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  • Mice, Inbred C57BL  (19)
  • *Fossils  (12)
  • ASTROPHYSICS
  • Life and Medical Sciences
  • Lunar and Planetary Science and Exploration
  • American Association for the Advancement of Science (AAAS)  (31)
  • 2010-2014  (31)
  • 1950-1954
  • 1930-1934
  • 2013  (31)
  • 1933
  • 1932
  • 1930
Collection
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  • 2010-2014  (31)
  • 1950-1954
  • 1930-1934
Year
  • 1
    Publication Date: 2013-09-28
    Description: A dense mucus layer in the large intestine prevents inflammation by shielding the underlying epithelium from luminal bacteria and food antigens. This mucus barrier is organized around the hyperglycosylated mucin MUC2. Here we show that the small intestine has a porous mucus layer, which permitted the uptake of MUC2 by antigen-sampling dendritic cells (DCs). Glycans associated with MUC2 imprinted DCs with anti-inflammatory properties by assembling a galectin-3-Dectin-1-FcgammaRIIB receptor complex that activated beta-catenin. This transcription factor interfered with DC expression of inflammatory but not tolerogenic cytokines by inhibiting gene transcription through nuclear factor kappaB. MUC2 induced additional conditioning signals in intestinal epithelial cells. Thus, mucus does not merely form a nonspecific physical barrier, but also constrains the immunogenicity of gut antigens by delivering tolerogenic signals.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4005805/" 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/PMC4005805/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shan, Meimei -- Gentile, Maurizio -- Yeiser, John R -- Walland, A Cooper -- Bornstein, Victor U -- Chen, Kang -- He, Bing -- Cassis, Linda -- Bigas, Anna -- Cols, Montserrat -- Comerma, Laura -- Huang, Bihui -- Blander, J Magarian -- Xiong, Huabao -- Mayer, Lloyd -- Berin, Cecilia -- Augenlicht, Leonard H -- Velcich, Anna -- Cerutti, Andrea -- AI073899/AI/NIAID NIH HHS/ -- AI095245/AI/NIAID NIH HHS/ -- AI57653/AI/NIAID NIH HHS/ -- AI61093/AI/NIAID NIH HHS/ -- AI74378/AI/NIAID NIH HHS/ -- AI95613/AI/NIAID NIH HHS/ -- AI96187/AI/NIAID NIH HHS/ -- DK072201/DK/NIDDK NIH HHS/ -- P01 AI061093/AI/NIAID NIH HHS/ -- P01 DK072201/DK/NIDDK NIH HHS/ -- P60 DK020541/DK/NIDDK NIH HHS/ -- R01 AI057653/AI/NIAID NIH HHS/ -- R01 AI093577/AI/NIAID NIH HHS/ -- U01 AI095613/AI/NIAID NIH HHS/ -- U19 AI096187/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2013 Oct 25;342(6157):447-53. doi: 10.1126/science.1237910. Epub 2013 Sep 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Immunology Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24072822" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Dendritic Cells/immunology ; Galectin 3/genetics/metabolism ; Glycosylation ; *Homeostasis ; Humans ; Immune Tolerance/genetics/*immunology ; Inflammation/immunology ; Intestinal Mucosa/immunology ; Intestine, Small/*immunology ; Lectins, C-Type/genetics/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Mutant Strains ; Mouth/*immunology ; Mucin-2/genetics/physiology ; Mucus/*immunology ; NF-kappa B/metabolism ; Receptors, IgG/genetics/metabolism ; Transcription, Genetic ; beta Catenin/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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  • 2
    Publication Date: 2013-08-10
    Description: Tree-building with diverse data maximizes explanatory power. Application of molecular clock models to ancient speciation events risks a bias against detection of fast radiations subsequent to the Cretaceous-Paleogene (K-Pg) event. Contrary to Springer et al., post-K-Pg placental diversification does not require "virus-like" substitution rates. Even constraining clade ages to their model, the explosive model best explains placental evolution.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉O'Leary, Maureen A -- Bloch, Jonathan I -- Flynn, John J -- Gaudin, Timothy J -- Giallombardo, Andres -- Giannini, Norberto P -- Goldberg, Suzann L -- Kraatz, Brian P -- Luo, Zhe-Xi -- Meng, Jin -- Ni, Xijun -- Novacek, Michael J -- Perini, Fernando A -- Randall, Zachary -- Rougier, Guillermo W -- Sargis, Eric J -- Silcox, Mary T -- Simmons, Nancy B -- Spaulding, Michelle -- Velazco, Paul M -- Weksler, Marcelo -- Wible, John R -- Cirranello, Andrea L -- New York, N.Y. -- Science. 2013 Aug 9;341(6146):613. doi: 10.1126/science.1238162.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomical Sciences, HSC T-8 (040), Stony Brook University, Stony Brook, NY 11794-8081, USA. maureen.oleary@stonybrook.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23929968" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Female ; *Fossils ; *Mammals ; *Phylogeny ; Pregnancy
