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  • Mice  (7)
  • American Association for the Advancement of Science (AAAS)  (7)
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  • 1
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    An iron-regulated ferric reductase associated with the absorption of dietary iron (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-03-07
    Description: The ability of intestinal mucosa to absorb dietary ferric iron is attributed to the presence of a brush-border membrane reductase activity that displays adaptive responses to iron status. We have isolated a complementary DNA, Dcytb (for duodenal cytochrome b), which encoded a putative plasma membrane di-heme protein in mouse duodenal mucosa. Dcytb shared between 45 and 50% similarity to the cytochrome b561 family of plasma membrane reductases, was highly expressed in the brush-border membrane of duodenal enterocytes, and induced ferric reductase activity when expressed in Xenopus oocytes and cultured cells. Duodenal expression levels of Dcytb messenger RNA and protein were regulated by changes in physiological modulators of iron absorption. Thus, Dcytb provides an important element in the iron absorption pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McKie, A T -- Barrow, D -- Latunde-Dada, G O -- Rolfs, A -- Sager, G -- Mudaly, E -- Mudaly, M -- Richardson, C -- Barlow, D -- Bomford, A -- Peters, T J -- Raja, K B -- Shirali, S -- Hediger, M A -- Farzaneh, F -- Simpson, R J -- New York, N.Y. -- Science. 2001 Mar 2;291(5509):1755-9. Epub 2001 Feb 1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Medicine, Guy's, King's and St. Thomas' School of Medicine, King's College London, Rayne Institute, Denmark Hill Campus, 123 Coldharbour Lane, London SE5 9NU, UK. andrew.t.mckie@kcl.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11230685" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Anemia/enzymology ; Animals ; Anoxia ; Cell Line ; Cloning, Molecular ; Cytochrome b Group/chemistry/genetics/*metabolism ; DNA, Complementary ; Duodenum/enzymology/*metabolism ; