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  • Mice, Inbred C57BL  (164)
  • American Association for the Advancement of Science (AAAS)  (164)
  • American Chemical Society
  • American Society of Hematology
  • 2020-2024
  • 2020-2023
  • 2010-2014  (102)
  • 2005-2009  (62)
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  • American Association for the Advancement of Science (AAAS)  (164)
  • American Chemical Society
  • American Society of Hematology
  • Nature Publishing Group (NPG)  (212)
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  • 1
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    Ribosomal protein S6 kinase 1 signaling regulates mammalian life span (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-10-03
    Description: Caloric restriction (CR) protects against aging and disease, but the mechanisms by which this affects mammalian life span are unclear. We show in mice that deletion of ribosomal S6 protein kinase 1 (S6K1), a component of the nutrient-responsive mTOR (mammalian target of rapamycin) signaling pathway, led to increased life span and resistance to age-related pathologies, such as bone, immune, and motor dysfunction and loss of insulin sensitivity. Deletion of S6K1 induced gene expression patterns similar to those seen in CR or with pharmacological activation of adenosine monophosphate (AMP)-activated protein kinase (AMPK), a conserved regulator of the metabolic response to CR. Our results demonstrate that S6K1 influences healthy mammalian life-span and suggest that therapeutic manipulation of S6K1 and AMPK might mimic CR and could provide broad protection against diseases of aging.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Selman, Colin -- Tullet, Jennifer M A -- Wieser, Daniela -- Irvine, Elaine -- Lingard, Steven J -- Choudhury, Agharul I -- Claret, Marc -- Al-Qassab, Hind -- Carmignac, Danielle -- Ramadani, Faruk -- Woods, Angela -- Robinson, Iain C A -- Schuster, Eugene -- Batterham, Rachel L -- Kozma, Sara C -- Thomas, George -- Carling, David -- Okkenhaug, Klaus -- Thornton, Janet M -- Partridge, Linda -- Gems, David -- Withers, Dominic J -- BBS/E/B/0000C236/Biotechnology and Biological Sciences Research Council/United Kingdom -- BBS/E/B/0000M979/Biotechnology and Biological Sciences Research Council/United Kingdom -- G0800339/Medical Research Council/United Kingdom -- G108/551/Medical Research Council/United Kingdom -- MC_U117531708/Medical Research Council/United Kingdom -- MC_U120027537/Medical Research Council/United Kingdom -- MC_U120097114/Medical Research Council/United Kingdom -- Biotechnology and Biological Sciences Research Council/United Kingdom -- Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2009 Oct 2;326(5949):140-4. doi: 10.1126/science.1177221.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Healthy Ageing, Centre for Diabetes and Endocrinology, Department of Medicine, University College London, London WC1E 6JJ, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19797661" target="_blank"〉PubMed〈/a〉
    Keywords: AMP-Activated Protein Kinases/metabolism ; Adipose Tissue, White/metabolism ; Aging/*physiology ; Animals ; Bone Density ; Caloric Restriction ; Female ; Gene Deletion ; Gene Expression ; Gene Expression Regulation ; Insulin/metabolism ; Liver/metabolism ; Longevity/*physiology ; Male ; Mice ; Mice, Inbred C57BL ; Motor Activity ; Muscle, Skeletal/metabolism ; Protein Kinases/metabolism ; Ribosomal Protein S6 Kinases, 90-kDa/genetics/*metabolism ; *Signal Transduction ; T-Lymphocyte Subsets/immunology ; TOR Serine-Threonine Kinases ; Transcription, Genetic
    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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  • 2
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    Rapamycin-induced insulin resistance is mediated by mTORC2 loss and uncoupled from longevity (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-03-31
