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  • Animals  (796)
  • Cell & Developmental Biology
  • Chemistry
  • General Physics: Statistical and Quantum Mechanics, Quantum Information, etc.
  • Man/System Technology and Life Support
  • Nature Publishing Group (NPG)  (798)
  • 2010-2014  (798)
  • 2013  (798)
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  • 2010-2014  (798)
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  • 1
    Publication Date: 2013-12-10
    Description: Evolution drives, and is driven by, demography. A genotype moulds its phenotype's age patterns of mortality and fertility in an environment; these two patterns in turn determine the genotype's fitness in that environment. Hence, to understand the evolution of ageing, age patterns of mortality and reproduction need to be compared for species across the tree of life. However, few studies have done so and only for a limited range of taxa. Here we contrast standardized patterns over age for 11 mammals, 12 other vertebrates, 10 invertebrates, 12 vascular plants and a green alga. Although it has been predicted that evolution should inevitably lead to increasing mortality and declining fertility with age after maturity, there is great variation among these species, including increasing, constant, decreasing, humped and bowed trajectories for both long- and short-lived species. This diversity challenges theoreticians to develop broader perspectives on the evolution of ageing and empiricists to study the demography of more species.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4157354/" 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/PMC4157354/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jones, Owen R -- Scheuerlein, Alexander -- Salguero-Gomez, Roberto -- Camarda, Carlo Giovanni -- Schaible, Ralf -- Casper, Brenda B -- Dahlgren, Johan P -- Ehrlen, Johan -- Garcia, Maria B -- Menges, Eric S -- Quintana-Ascencio, Pedro F -- Caswell, Hal -- Baudisch, Annette -- Vaupel, James W -- P01 AG-031719/AG/NIA NIH HHS/ -- P01 AG031719/AG/NIA NIH HHS/ -- England -- Nature. 2014 Jan 9;505(7482):169-73. doi: 10.1038/nature12789. Epub 2013 Dec 8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Max-Planck Odense Center on the Biodemography of Aging, Campusvej 55, 5230 Odense M, Denmark [2] Department of Biology, University of Southern Denmark, Campusvej 55, 5230 Odense M, Denmark [3]. ; 1] Max Planck Institute for Demographic Research, Konrad-Zuse-Strasse 1, 18057 Rostock, Germany [2]. ; 1] Max Planck Institute for Demographic Research, Konrad-Zuse-Strasse 1, 18057 Rostock, Germany [2] School of Biological Sciences, Centre for Biodiversity and Conservation Science, University of Queensland, Brisbane QLD 4072, Australia. ; Institut National d'Etudes Demographiques, 133 Boulevard Davout, 75980 Paris Cedex 20, France. ; Max Planck Institute for Demographic Research, Konrad-Zuse-Strasse 1, 18057 Rostock, Germany. ; Department of Biology, University of Pennsylvania, 433 South University Avenue, Philadelphia, Pennsylvania 19104-6018, USA. ; 1] Max-Planck Odense Center on the Biodemography of Aging, Campusvej 55, 5230 Odense M, Denmark [2] Department of Biology, University of Southern Denmark, Campusvej 55, 5230 Odense M, Denmark. ; Department of Ecology, Environment and Plant Sciences, Stockholm University, Lilla Frescativagen 5, 10691 Stockholm, Sweden. ; Pyrenean Institute of Ecology (CSIC), Avenida Montanana 1005, 50059 Zaragoza, Spain. ; Archbold Biological Station, 123 Main Drive, Venus, Florida 33960, USA. ; Department of Biology, University of Central Florida, 4110 Libra Drive, Orlando, Florida 32816-2368, USA. ; 1] Department of Biology, University of Southern Denmark, Campusvej 55, 5230 Odense M, Denmark [2] Max Planck Institute for Demographic Research, Konrad-Zuse-Strasse 1, 18057 Rostock, Germany [3] Woods Hole Oceanographic Institution, Biology Department MS-34, Woods Hole, Massachusetts 02543 USA [4] Institute for Biodiversity and Ecosystem Dynamics, University of Amsterdam, PO Box 94248, 1090GE Amsterdam, The Netherlands. ; 1] Max-Planck Odense Center on the Biodemography of Aging, Campusvej 55, 5230 Odense M, Denmark [2] Max Planck Institute for Demographic Research, Konrad-Zuse-Strasse 1, 18057 Rostock, Germany [3] Duke Population Research Institute, Duke University, Durham, North Carolina 27705, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24317695" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/*physiology ; Animals ; Biological Evolution ; Chlorophyta ; Fertility/*physiology ; Longevity/*physiology ; *Phylogeny ; Plants ; Reproduction/physiology
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    Electronic ISSN: 1476-4687
