the body with microbes is assumed to be the main stimulus to postnatal immune development. By transiently colonizing pregnant female mice, we show that the maternal microbiota shapes the immune system of the offspring. Gestational colonization increases intestinal group 3 innate lymphoid cells and F4/80(+)CD11c(+) mononuclear cells in the pups. Maternal colonization reprograms intestinal transcriptional profiles of the offspring, including increased expression of genes encoding epithelial antibacterial peptides and metabolism of microbial molecules. Some of these effects are dependent on maternal antibodies that potentially retain microbial molecules and transmit them to the offspring during pregnancy and in milk. Pups born to mothers transiently colonized in pregnancy are better able to avoid inflammatory responses to microbial molecules and penetration of intestinal microbes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gomez de Aguero, Mercedes -- Ganal-Vonarburg, Stephanie C -- Fuhrer, Tobias -- Rupp, Sandra -- Uchimura, Yasuhiro -- Li, Hai -- Steinert, Anna -- Heikenwalder, Mathias -- Hapfelmeier, Siegfried -- Sauer, Uwe -- McCoy, Kathy D -- Macpherson, Andrew J -- New York, N.Y. -- Science. 2016 Mar 18;351(6279):1296-302. doi: 10.1126/science.aad2571.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Maurice Muller Laboratories (DKF), Universitatsklinik fur Viszerale Chirurgie und Medizin Inselspital, Murtenstrasse 35, University of Bern, 3010 Bern, Switzerland. ; Institute of Molecular Systems Biology, Swiss Federal Institute of Technology (ETH) Zurich, 8093 Zurich, Switzerland. ; Division of Chronic Inflammation and Cancer, German Cancer Research Center (DKFZ), Heidelberg, Germany. ; Institute for Infectious Diseases, University of Bern, 3010 Bern, Switzerland. ; Maurice Muller Laboratories (DKF), Universitatsklinik fur Viszerale Chirurgie und Medizin Inselspital, Murtenstrasse 35, University of Bern, 3010 Bern, Switzerland. andrew.macpherson@insel.ch.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26989247" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies/immunology ; Escherichia coli/immunology ; Female ; Gastrointestinal Microbiome/*immunology ; Germ-Free Life ; Immune System/*growth & development/*microbiology ; Immunity, Innate/genetics/*immunology ; Immunity, Maternally-Acquired/genetics/*immunology ; Intestines/*immunology ; Lymphocytes/immunology ; Mice ; Mice, Inbred C57BL ; Pregnancy ; Symbiosis ; Transcription, Genetic
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  • 38
    Publication Date: 2016-04-16
    Description: Drug resistance compromises control of malaria. Here, we show that resistance to a commonly used antimalarial medication, atovaquone, is apparently unable to spread. Atovaquone pressure selects parasites with mutations in cytochrome b, a respiratory protein with low but essential activity in the mammalian blood phase of the parasite life cycle. Resistance mutations rescue parasites from the drug but later prove lethal in the mosquito phase, where parasites require full respiration. Unable to respire efficiently, resistant parasites fail to complete mosquito development, arresting their life cycle. Because cytochrome b is encoded by the maternally inherited parasite mitochondrion, even outcrossing with wild-type strains cannot facilitate spread of resistance. Lack of transmission suggests that resistance will be unable to spread in the field, greatly enhancing the utility of atovaquone in malaria control.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Goodman, Christopher D -- Siregar, Josephine E -- Mollard, Vanessa -- Vega-Rodriguez, Joel -- Syafruddin, Din -- Matsuoka, Hiroyuki -- Matsuzaki, Motomichi -- Toyama, Tomoko -- Sturm, Angelika -- Cozijnsen, Anton -- Jacobs-Lorena, Marcelo -- Kita, Kiyoshi -- Marzuki, Sangkot -- McFadden, Geoffrey I -- AI031478/AI/NIAID NIH HHS/ -- RR00052/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2016 Apr 15;352(6283):349-53. doi: 10.1126/science.aad9279.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of BioSciences, University of Melbourne, Melbourne, VIC 3010, Australia. gim@unimelb.edu.au deang@unimelb.edu.au. ; School of BioSciences, University of Melbourne, Melbourne, VIC 3010, Australia. Eijkman Institute for Molecular Biology, JI Diponegoro no. 69, Jakarta, 10430, Indonesia. Department of Biomedical Chemistry, Graduate School of Medicine, The University of Tokyo, Hongo, Bunkyo-ku, Tokyo 113-0033, Japan. ; School of BioSciences, University of Melbourne, Melbourne, VIC 3010, Australia. ; Johns Hopkins University Bloomberg School of Public Health, Department of Molecular Microbiology and Immunology, Malaria Research Institute, Baltimore, MD 21205, USA. ; Eijkman Institute for Molecular Biology, JI Diponegoro no. 69, Jakarta, 10430, Indonesia. Department of Parasitology, Faculty of Medicine, Hasanuddin University, Jalan Perintis Kemerdekaan Km10, Makassar 90245, Indonesia. ; Division of Medical Zoology, Jichi Medical University, 3311-1 Yakushiji, Shimotsuke, Tochigi 329-0498, Japan. ; Department of Biomedical Chemistry, Graduate School of Medicine, The University of Tokyo, Hongo, Bunkyo-ku, Tokyo 113-0033, Japan. ; Department of Biomedical Chemistry, Graduate School of Medicine, The University of Tokyo, Hongo, Bunkyo-ku, Tokyo 113-0033, Japan. School of Tropical Medicine and Global Health, Nagasaki University, Sakamoto, Nagasaki 852-8523, Japan. ; Eijkman Institute for Molecular Biology, JI Diponegoro no. 69, Jakarta, 10430, Indonesia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27081071" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anopheles/*parasitology ; Antimalarials/*pharmacology/therapeutic use ; Atovaquone/*pharmacology/therapeutic use ; Cell Line ; Cytochromes b/*genetics ; Drug Resistance/*genetics ; Genes, Mitochondrial/genetics ; Humans ; Life Cycle Stages/drug effects/genetics ; Malaria/drug therapy/*parasitology/transmission ; Male ; Mice ; Mitochondria/*genetics ; Mutation ; Plasmodium berghei/*drug effects/genetics/growth & development ; Selection, Genetic
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  • 39
    Publication Date: 2016-04-30
    Description: Recent studies in human populations and mouse models reveal notable congruences in gut microbial taxa whose abundances are partly regulated by host genotype. Host genes associating with these taxa are related to diet sensing, metabolism, and immunity. These broad patterns are further validated in similar studies of nonmammalian microbiomes. The next generation of genome-wide association studies will expand the size of the data sets and refine the microbial phenotypes to fully capture these intriguing signatures of host-microbiome coevolution.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Goodrich, Julia K -- Davenport, Emily R -- Waters, Jillian L -- Clark, Andrew G -- Ley, Ruth E -- R01 DK093595/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2016 Apr 29;352(6285):532-5. doi: 10.1126/science.aad9379.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology and Genetics, Cornell University, Ithaca NY, USA. ; Department of Molecular Biology and Genetics, Cornell University, Ithaca NY, USA. Department of Microbiome Science, Max Planck Institute for Developmental Biology, Tubingen, Germany. ; Department of Molecular Biology and Genetics, Cornell University, Ithaca NY, USA. Department of Microbiology, Cornell University, Ithaca NY, USA. Department of Microbiome Science, Max Planck Institute for Developmental Biology, Tubingen, Germany. rel222@cornell.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27126034" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacteria/*classification/genetics ; Diet ; *Genome-Wide Association Study ; Genotype ; Humans ; Mice ; Microbiota/genetics/*physiology ; Phenotype ; *Quantitative Trait Loci ; Species Specificity
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  • 40
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-03-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Harris, Nicola -- New York, N.Y. -- Science. 2016 Mar 18;351(6279):1264-5. doi: 10.1126/science.aaf5215. Epub 2016 Mar 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Ecole polytechnique federeale de Lausanne, 1015 Lausanne, Switzerland. nicola.harris@epfl.ch.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26989236" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chemoreceptor Cells/*immunology ; Intestinal Diseases, Parasitic/*immunology ; Intestinal Mucosa/*immunology/*parasitology ; Microbiota/*immunology ; TRPM Cation Channels/*immunology
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  • 41
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-04-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Badylak, Stephen F -- New York, N.Y. -- Science. 2016 Apr 15;352(6283):298. doi: 10.1126/science.aaf7587.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉McGowan Institute for Regenerative Medicine, University of Pittsburgh, Pittsburgh, PA, USA. Department of Surgery, University of Pittsburgh, PA, USA. Department of Bioengineering, University of Pittsburgh, Pittsburgh, PA, USA. badylaks@upmc.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27081059" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biocompatible Materials ; Muscle, Skeletal/*injuries/*physiology ; *Tissue Scaffolds ; Wound Healing/*immunology
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  • 42
    Publication Date: 2016-04-16
    Description: Coral bleaching events threaten the sustainability of the Great Barrier Reef (GBR). Here we show that bleaching events of the past three decades have been mitigated by induced thermal tolerance of reef-building corals, and this protective mechanism is likely to be lost under near-future climate change scenarios. We show that 75% of past thermal stress events have been characterized by a temperature trajectory that subjects corals to a protective, sub-bleaching stress, before reaching temperatures that cause bleaching. Such conditions confer thermal tolerance, decreasing coral cell mortality and symbiont loss during bleaching by over 50%. We find that near-future increases in local temperature of as little as 0.5 degrees C result in this protective mechanism being lost, which may increase the rate of degradation of the GBR.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ainsworth, Tracy D -- Heron, Scott F -- Ortiz, Juan Carlos -- Mumby, Peter J -- Grech, Alana -- Ogawa, Daisie -- Eakin, C Mark -- Leggat, William -- New York, N.Y. -- Science. 2016 Apr 15;352(6283):338-42. doi: 10.1126/science.aac7125.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Australian Research Council Centre of Excellence for Coral Reef Studies, James Cook University, Townsville 4810, Australia. ; Coral Reef Watch, U.S. National Oceanic and Atmospheric Administration (NOAA), College Park, MD 20740, USA. Marine Geophysical Laboratory, College of Science, Technology and Engineering, James Cook University, Townsville 4811, Australia. ; Marine Spatial Ecology Lab, School of Biological Sciences, University of Queensland, Brisbane 4072, Australia. Australian Research Council Centre of Excellence for Coral Reef Studies, University of Queensland, Brisbane 4072, Australia. ; Department of Environmental Sciences, Macquarie University, Sydney 2109, Australia. ; Australian Research Council Centre of Excellence for Coral Reef Studies, James Cook University, Townsville 4810, Australia. The College of Public Health, Medical and Veterinary Sciences, James Cook University, Townsville 4810, Australia. ; Coral Reef Watch, U.S. National Oceanic and Atmospheric Administration (NOAA), College Park, MD 20740, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27081069" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anthozoa/cytology/*physiology ; Cell Count ; Cell Death ; *Climate Change ; *Coral Reefs ; Dinoflagellida/cytology/physiology ; *Heat-Shock Response ; Hot Temperature ; Photosynthesis ; Pigments, Biological/*physiology ; Symbiosis
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 43
    Publication Date: 2016-03-12
    Description: Scavenger receptor BI (SR-BI) is the major receptor for high-density lipoprotein (HDL) cholesterol (HDL-C). In humans, high amounts of HDL-C in plasma are associated with a lower risk of coronary heart disease (CHD). Mice that have depleted Scarb1 (SR-BI knockout mice) have markedly elevated HDL-C levels but, paradoxically, increased atherosclerosis. The impact of SR-BI on HDL metabolism and CHD risk in humans remains unclear. Through targeted sequencing of coding regions of lipid-modifying genes in 328 individuals with extremely high plasma HDL-C levels, we identified a homozygote for a loss-of-function variant, in which leucine replaces proline 376 (P376L), in SCARB1, the gene encoding SR-BI. The P376L variant impairs posttranslational processing of SR-BI and abrogates selective HDL cholesterol uptake in transfected cells, in hepatocyte-like cells derived from induced pluripotent stem cells from the homozygous subject, and in mice. Large population-based studies revealed that subjects who are heterozygous carriers of the P376L variant have significantly increased levels of plasma HDL-C. P376L carriers have a profound HDL-related phenotype and an increased risk of CHD (odds ratio = 1.79, which is statistically significant).〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zanoni, Paolo -- Khetarpal, Sumeet A -- Larach, Daniel B -- Hancock-Cerutti, William F -- Millar, John S -- Cuchel, Marina -- DerOhannessian, Stephanie -- Kontush, Anatol -- Surendran, Praveen -- Saleheen, Danish -- Trompet, Stella -- Jukema, J Wouter -- De Craen, Anton -- Deloukas, Panos -- Sattar, Naveed -- Ford, Ian -- Packard, Chris -- Majumder, Abdullah al Shafi -- Alam, Dewan S -- Di Angelantonio, Emanuele -- Abecasis, Goncalo -- Chowdhury, Rajiv -- Erdmann, Jeanette -- Nordestgaard, Borge G -- Nielsen, Sune F -- Tybjaerg-Hansen, Anne -- Schmidt, Ruth Frikke -- Kuulasmaa, Kari -- Liu, Dajiang J -- Perola, Markus -- Blankenberg, Stefan -- Salomaa, Veikko -- Mannisto, Satu -- Amouyel, Philippe -- Arveiler, Dominique -- Ferrieres, Jean -- Muller-Nurasyid, Martina -- Ferrario, Marco -- Kee, Frank -- Willer, Cristen J -- Samani, Nilesh -- Schunkert, Heribert -- Butterworth, Adam S -- Howson, Joanna M M -- Peloso, Gina M -- Stitziel, Nathan O -- Danesh, John -- Kathiresan, Sekar -- Rader, Daniel J -- CHD Exome+ Consortium -- CARDIoGRAM Exome Consortium -- Global Lipids Genetics Consortium -- R01 DK089256/DK/NIDDK NIH HHS/ -- R01 HL117078/HL/NHLBI NIH HHS/ -- TL1 RR024133/RR/NCRR NIH HHS/ -- TL1R000138/PHS HHS/ -- TL1RR024133/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2016 Mar 11;351(6278):1166-71. doi: 10.1126/science.aad3517.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departments of Genetics and Medicine, Division of Translational Medicine and Human Genetics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. ; Departments of Genetics and Medicine, Division of Translational Medicine and Human Genetics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. INSERM UMR 1166 ICAN, Universite Pierre et Marie Curie Paris 6, Hopital de la Pitie, Paris, France. ; INSERM UMR 1166 ICAN, Universite Pierre et Marie Curie Paris 6, Hopital de la Pitie, Paris, France. ; Cardiovascular Epidemiology Unit, Department of Public Health and Primary Care, University of Cambridge, Cambridge, UK. ; Cardiovascular Epidemiology Unit, Department of Public Health and Primary Care, University of Cambridge, Cambridge, UK. Department of Biostatistics and Epidemiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. Centre for Non-Communicable Diseases, Karachi, Pakistan. ; Department of Gerontology and Geriatrics, Leiden University Medical Center, Leiden, Netherlands. Department of Cardiology, Leiden University Medical Center, Leiden, Netherlands. ; Department of Cardiology, Leiden University Medical Center, Leiden, Netherlands. The Interuniversity Cardiology Institute of the Netherlands, Utrecht, Netherlands. ; Department of Gerontology and Geriatrics, Leiden University Medical Center, Leiden, Netherlands. ; Wellcome Trust Sanger Institute, Genome Campus, Hinxton, UK. ; Institute of Cardiovascular and Medical Sciences, British Heart Foundation, Glasgow Cardiovascular Research Centre, University of Glasgow, Glasgow, UK. ; Robertson Center for Biostatistics, University of Glasgow, Glasgow, UK. ; Glasgow Clinical Research Facility, Western Infirmary, Glasgow, UK. ; National Institute of Cardiovascular Diseases, Sher-e-Bangla Nagar, Dhaka, Bangladesh. ; International Centre for Diarrhoeal Disease Research, Mohakhali, Dhaka, Bangladesh. ; Center for Statistical Genetics, Department of Biostatistics, University of Michigan School of Public Health, Ann Arbor, MI 48109, USA. ; Institute for Integrative and Experimental Genomics, University of Lubeck, Lubeck 23562, Germany. ; Department of Clinical Biochemistry, Herlev Hospital, Copenhagen University Hospital, Herlev, Denmark. ; Copenhagen University Hospital, University of Copenhagen, Copenhagen, Denmark. ; Department of Clinical Biochemistry, Rigshospitalet, Copenhagen University Hospitals, Copenhagen, Denmark. ; Department of Health, National Institute for Health and Welfare, Helsinki, Finland. ; Department of Public Health Sciences, College of Medicine, Pennsylvania State University, Hershey, PA 17033, USA. ; Department of Health, National Institute for Health and Welfare, Helsinki, Finland. Institute of Molecular Medicine FIMM, University of Helsinki, Helsinki, Finland. ; Department of General and Interventional Cardiology, University Heart Center Hamburg, Hamburg, Germany. University Medical Center Hamburg-Eppendorf, Hamburg, Germany. ; Department of Epidemiology and Public Health, Institut Pasteur de Lille, Lille, France. ; Department of Epidemiology and Public Health, University of Strasbourg, Strasbourg, France. ; Department of Epidemiology, Toulouse University-CHU Toulouse, Toulouse, France. ; Institute of Genetic Epidemiology, Helmholtz Zentrum Munchen-German Research Center for Environmental Health, Neuherberg, Germany. Department of Medicine I, Ludwig-Maximilians-University Munich, Munich, Germany. ; Research Centre in Epidemiology and Preventive Medicine, Department of Clinical and Experimental Medicine, University of Insubria, Varese, Italy. ; UKCRC Centre of Excellence for Public Health, Queens University, Belfast, Northern Ireland. ; Department of Computational Medicine and Bioinformatics, Department of Human Genetics, and Department of Internal Medicine, University of Michigan, Ann Arbor, MI 48109, USA. ; Department of Cardiovascular Sciences, University of Leicester, Leicester, UK. National Institute for Health Research (NIHR) Leicester Cardiovascular Biomedical Research Unit, Glenfield Hotel, Leicester, UK. ; Deutsches Herzzentrum Munchen, Technische Universitat Munchen, Munich, Germany. ; Broad Institute and Center for Human Genetic Research, Massachusetts General Hospital, Boston, MA 02114, USA. ; Department of Medicine, Division of Cardiology, Department of Genetics, and the McDonnell Genome Institute, Washington University School of Medicine, St. Louis, MO 63110, USA. ; Cardiovascular Epidemiology Unit, Department of Public Health and Primary Care, University of Cambridge, Cambridge, UK. Wellcome Trust Sanger Institute, Genome Campus, Hinxton, UK. ; Departments of Genetics and Medicine, Division of Translational Medicine and Human Genetics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. rader@mail.med.upenn.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26965621" target="_blank"〉PubMed〈/a〉
    Keywords: Aged ; Amino Acid Substitution ; Animals ; Cholesterol, HDL/*blood ; Coronary Disease/*blood/*genetics ; DNA Mutational Analysis ; Female ; Genetic Variation ; Heterozygote ; Homozygote ; Humans ; Leucine/genetics ; Male ; Mice ; Middle Aged ; Proline/genetics ; Protein Processing, Post-Translational ; Risk ; Scavenger Receptors, Class B/*genetics/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 44
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-01-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennisi, Elizabeth -- New York, N.Y. -- Science. 2016 Jan 29;351(6272):433. doi: 10.1126/science.351.6272.433.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26823406" target="_blank"〉PubMed〈/a〉