    Description: Rapamycin, an inhibitor of mechanistic target of rapamycin complex 1 (mTORC1), extends the life spans of yeast, flies, and mice. Calorie restriction, which increases life span and insulin sensitivity, is proposed to function by inhibition of mTORC1, yet paradoxically, chronic administration of rapamycin substantially impairs glucose tolerance and insulin action. We demonstrate that rapamycin disrupted a second mTOR complex, mTORC2, in vivo and that mTORC2 was required for the insulin-mediated suppression of hepatic gluconeogenesis. Further, decreased mTORC1 signaling was sufficient to extend life span independently from changes in glucose homeostasis, as female mice heterozygous for both mTOR and mLST8 exhibited decreased mTORC1 activity and extended life span but had normal glucose tolerance and insulin sensitivity. Thus, mTORC2 disruption is an important mediator of the effects of rapamycin in vivo.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3324089/" 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/PMC3324089/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lamming, Dudley W -- Ye, Lan -- Katajisto, Pekka -- Goncalves, Marcus D -- Saitoh, Maki -- Stevens, Deanna M -- Davis, James G -- Salmon, Adam B -- Richardson, Arlan -- Ahima, Rexford S -- Guertin, David A -- Sabatini, David M -- Baur, Joseph A -- 1F32AG032833-01A1/AG/NIA NIH HHS/ -- CA129105/CA/NCI NIH HHS/ -- F32 AG032833/AG/NIA NIH HHS/ -- P30DK19525/DK/NIDDK NIH HHS/ -- R01 CA129105/CA/NCI NIH HHS/ -- R01 CA129105-05/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2012 Mar 30;335(6076):1638-43. doi: 10.1126/science.1215135.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research, Cambridge, MA 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22461615" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue, White/metabolism ; Animals ; Carrier Proteins/genetics/metabolism ; Female ; Gluconeogenesis ; Glucose/metabolism ; Glucose Clamp Technique ; Homeostasis ; Insulin/administration & dosage/blood ; *Insulin Resistance ; Liver/metabolism ; *Longevity ; Male ; Mice ; Mice, Inbred C57BL ; Multiprotein Complexes ; Muscle, Skeletal/metabolism ; Phosphorylation ; Proteins/antagonists & inhibitors/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; Signal Transduction ; Sirolimus/*pharmacology ; TOR Serine-Threonine Kinases/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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  • 3
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    Shear-activated nanotherapeutics for drug targeting to obstructed blood vessels (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-07-07
    Description: Obstruction of critical blood vessels due to thrombosis or embolism is a leading cause of death worldwide. Here, we describe a biomimetic strategy that uses high shear stress caused by vascular narrowing as a targeting mechanism--in the same way platelets do--to deliver drugs to obstructed blood vessels. Microscale aggregates of nanoparticles were fabricated to break up into nanoscale components when exposed to abnormally high fluid shear stress. When coated with tissue plasminogen activator and administered intravenously in mice, these shear-activated nanotherapeutics induce rapid clot dissolution in a mesenteric injury model, restore normal flow dynamics, and increase survival in an otherwise fatal mouse pulmonary embolism model. This biophysical strategy for drug targeting, which lowers required doses and minimizes side effects while maximizing drug efficacy, offers a potential new approach for treatment of life-threatening diseases that result from acute vascular occlusion.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Korin, Netanel -- Kanapathipillai, Mathumai -- Matthews, Benjamin D -- Crescente, Marilena -- Brill, Alexander -- Mammoto, Tadanori -- Ghosh, Kaustabh -- Jurek, Samuel -- Bencherif, Sidi A -- Bhatta, Deen -- Coskun, Ahmet U -- Feldman, Charles L -- Wagner, Denisa D -- Ingber, Donald E -- New York, N.Y. -- Science. 2012 Aug 10;337(6095):738-42. doi: 10.1126/science.1217815. Epub 2012 Jul 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wyss Institute for Biologically Inspired Engineering, Harvard University, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22767894" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biomimetic Materials ; Blood Circulation ; Drug Delivery Systems/*methods ; Fibrinolytic Agents/*administration & dosage ; Hemodynamics ; Hemorheology ; Lactic Acid ; Male ; Mesenteric Arteries ; Mesenteric Vascular Occlusion/*drug therapy ; Mice ; Mice, Inbred C57BL ; Microfluidic Analytical Techniques ; Models, Anatomic ; *Nanoparticles ; Polyglycolic Acid ; Pulmonary Embolism/*drug therapy ; Stress, Mechanical ; Thrombosis/*drug therapy/prevention & control ; Tissue Plasminogen Activator/*administration & dosage