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  • 2
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    Nature Publishing Group (NPG)
    Publication Date: 2013-01-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gatenby, Robert -- England -- Nature. 2012 Nov 22;491(7425):S55.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departments of Radiology andIntegrated Mathematical Oncology at the H. Lee Moffitt CancerCenter in Tampa, Florida, USA.robert.gatenby@moffitt.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23320287" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Evolution ; Biomedical Research/*methods ; Caves ; Fishes/genetics/physiology ; Humans ; *Models, Biological ; Molecular Biology ; Molecular Targeted Therapy ; *Neoplasms/genetics/metabolism/pathology ; Physics/*methods
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  • 3
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    Nature Publishing Group (NPG)
    Publication Date: 2013-01-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bourzac, Katherine -- England -- Nature. 2012 Nov 22;491(7425):S58-60.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23320289" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antineoplastic Agents/*administration & dosage/adverse effects/*pharmacokinetics ; Cisplatin/adverse effects/pharmacokinetics ; Clinical Trials as Topic ; Doxorubicin/administration & dosage/pharmacokinetics ; Drug Carriers/administration & dosage/*chemistry/*pharmacokinetics ; Drug Resistance, Neoplasm ; Humans ; Leukemia/drug therapy/metabolism ; Logic ; Nanomedicine/*methods ; Nanoparticles/administration & dosage/*chemistry ; Neoplasm Metastasis ; Neoplasms/*drug therapy/genetics ; Pancreatic Neoplasms/drug therapy ; RNA Interference ; RNA, Small Interfering/administration & dosage/genetics/pharmacokinetics ; Robotics ; Substrate Specificity
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  • 4
    Publication Date: 2013-02-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brown, Peter -- England -- Nature. 2013 Feb 21;494(7437):316-7. doi: 10.1038/494316a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23426319" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anthropology ; Australia ; Chromosomes, Human, Y/genetics ; Continental Population Groups/genetics ; DNA, Mitochondrial/genetics ; *Dogs/genetics ; Female ; Gene Flow/genetics ; History, Ancient ; Human Migration/*history ; Humans ; India ; Paleontology ; Papua New Guinea ; Phylogeny
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
    Publication Date: 2013-03-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kosik, Kenneth S -- England -- Nature. 2013 Mar 21;495(7441):322-4. doi: 10.1038/nature11956. Epub 2013 Feb 27.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23446351" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Female ; *Gene Expression Regulation ; Humans ; Male ; MicroRNAs/*metabolism ; RNA/*metabolism
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  • 6
    Publication Date: 2013-10-25
    Description: Mutations in SHANK3 and large duplications of the region spanning SHANK3 both cause a spectrum of neuropsychiatric disorders, indicating that proper SHANK3 dosage is critical for normal brain function. However, SHANK3 overexpression per se has not been established as a cause of human disorders because 22q13 duplications involve several genes. Here we report that Shank3 transgenic mice modelling a human SHANK3 duplication exhibit manic-like behaviour and seizures consistent with synaptic excitatory/inhibitory imbalance. We also identified two patients with hyperkinetic disorders carrying the smallest SHANK3-spanning duplications reported so far. These findings indicate that SHANK3 overexpression causes a hyperkinetic neuropsychiatric disorder. To probe the mechanism underlying the phenotype, we generated a Shank3 in vivo interactome and found that Shank3 directly interacts with the Arp2/3 complex to increase F-actin levels in Shank3 transgenic mice. The mood-stabilizing drug valproate, but not lithium, rescues the manic-like behaviour of Shank3 transgenic mice raising the possibility that this hyperkinetic disorder has a unique pharmacogenetic profile.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3923348/" 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/PMC3923348/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Han, Kihoon -- Holder, J Lloyd Jr -- Schaaf, Christian P -- Lu, Hui -- Chen, Hongmei -- Kang, Hyojin -- Tang, Jianrong -- Wu, Zhenyu -- Hao, Shuang -- Cheung, Sau Wai -- Yu, Peng -- Sun, Hao -- Breman, Amy M -- Patel, Ankita -- Lu, Hui-Chen -- Zoghbi, Huda Y -- 1R01NS070302/NS/NINDS NIH HHS/ -- 2T32NS043124/NS/NINDS NIH HHS/ -- P30HD024064/HD/NICHD NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2013 Nov 7;503(7474):72-7. doi: 10.1038/nature12630. Epub 2013 Oct 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas 77030, USA [2] Howard Hughes Medical Institute, Baylor College of Medicine, Houston, Texas 77030, USA [3] Jan and Dan Duncan Neurological Research Institute at Texas Children's Hospital, Houston, Texas 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24153177" target="_blank"〉PubMed〈/a〉