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
    Publication Date: 2013-02-01
    Description: Kwashiorkor, an enigmatic form of severe acute malnutrition, is the consequence of inadequate nutrient intake plus additional environmental insults. To investigate the role of the gut microbiome, we studied 317 Malawian twin pairs during the first 3 years of life. During this time, half of the twin pairs remained well nourished, whereas 43% became discordant, and 7% manifested concordance for acute malnutrition. Both children in twin pairs discordant for kwashiorkor were treated with a peanut-based, ready-to-use therapeutic food (RUTF). Time-series metagenomic studies revealed that RUTF produced a transient maturation of metabolic functions in kwashiorkor gut microbiomes that regressed when administration of RUTF was stopped. Previously frozen fecal communities from several discordant pairs were each transplanted into gnotobiotic mice. The combination of Malawian diet and kwashiorkor microbiome produced marked weight loss in recipient mice, accompanied by perturbations in amino acid, carbohydrate, and intermediary metabolism that were only transiently ameliorated with RUTF. These findings implicate the gut microbiome as a causal factor in kwashiorkor.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3667500/" 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/PMC3667500/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Smith, Michelle I -- Yatsunenko, Tanya -- Manary, Mark J -- Trehan, Indi -- Mkakosya, Rajhab -- Cheng, Jiye -- Kau, Andrew L -- Rich, Stephen S -- Concannon, Patrick -- Mychaleckyj, Josyf C -- Liu, Jie -- Houpt, Eric -- Li, Jia V -- Holmes, Elaine -- Nicholson, Jeremy -- Knights, Dan -- Ursell, Luke K -- Knight, Rob -- Gordon, Jeffrey I -- DK078669/DK/NIDDK NIH HHS/ -- DK30292/DK/NIDDK NIH HHS/ -- F32 DK091044/DK/NIDDK NIH HHS/ -- P01 DK078669/DK/NIDDK NIH HHS/ -- P30 DK056341/DK/NIDDK NIH HHS/ -- R37 DK030292/DK/NIDDK NIH HHS/ -- T32 HD049338/HD/NICHD NIH HHS/ -- T32-HD049338/HD/NICHD NIH HHS/ -- T35 DK074375/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2013 Feb 1;339(6119):548-54. doi: 10.1126/science.1229000. Epub 2013 Jan 30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Genome Sciences and Systems Biology, Washington University in St. Louis, St. Louis, MO 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23363771" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acids/metabolism ; Animals ; Arachis ; Carbohydrate Metabolism ; Child, Preschool ; Diseases in Twins/*microbiology ; Feces/microbiology ; Female ; Gastrointestinal Tract/*microbiology ; Germ-Free Life ; Humans ; Infant ; Kwashiorkor/diet therapy/epidemiology/*microbiology ; Longitudinal Studies ; Malawi/epidemiology ; Male ; *Metagenome ; Mice ; Mice, Inbred C57BL
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  • 4
    Publication Date: 2013-08-21
    Description: Proteinases and the innate immune receptor Toll-like receptor 4 (TLR4) are essential for expression of allergic inflammation and diseases such as asthma. A mechanism that links these inflammatory mediators is essential for explaining the fundamental basis of allergic disease but has been elusive. Here, we demonstrate that TLR4 is activated by airway proteinase activity to initiate both allergic airway disease and antifungal immunity. These outcomes were induced by proteinase cleavage of the clotting protein fibrinogen, yielding fibrinogen cleavage products that acted as TLR4 ligands on airway epithelial cells and macrophages. Thus, allergic airway inflammation represents an antifungal defensive strategy that is driven by fibrinogen cleavage and TLR4 activation. These findings clarify the molecular basis of allergic disease and suggest new therapeutic strategies.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3898200/" 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/PMC3898200/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Millien, Valentine Ongeri -- Lu, Wen -- Shaw, Joanne -- Yuan, Xiaoyi -- Mak, Garbo -- Roberts, Luz -- Song, Li-Zhen -- Knight, J Morgan -- Creighton, Chad J -- Luong, Amber -- Kheradmand, Farrah -- Corry, David B -- AI057696/AI/NIAID NIH HHS/ -- AI070973/AI/NIAID NIH HHS/ -- CA125123/CA/NCI NIH HHS/ -- HL75243/HL/NHLBI NIH HHS/ -- K02 HL075243/HL/NHLBI NIH HHS/ -- R01 AI057696/AI/NIAID NIH HHS/ -- R01 HL095382/HL/NHLBI NIH HHS/ -- R01 HL117181/HL/NHLBI NIH HHS/ -- R25GM56929/GM/NIGMS NIH HHS/ -- T32 GM088129/GM/NIGMS NIH HHS/ -- T32GM088129/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2013 Aug 16;341(6147):792-6. doi: 10.1126/science.1240342.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Translational Biology and Molecular Medicine Program, Baylor College of Medicine, Houston, TX, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23950537" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aspergillus niger/growth & development/*immunology ; Aspergillus oryzae/enzymology ; Bronchoalveolar Lavage Fluid/cytology ; Epithelial Cells/immunology/metabolism ; Fibrinogen/*metabolism ; Immunity, Innate ; Ligands ; Macrophage Activation ; Macrophages/immunology/metabolism/microbiology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Peptide Hydrolases/immunology/*metabolism ; Respiratory Hypersensitivity/*immunology/*metabolism ; Respiratory Mucosa/cytology/immunology/metabolism ; Th2 Cells/immunology ; Toll-Like Receptor 4/genetics/*metabolism
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  • 5
    Publication Date: 2013-04-13
    Description: Since the announcement of the species Australopithecus sediba, questions have been raised over whether the Malapa fossils represent a valid taxon or whether inadequate allowance was made for intraspecific variation, in particular with reference to the temporally and geographically proximate species Au. africanus. The morphology of mandibular remains of Au. sediba, including newly recovered material discussed here, shows that it is not merely a late-surviving morph of Au. africanus. Rather-as is seen elsewhere in the cranium, dentition, and postcranial skeleton-these mandibular remains share similarities with other australopiths but can be differentiated from the hypodigm of Au. africanus in both size and shape as well as in their ontogenetic growth trajectory.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉de Ruiter, Darryl J -- DeWitt, Thomas J -- Carlson, Keely B -- Brophy, Juliet K -- Schroeder, Lauren -- Ackermann, Rebecca R -- Churchill, Steven E -- Berger, Lee R -- New York, N.Y. -- Science. 2013 Apr 12;340(6129):1232997. doi: 10.1126/science.1232997.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anthropology, Texas A&M University, College Station, TX 77843, USA. deruiter@tamu.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23580533" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Dentition ; Female ; *Fossils ; Hominidae/*anatomy & histology/*classification/growth & development ; Male ; Mandible/*anatomy & histology/growth & development ; Paleodontology ; South Africa ; Tooth/anatomy & histology
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  • 6
    Publication Date: 2013-04-13
    Description: The evolution of the human upper limb involved a change in function from its use for both locomotion and prehension (as in apes) to a predominantly prehensile and manipulative role. Well-preserved forelimb remains of 1.98-million-year-old Australopithecus sediba from Malapa, South Africa, contribute to our understanding of this evolutionary transition. Whereas other aspects of their postcranial anatomy evince mosaic combinations of primitive (australopith-like) and derived (Homo-like) features, the upper limbs (excluding the hand and wrist) of the Malapa hominins are predominantly primitive and suggest the retention of substantial climbing and suspensory ability. The use of the forelimb primarily for prehension and manipulation appears to arise later, likely with the emergence of Homo erectus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Churchill, Steven E -- Holliday, Trenton W -- Carlson, Kristian J -- Jashashvili, Tea -- Macias, Marisa E -- Mathews, Sandra -- Sparling, Tawnee L -- Schmid, Peter -- de Ruiter, Darryl J -- Berger, Lee R -- New York, N.Y. -- Science. 2013 Apr 12;340(6129):1233477. doi: 10.1126/science.1233477.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Evolutionary Anthropology, Duke University, Durham, NC 27708, USA. churchy@duke.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23580536" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arm Bones/anatomy & histology ; Biological Evolution ; Biomechanical Phenomena ; Bones of Upper Extremity/*anatomy & histology/physiology ; Clavicle/anatomy & histology ; Female ; *Fossils ; Hominidae/*anatomy & histology/*physiology ; Humans ; Locomotion ; Male ; Principal Component Analysis ; Scapula/anatomy & histology ; South Africa ; Upper Extremity/*anatomy & histology/*physiology
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  • 7
    Publication Date: 2013-11-02
    Description: Synapse formation in the developing brain depends on the coordinated activity of synaptogenic proteins, some of which have been implicated in a number of neurodevelopmental disorders. Here, we show that the sushi repeat-containing protein X-linked 2 (SRPX2) gene encodes a protein that promotes synaptogenesis in the cerebral cortex. In humans, SRPX2 is an epilepsy- and language-associated gene that is a target of the foxhead box protein P2 (FoxP2) transcription factor. We also show that FoxP2 modulates synapse formation through regulating SRPX2 levels and that SRPX2 reduction impairs development of ultrasonic vocalization in mice. Our results suggest FoxP2 modulates the development of neural circuits through regulating synaptogenesis and that SRPX2 is a synaptogenic factor that plays a role in the pathogenesis of language disorders.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3903157/" 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/PMC3903157/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sia, G M -- Clem, R L -- Huganir, R L -- NS050274/NS/NINDS NIH HHS/ -- P30 NS050274/NS/NINDS NIH HHS/ -- P50 MH084020/MH/NIMH NIH HHS/ -- P50MH084020/MH/NIMH NIH HHS/ -- R01 MH095058/MH/NIMH NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2013 Nov 22;342(6161):987-91. doi: 10.1126/science.1245079. Epub 2013 Oct 31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Johns Hopkins University School of Medicine, 725 North Wolfe Street, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24179158" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cerebral Cortex/cytology ; Epilepsy/genetics ; Forkhead Transcription Factors/genetics/*metabolism ; Humans ; *Language ; Language Disorders/*genetics ; Mice ; Mice, Inbred C57BL ; Nerve Tissue Proteins/genetics/*physiology ; Neurons/physiology ; Synapses/*physiology ; Transfection ; *Vocalization, Animal
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  • 8
    Publication Date: 2013-02-09
    Description: To discover interordinal relationships of living and fossil placental mammals and the time of origin of placentals relative to the Cretaceous-Paleogene (K-Pg) boundary, we scored 4541 phenomic characters de novo for 86 fossil and living species. Combining these data with molecular sequences, we obtained a phylogenetic tree that, when calibrated with fossils, shows that crown clade Placentalia and placental orders originated after the K-Pg boundary. Many nodes discovered using molecular data are upheld, but phenomic signals overturn molecular signals to show Sundatheria (Dermoptera + Scandentia) as the sister taxon of Primates, a close link between Proboscidea (elephants) and Sirenia (sea cows), and the monophyly of echolocating Chiroptera (bats). Our tree suggests that Placentalia first split into Xenarthra and Epitheria; extinct New World species are the oldest members of Afrotheria.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉O'Leary, Maureen A -- Bloch, Jonathan I -- Flynn, John J -- Gaudin, Timothy J -- Giallombardo, Andres -- Giannini, Norberto P -- Goldberg, Suzann L -- Kraatz, Brian P -- Luo, Zhe-Xi -- Meng, Jin -- Ni, Xijun -- Novacek, Michael J -- Perini, Fernando A -- Randall, Zachary S -- Rougier, Guillermo W -- Sargis, Eric J -- Silcox, Mary T -- Simmons, Nancy B -- Spaulding, Michelle -- Velazco, Paul M -- Weksler, Marcelo -- Wible, John R -- Cirranello, Andrea L -- New York, N.Y. -- Science. 2013 Feb 8;339(6120):662-7. doi: 10.1126/science.1229237.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomical Sciences, School of Medicine, HSC T-8 (040), Stony Brook University, Stony Brook, NY 11794-8081, USA. maureen.oleary@stonybrook.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23393258" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; *Biological Evolution ; Dentition ; Ecosystem ; Extinction, Biological ; Female ; *Fossils ; *Mammals/anatomy & histology/classification/genetics ; Paleodontology ; *Phylogeny ; Phylogeography ; Placenta ; Pregnancy ; Sequence Alignment ; Time ; Xenarthra/anatomy & histology/classification/genetics
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  • 9
    Publication Date: 2013-09-07
    Description: The role of specific gut microbes in shaping body composition remains unclear. We transplanted fecal microbiota from adult female twin pairs discordant for obesity into germ-free mice fed low-fat mouse chow, as well as diets representing different levels of saturated fat and fruit and vegetable consumption typical of the U.S. diet. Increased total body and fat mass, as well as obesity-associated metabolic phenotypes, were transmissible with uncultured fecal communities and with their corresponding fecal bacterial culture collections. Cohousing mice harboring an obese twin's microbiota (Ob) with mice containing the lean co-twin's microbiota (Ln) prevented the development of increased body mass and obesity-associated metabolic phenotypes in Ob cage mates. Rescue correlated with invasion of specific members of Bacteroidetes from the Ln microbiota into Ob microbiota and was diet-dependent. These findings reveal transmissible, rapid, and modifiable effects of diet-by-microbiota interactions.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3829625/" 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/PMC3829625/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ridaura, Vanessa K -- Faith, Jeremiah J -- Rey, Federico E -- Cheng, Jiye -- Duncan, Alexis E -- Kau, Andrew L -- Griffin, Nicholas W -- Lombard, Vincent -- Henrissat, Bernard -- Bain, James R -- Muehlbauer, Michael J -- Ilkayeva, Olga -- Semenkovich, Clay F -- Funai, Katsuhiko -- Hayashi, David K -- Lyle, Barbara J -- Martini, Margaret C -- Ursell, Luke K -- Clemente, Jose C -- Van Treuren, William -- Walters, William A -- Knight, Rob -- Newgard, Christopher B -- Heath, Andrew C -- Gordon, Jeffrey I -- DK078669/DK/NIDDK NIH HHS/ -- DK58398/DK/NIDDK NIH HHS/ -- DK70977/DK/NIDDK NIH HHS/ -- F32 DK091044/DK/NIDDK NIH HHS/ -- K01 DK095774/DK/NIDDK NIH HHS/ -- K05 AA017688/AA/NIAAA NIH HHS/ -- P01 DK078669/DK/NIDDK NIH HHS/ -- P30 AG028716/AG/NIA NIH HHS/ -- P30 DK020579/DK/NIDDK NIH HHS/ -- P30 DK056341/DK/NIDDK NIH HHS/ -- P30-AG028716/AG/NIA NIH HHS/ -- R01 DK070977/DK/NIDDK NIH HHS/ -- R01 DK076729/DK/NIDDK NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2013 Sep 6;341(6150):1241214. doi: 10.1126/science.1241214.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Genome Sciences and Systems Biology, Washington University School of Medicine, St. Louis, MO 63108, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24009397" target="_blank"〉PubMed〈/a〉
    Keywords: *Adiposity ; Adult ; Animals ; Bacteroidetes/genetics/*physiology ; Cecum/metabolism/microbiology ; Diet, Fat-Restricted ; Feces/microbiology ; Female ; Gastrointestinal Tract/*microbiology ; Germ-Free Life ; Humans ; Metabolome ; Metagenome/genetics/*physiology ; Mice ; Mice, Inbred C57BL ; Mice, Obese ; Obesity/genetics/*metabolism ; Thinness/microbiology ; Twins ; Weight Gain ; Young Adult
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  • 10
    Publication Date: 2013-04-27
    Description: Secondary bacterial pneumonia leads to increased morbidity and mortality from influenza virus infections. What causes this increased susceptibility, however, is not well defined. Host defense from infection relies not only on immune resistance mechanisms but also on the ability to tolerate a given level of pathogen burden. Failure of either resistance or tolerance can contribute to disease severity, making it hard to distinguish their relative contribution. We employ a coinfection mouse model of influenza virus and Legionella pneumophila in which we can separate resistance and tolerance. We demonstrate that influenza virus can promote susceptibility to lethal bacterial coinfection, even when bacterial infection is controlled by the immune system. We propose that this failure of host defense is due to impaired ability to tolerate tissue damage.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3933032/" 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/PMC3933032/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jamieson, Amanda M -- Pasman, Lesley -- Yu, Shuang -- Gamradt, Pia -- Homer, Robert J -- Decker, Thomas -- Medzhitov, Ruslan -- AI R01 055502/AI/NIAID NIH HHS/ -- R01 046688/PHS HHS/ -- R01 AI046688/AI/NIAID NIH HHS/ -- R01 AI055502/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2013 Jun 7;340(6137):1230-4. doi: 10.1126/science.1233632. Epub 2013 Apr 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA. amanda_jamieson@brown.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23618765" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caspase 1 ; Coinfection/*immunology/pathology ; Disease Models, Animal ; Host-Pathogen Interactions/immunology ; Interleukin-1beta/metabolism ; *Legionella pneumophila ; Legionnaires' Disease/*immunology/pathology ; Lung/microbiology/pathology/virology ; Mice ; Mice, Inbred C57BL ; *Orthomyxoviridae ; Orthomyxoviridae Infections/*immunology/pathology ; Pneumonia, Bacterial/*immunology/pathology ; Toll-Like Receptor 2/metabolism ; Toll-Like Receptor 3/metabolism ; Toll-Like Receptor 4/metabolism ; Tumor Necrosis Factor-alpha/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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