    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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  • 4
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    Interactions between commensal fungi and the C-type lectin receptor Dectin-1 influence colitis (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-06-08
    Description: The intestinal microflora, typically equated with bacteria, influences diseases such as obesity and inflammatory bowel disease. Here, we show that the mammalian gut contains a rich fungal community that interacts with the immune system through the innate immune receptor Dectin-1. Mice lacking Dectin-1 exhibited increased susceptibility to chemically induced colitis, which was the result of altered responses to indigenous fungi. In humans, we identified a polymorphism in the gene for Dectin-1 (CLEC7A) that is strongly linked to a severe form of ulcerative colitis. Together, our findings reveal a eukaryotic fungal community in the gut (the "mycobiome") that coexists with bacteria and substantially expands the repertoire of organisms interacting with the intestinal immune system to influence health and disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3432565/" 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/PMC3432565/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Iliev, Iliyan D -- Funari, Vincent A -- Taylor, Kent D -- Nguyen, Quoclinh -- Reyes, Christopher N -- Strom, Samuel P -- Brown, Jordan -- Becker, Courtney A -- Fleshner, Phillip R -- Dubinsky, Marla -- Rotter, Jerome I -- Wang, Hanlin L -- McGovern, Dermot P B -- Brown, Gordon D -- Underhill, David M -- 086558/Wellcome Trust/United Kingdom -- AI071116/AI/NIAID NIH HHS/ -- P01-DK046763/DK/NIDDK NIH HHS/ -- R01 DK093426/DK/NIDDK NIH HHS/ -- UL1 RR033176/RR/NCRR NIH HHS/ -- UL1 TR000124/TR/NCATS NIH HHS/ -- UL1RR033176/RR/NCRR NIH HHS/ -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2012 Jun 8;336(6086):1314-7. doi: 10.1126/science.1221789. Epub 2012 Jun 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Inflammatory Bowel and Immunobiology Research Institute, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22674328" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Fungal/blood ; Candida tropicalis/immunology/isolation & purification/pathogenicity/physiology ; Colitis, Ulcerative/chemically induced/*immunology/*microbiology ; Colon/immunology/*microbiology ; Colony Count, Microbial ; Dextran Sulfate ; Disease Susceptibility ; Female ; Fungi/classification/*immunology/isolation & purification/*physiology ; Haplotypes ; Humans ; Immunity, Innate ; Immunity, Mucosal ; Intestinal Mucosa/immunology/*microbiology ; Intestines/immunology/microbiology ; Lectins, C-Type/deficiency/*genetics/*metabolism ; Metagenome ; Mice ; Mice, Inbred C57BL ; Polymorphism, Single Nucleotide
    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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  • 5
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    Neurokinin 1 receptor antagonism as a possible therapy for alcoholism (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-02-16
    Description: Alcohol dependence is a major public health challenge in need of new treatments. As alcoholism evolves, stress systems in the brain play an increasing role in motivating continued alcohol use and relapse. We investigated the role of the neurokinin 1 receptor (NK1R), a mediator of behavioral stress responses, in alcohol dependence and treatment. In preclinical studies, mice genetically deficient in NK1R showed a marked decrease in voluntary alcohol consumption and had an increased sensitivity to the sedative effects of alcohol. In a randomized controlled experimental study, we treated recently detoxified alcoholic inpatients with an NK1R antagonist (LY686017; n = 25) or placebo (n = 25). LY686017 suppressed spontaneous alcohol cravings, improved overall well-being, blunted cravings induced by a challenge procedure, and attenuated concomitant cortisol responses. Brain functional magnetic resonance imaging responses to affective stimuli likewise suggested beneficial LY686017 effects. Thus, as assessed by these surrogate markers of efficacy, NK1R antagonism warrants further investigation as a treatment in alcoholism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉George, David T -- Gilman, Jodi -- Hersh, Jacqueline -- Thorsell, Annika -- Herion, David -- Geyer, Christopher -- Peng, Xiaomei -- Kielbasa, William -- Rawlings, Robert -- Brandt, John E -- Gehlert, Donald R -- Tauscher, Johannes T -- Hunt, Stephen P -- Hommer, Daniel -- Heilig, Markus -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2008 Mar 14;319(5869):1536-9. doi: 10.1126/science.1153813. Epub 2008 Feb 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Clinical and Translational Studies, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18276852" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aged ; *Alcohol Drinking/drug therapy ; Alcoholism/*drug therapy ; Animals ; Behavior, Addictive/drug therapy ; Brain/drug effects/physiology ; Emotions/drug effects ; Ethanol/administration & dosage/pharmacology ; Female ; Humans ; Hydrocortisone/blood ; Magnetic Resonance Imaging ; Male ; Mice ; Mice, Inbred C57BL ; Middle Aged ; *Neurokinin-1 Receptor Antagonists ; Pyridines/administration & dosage/pharmacology/*therapeutic use ; Receptors, Neurokinin-1/deficiency/genetics/*physiology ; Triazoles/administration & dosage/pharmacology/*therapeutic use
    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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  • 6
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    Host genetic diversity enables Ebola hemorrhagic fever pathogenesis and resistance (2014)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2014-11-02
    Description: Existing mouse models of lethal Ebola virus infection do not reproduce hallmark symptoms of Ebola hemorrhagic fever, neither delayed blood coagulation and disseminated intravascular coagulation nor death from shock, thus restricting pathogenesis studies to nonhuman primates. Here we show that mice from the Collaborative Cross panel of recombinant inbred mice exhibit distinct disease phenotypes after mouse-adapted Ebola virus infection. Phenotypes range from complete resistance to lethal disease to severe hemorrhagic fever characterized by prolonged coagulation times and 100% mortality. Inflammatory signaling was associated with vascular permeability and endothelial activation, and resistance to lethal infection arose by induction of lymphocyte differentiation and cellular adhesion, probably mediated by the susceptibility allele Tek. These data indicate that genetic background determines susceptibility to Ebola hemorrhagic fever.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4241145/" 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/PMC4241145/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rasmussen, Angela L -- Okumura, Atsushi -- Ferris, Martin T -- Green, Richard -- Feldmann, Friederike -- Kelly, Sara M -- Scott, Dana P -- Safronetz, David -- Haddock, Elaine -- LaCasse, Rachel -- Thomas, Matthew J -- Sova, Pavel -- Carter, Victoria S -- Weiss, Jeffrey M -- Miller, Darla R -- Shaw, Ginger D -- Korth, Marcus J -- Heise, Mark T -- Baric, Ralph S -- de Villena, Fernando Pardo-Manuel -- Feldmann, Heinz -- Katze, Michael G -- P51 OD010425/OD/NIH HHS/ -- U19 AI100625/AI/NIAID NIH HHS/ -- U19 AI109761/AI/NIAID NIH HHS/ -- U54 AI081680/AI/NIAID NIH HHS/ -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2014 Nov 21;346(6212):987-91. doi: 10.1126/science.1259595. Epub 2014 Oct 30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, University of Washington, Seattle, WA, USA. ; Department of Microbiology, University of Washington, Seattle, WA, USA. Laboratory of Virology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rocky Mountain Laboratories, Hamilton, MT, USA. ; Department of Genetics, University of North Carolina, Chapel Hill, NC, USA. ; Rocky Mountain Veterinary Branch, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rocky Mountain Laboratories, Hamilton, MT, USA. ; Laboratory of Virology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rocky Mountain Laboratories, Hamilton, MT, USA. ; Department of Genetics, University of North Carolina, Chapel Hill, NC, USA. Department of Microbiology and Immunology, University of North Carolina, Chapel Hill, NC, USA. ; Department of Microbiology and Immunology, University of North Carolina, Chapel Hill, NC, USA. ; Department of Microbiology, University of Washington, Seattle, WA, USA. Washington National Primate Research Center, Seattle, WA, USA. honey@uw.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25359852" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Blood Coagulation/genetics ; Capillary Permeability/genetics ; *Disease Models, Animal ; Endothelium, Vascular/physiopathology ; *Genetic Predisposition to Disease ; Hemorrhagic Fever, Ebola/blood/*genetics/*immunology ; Host-Pathogen Interactions/*genetics ; Liver/blood supply/metabolism/pathology ; Lymphocyte Activation/immunology ; *Mice ; Mice, Inbred C57BL ; Neovascularization, Physiologic/genetics ; Receptor, TIE-2/*genetics
    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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  • 7
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    Innate lymphoid cells promote anatomical containment of lymphoid-resident commensal bacteria (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-06-08
    Description: The mammalian intestinal tract is colonized by trillions of beneficial commensal bacteria that are anatomically restricted to specific niches. However, the mechanisms that regulate anatomical containment remain unclear. Here, we show that interleukin-22 (IL-22)-producing innate lymphoid cells (ILCs) are present in intestinal tissues of healthy mammals. Depletion of ILCs resulted in peripheral dissemination of commensal bacteria and systemic inflammation, which was prevented by administration of IL-22. Disseminating bacteria were identified as Alcaligenes species originating from host lymphoid tissues. Alcaligenes was sufficient to promote systemic inflammation after ILC depletion in mice, and Alcaligenes-specific systemic immune responses were associated with Crohn's disease and progressive hepatitis C virus infection in patients. Collectively, these data indicate that ILCs regulate selective containment of lymphoid-resident bacteria to prevent systemic inflammation associated with chronic diseases.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3659421/" 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/PMC3659421/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sonnenberg, Gregory F -- Monticelli, Laurel A -- Alenghat, Theresa -- Fung, Thomas C -- Hutnick, Natalie A -- Kunisawa, Jun -- Shibata, Naoko -- Grunberg, Stephanie -- Sinha, Rohini -- Zahm, Adam M -- Tardif, Melanie R -- Sathaliyawala, Taheri -- Kubota, Masaru -- Farber, Donna L -- Collman, Ronald G -- Shaked, Abraham -- Fouser, Lynette A -- Weiner, David B -- Tessier, Philippe A -- Friedman, Joshua R -- Kiyono, Hiroshi -- Bushman, Frederic D -- Chang, Kyong-Mi -- Artis, David -- 2-P30 CA016520/CA/NCI NIH HHS/ -- AI061570/AI/NIAID NIH HHS/ -- AI074878/AI/NIAID NIH HHS/ -- AI083480/AI/NIAID NIH HHS/ -- AI087990/AI/NIAID NIH HHS/ -- AI095466/AI/NIAID NIH HHS/ -- AI095608/AI/NIAID NIH HHS/ -- AI47619/AI/NIAID NIH HHS/ -- K08 DK093784/DK/NIDDK NIH HHS/ -- K08-DK093784/DK/NIDDK NIH HHS/ -- P30 AI 045008/AI/NIAID NIH HHS/ -- P30DK50306/DK/NIDDK NIH HHS/ -- R01 AI061570/AI/NIAID NIH HHS/ -- R01 AI074878/AI/NIAID NIH HHS/ -- R01 AI095466/AI/NIAID NIH HHS/ -- R01 AI102942/AI/NIAID NIH HHS/ -- R21 AI083480/AI/NIAID NIH HHS/ -- R21 AI087990/AI/NIAID NIH HHS/ -- T32 AI007532/AI/NIAID NIH HHS/ -- T32 AI055428/AI/NIAID NIH HHS/ -- T32 RR007063/RR/NCRR NIH HHS/ -- T32-AI007532/AI/NIAID NIH HHS/ -- T32-AI055428/AI/NIAID NIH HHS/ -- T32-RR007063/RR/NCRR NIH HHS/ -- U01 AI095608/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2012 Jun 8;336(6086):1321-5. doi: 10.1126/science.1222551. Epub 2012 Jun 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22674331" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Alcaligenes/immunology/isolation & purification/*physiology ; Animals ; Bacterial Translocation ; Crohn Disease/immunology/microbiology ; Hepatitis C, Chronic/immunology/microbiology ; Humans ; Immunity, Innate ; Inflammation ; Interleukins/administration & dosage/biosynthesis/*immunology ; Intestines/*immunology/microbiology ; Leukocyte L1 Antigen Complex/metabolism ; Liver/microbiology ; Lymph Nodes/immunology ; Lymphocytes/*immunology ; Lymphoid Tissue/*immunology/*microbiology ; Macaca mulatta ; Mice ; Mice, Inbred C57BL ; Middle Aged ; Spleen/microbiology ; Young Adult
    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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  • 8
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    BDNF is a negative modulator of morphine action (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-10-09
    Description: Brain-derived neurotrophic factor (BDNF) is a key positive regulator of neural plasticity, promoting, for example, the actions of stimulant drugs of abuse such as cocaine. We discovered a surprising opposite role for BDNF in countering responses to chronic morphine exposure. The suppression of BDNF in the ventral tegmental area (VTA) enhanced the ability of morphine to increase dopamine (DA) neuron excitability and promote reward. In contrast, optical stimulation of VTA DA terminals in nucleus accumbens (NAc) completely reversed the suppressive effect of BDNF on morphine reward. Furthermore, we identified numerous genes in the NAc, a major target region of VTA DA neurons, whose regulation by BDNF in the context of chronic morphine exposure mediated this counteractive function. These findings provide insight into the molecular basis of morphine-induced neuroadaptations in the brain's reward circuitry.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3547365/" 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/PMC3547365/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koo, Ja Wook -- Mazei-Robison, Michelle S -- Chaudhury, Dipesh -- Juarez, Barbara -- LaPlant, Quincey -- Ferguson, Deveroux -- Feng, Jian -- Sun, Haosheng -- Scobie, Kimberly N -- Damez-Werno, Diane -- Crumiller, Marshall -- Ohnishi, Yoshinori N -- Ohnishi, Yoko H -- Mouzon, Ezekiell -- Dietz, David M -- Lobo, Mary Kay -- Neve, Rachael L -- Russo, Scott J -- Han, Ming-Hu -- Nestler, Eric J -- K99 MH094405/MH/NIMH NIH HHS/ -- P01 DA008227/DA/NIDA NIH HHS/ -- R01 DA014133/DA/NIDA NIH HHS/ -- R01 MH092306/MH/NIMH NIH HHS/ -- T32 MH087004/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2012 Oct 5;338(6103):124-8. doi: 10.1126/science.1222265.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Fishberg Department of Neuroscience and Friedman Brain Institute, Mount Sinai School of Medicine, New York, NY 10029, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23042896" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain-Derived Neurotrophic Factor/genetics/*physiology ; Dopamine/metabolism ; Dopaminergic Neurons/*drug effects/physiology ; Gene Expression Regulation ; Gene Knockdown Techniques ; Gene Knockout Techniques ; Male ; Mice ; Mice, Inbred C57BL ; Morphine/*pharmacology ; Morphine Dependence/genetics/*physiopathology ; Nucleus Accumbens/drug effects/physiopathology ; Photic Stimulation ; Receptor, trkB/genetics/physiology ; Ventral Tegmental Area/*drug effects/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 9
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    Modulation of gene expression via disruption of NF-kappaB signaling by a bacterial small molecule (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-06-21
    Description: The control of innate immune responses through activation of the nuclear transcription factor NF-kappaB is essential for the elimination of invading microbial pathogens. We showed that the bacterial N-(3-oxo-dodecanoyl) homoserine lactone (C12) selectively impairs the regulation of NF-kappaB functions in activated mammalian cells. The consequence is specific repression of stimulus-mediated induction of NF-kappaB-responsive genes encoding inflammatory cytokines and other immune regulators. These findings uncover a strategy by which C12-producing opportunistic pathogens, such as Pseudomonas aeruginosa, attenuate the innate immune system to establish and maintain local persistent infection in humans, for example, in cystic fibrosis patients.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kravchenko, Vladimir V -- Kaufmann, Gunnar F -- Mathison, John C -- Scott, David A -- Katz, Alexander Z -- Grauer, David C -- Lehmann, Mandy -- Meijler, Michael M -- Janda, Kim D -- Ulevitch, Richard J -- New York, N.Y. -- Science. 2008 Jul 11;321(5886):259-63. doi: 10.1126/science.1156499. Epub 2008 Jun 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology and Microbial Sciences, Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18566250" target="_blank"〉PubMed〈/a〉
    Keywords: 4-Butyrolactone/*analogs & derivatives/physiology ; Adult ; Animals ; Cyclic AMP Response Element-Binding Protein/metabolism ; Cystic Fibrosis/microbiology ; Female ; *Gene Expression Regulation ; Homoserine/*analogs & derivatives/physiology ; Humans ; I-kappa B Kinase/metabolism ; I-kappa B Proteins/metabolism ; Immunity, Innate ; Interferon-gamma/immunology ; Lipopolysaccharides/immunology ; Macrophage Activation ; Macrophages/*immunology/*metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Middle Aged ; NF-kappa B/*metabolism ; Phosphorylation ; Pseudomonas Infections/immunology/microbiology ; Pseudomonas aeruginosa/immunology/*pathogenicity/physiology ; *Signal Transduction ; Toll-Like Receptors/metabolism ; Transcription Factor RelA/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 10
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    ApoE-directed therapeutics rapidly clear beta-amyloid and reverse deficits in AD mouse models (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-02-11
    Description: Alzheimer's disease (AD) is associated with impaired clearance of beta-amyloid (Abeta) from the brain, a process normally facilitated by apolipoprotein E (apoE). ApoE expression is transcriptionally induced through the action of the nuclear receptors peroxisome proliferator-activated receptor gamma and liver X receptors in coordination with retinoid X receptors (RXRs). Oral administration of the RXR agonist bexarotene to a mouse model of AD resulted in enhanced clearance of soluble Abeta within hours in an apoE-dependent manner. Abeta plaque area was reduced more than 50% within just 72 hours. Furthermore, bexarotene stimulated the rapid reversal of cognitive, social, and olfactory deficits and improved neural circuit function. Thus, RXR activation stimulates physiological Abeta clearance mechanisms, resulting in the rapid reversal of a broad range of Abeta-induced deficits.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3651582/" 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/PMC3651582/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cramer, Paige E -- Cirrito, John R -- Wesson, Daniel W -- Lee, C Y Daniel -- Karlo, J Colleen -- Zinn, Adriana E -- Casali, Brad T -- Restivo, Jessica L -- Goebel, Whitney D -- James, Michael J -- Brunden, Kurt R -- Wilson, Donald A -- Landreth, Gary E -- AG030482-03S1/AG/NIA NIH HHS/ -- DC003906/DC/NIDCD NIH HHS/ -- K01 AG029524/AG/NIA NIH HHS/ -- P50-AG005681/AG/NIA NIH HHS/ -- R01 AG030482/AG/NIA NIH HHS/ -- R01 AG037693/AG/NIA NIH HHS/ -- R01 DC003906/DC/NIDCD NIH HHS/ -- R01-AG037693/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2012 Mar 23;335(6075):1503-6. doi: 10.1126/science.1217697. Epub 2012 Feb 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurosciences, Case Western Reserve University School of Medicine, Cleveland, OH 44106, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22323736" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/*drug therapy/*metabolism ; Amyloid beta-Peptides/*metabolism ; Amyloidosis/drug therapy/metabolism ; Animals ; Apolipoproteins E/*metabolism ; Astrocytes/drug effects/metabolism ; Behavior, Animal/drug effects ; Brain/drug effects/*metabolism ; Disease Models, Animal ; Extracellular Fluid/drug effects/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Microglia/drug effects/metabolism ; Molecular Targeted Therapy ; Odors ; Olfactory Pathways/drug effects/physiology ; Orphan Nuclear Receptors/metabolism ; PPAR gamma/metabolism ; Phagocytosis ; Plaque, Amyloid/drug therapy ; Retinoid X Receptors/agonists/metabolism ; Tetrahydronaphthalenes/*pharmacology/*therapeutic use
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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