    Keywords: Actin-Related Protein 2-3 Complex/metabolism ; Actins/metabolism ; Adult ; Animals ; Behavior, Animal ; Bipolar Disorder/*drug therapy/genetics/*physiopathology ; Chromosomes, Human, Pair 22/genetics ; Disease Models, Animal ; Excitatory Postsynaptic Potentials ; Female ; Gene Dosage/genetics ; Gene Expression/genetics ; Genes, Duplicate/genetics ; Humans ; Hyperkinesis/genetics/physiopathology ; Inhibitory Postsynaptic Potentials ; Lithium/pharmacology ; Male ; Mice ; Mice, Transgenic ; Nerve Tissue Proteins/*genetics/*metabolism ; Seizures/genetics ; Valproic Acid/pharmacology/therapeutic use
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  • 7
    Publication Date: 2013-03-12
    Description: CLP1 was the first mammalian RNA kinase to be identified. However, determining its in vivo function has been elusive. Here we generated kinase-dead Clp1 (Clp1(K/K)) mice that show a progressive loss of spinal motor neurons associated with axonal degeneration in the peripheral nerves and denervation of neuromuscular junctions, resulting in impaired motor function, muscle weakness, paralysis and fatal respiratory failure. Transgenic rescue experiments show that CLP1 functions in motor neurons. Mechanistically, loss of CLP1 activity results in accumulation of a novel set of small RNA fragments, derived from aberrant processing of tyrosine pre-transfer RNA. These tRNA fragments sensitize cells to oxidative-stress-induced p53 (also known as TRP53) activation and p53-dependent cell death. Genetic inactivation of p53 rescues Clp1(K/K) mice from the motor neuron loss, muscle denervation and respiratory failure. Our experiments uncover a mechanistic link between tRNA processing, formation of a new RNA species and progressive loss of lower motor neurons regulated by p53.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3674495/" 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/PMC3674495/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hanada, Toshikatsu -- Weitzer, Stefan -- Mair, Barbara -- Bernreuther, Christian -- Wainger, Brian J -- Ichida, Justin -- Hanada, Reiko -- Orthofer, Michael -- Cronin, Shane J -- Komnenovic, Vukoslav -- Minis, Adi -- Sato, Fuminori -- Mimata, Hiromitsu -- Yoshimura, Akihiko -- Tamir, Ido -- Rainer, Johannes -- Kofler, Reinhard -- Yaron, Avraham -- Eggan, Kevin C -- Woolf, Clifford J -- Glatzel, Markus -- Herbst, Ruth -- Martinez, Javier -- Penninger, Josef M -- K99NS077435-01A1/NS/NINDS NIH HHS/ -- NS038253/NS/NINDS NIH HHS/ -- P 19223/Austrian Science Fund FWF/Austria -- P 21667/Austrian Science Fund FWF/Austria -- R00 NS077435/NS/NINDS NIH HHS/ -- R01 NS038253/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2013 Mar 28;495(7442):474-80. doi: 10.1038/nature11923. Epub 2013 Mar 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉IMBA, Institute of Molecular Biotechnology of the Austrian Academy of Sciences, Vienna 1030, Austria.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23474986" target="_blank"〉PubMed〈/a〉
    Keywords: Amyotrophic Lateral Sclerosis ; Animals ; Animals, Newborn ; Axons/metabolism/pathology ; Cell Death ; Diaphragm/innervation ; Embryo Loss ; Embryo, Mammalian/metabolism/pathology ; Exons/genetics ; Female ; Fibroblasts ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Transgenic ; Motor Neurons/*metabolism/*pathology ; Muscular Atrophy, Spinal ; Neuromuscular Diseases/metabolism/pathology ; Oxidative Stress ; RNA Processing, Post-Transcriptional ; RNA, Transfer, Tyr/genetics/*metabolism ; Respiration ; Spinal Nerves/cytology ; Transcription Factors/deficiency/*metabolism ; Tumor Suppressor Protein p53/metabolism ; Tyrosine/genetics/metabolism
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  • 8
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    Nature Publishing Group (NPG)
    Publication Date: 2013-07-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mole, Beth -- England -- Nature. 2013 Jul 25;499(7459):398-400. doi: 10.1038/499398a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23887415" target="_blank"〉PubMed〈/a〉
    Keywords: Agriculture ; Animals ; Animals, Domestic/*microbiology/virology ; Anti-Bacterial Agents/pharmacology/supply & distribution ; European Union ; Fomites/microbiology/statistics & numerical data ; Humans ; Iowa/epidemiology ; Meat/*microbiology ; Methicillin Resistance ; Methicillin-Resistant Staphylococcus aureus/classification/genetics/*isolation & ; purification/pathogenicity ; Staphylococcal Infections/epidemiology/microbiology/*transmission/*veterinary ; Swine/microbiology/virology ; Swine Diseases/microbiology/transmission/virology ; Zoonoses/epidemiology/*microbiology/*transmission/virology
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  • 9
    Publication Date: 2013-08-24
    Description: The RAG1/RAG2 endonuclease (RAG) initiates the V(D)J recombination reaction that assembles immunoglobulin heavy (IgH) and light (IgL) chain variable region exons from germline gene segments to generate primary antibody repertoires. IgH V(D)J assembly occurs in progenitor (pro-) B cells followed by that of IgL in precursor (pre-) B cells. Expression of IgH mu and IgL (Igkappa or Iglambda) chains generates IgM, which is expressed on immature B cells as the B-cell antigen-binding receptor (BCR). Rag expression can continue in immature B cells, allowing continued Igkappa V(D)J recombination that replaces the initial VkappaJkappa exon with one that generates a new specificity. This 'receptor editing' process, which can also lead to Iglambda V(D)J recombination and expression, provides a mechanism whereby antigen encounter at the Rag-expressing immature B-cell stage helps shape pre-immune BCR repertoires. As the major site of postnatal B-cell development, the bone marrow is the principal location of primary immunoglobulin repertoire diversification in mice. Here we report that early B-cell development also occurs within the mouse intestinal lamina propria (LP), where the associated V(D)J recombination/receptor editing processes modulate primary LP immunoglobulin repertoires. At weanling age in normally housed mice, the LP contains a population of Rag-expressing B-lineage cells that harbour intermediates indicative of ongoing V(D)J recombination and which contain cells with pro-B, pre-B and editing phenotypes. Consistent with LP-specific receptor editing, Rag-expressing LP B-lineage cells have similar VH repertoires, but significantly different Vkappa repertoires, compared to those of Rag2-expressing bone marrow counterparts. Moreover, colonization of germ-free mice leads to an increased ratio of Iglambda-expressing versus Igkappa-expressing B cells specifically in the LP. We conclude that B-cell development occurs in the intestinal mucosa, where it is regulated by extracellular signals from commensal microbes that influence gut immunoglobulin repertoires.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3807868/" 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/PMC3807868/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wesemann, Duane R -- Portuguese, Andrew J -- Meyers, Robin M -- Gallagher, Michael P -- Cluff-Jones, Kendra -- Magee, Jennifer M -- Panchakshari, Rohit A -- Rodig, Scott J -- Kepler, Thomas B -- Alt, Frederick W -- AI020047/AI/NIAID NIH HHS/ -- AI89972/AI/NIAID NIH HHS/ -- HHSN272201000053C/PHS HHS/ -- K08 AI089972/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2013 Sep 5;501(7465):112-5. doi: 10.1038/nature12496. Epub 2013 Aug 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program in Cellular and Molecular Medicine and Department of Medicine, Children's Hospital Boston, Boston, Massachusetts 02115, USA. dwesemann@research.bwh.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23965619" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/*cytology/*immunology/metabolism ; Bone Marrow Cells/cytology/immunology ; *Cell Lineage ; DNA-Binding Proteins/genetics/metabolism ; Gene Rearrangement, B-Lymphocyte/genetics ; Germ-Free Life ; Immunoglobulins/genetics/immunology ; Intestinal Mucosa/*cytology/*immunology ; Mice ; Precursor Cells, B-Lymphoid/cytology/metabolism ; Symbiosis ; Weaning
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  • 10
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    Nature Publishing Group (NPG)
    Publication Date: 2013-10-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉DeWeerdt, Sarah -- England -- Nature. 2013 Oct 10;502(7470):S8-9. doi: 10.1038/502S8a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24108081" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; BCG Vaccine/immunology ; Clinical Trials as Topic ; Humans ; Immunity, Cellular ; Immunity, Humoral ; Tuberculosis Vaccines/administration & dosage/*immunology/*standards ; Tuberculosis, Pulmonary/immunology/*prevention & control
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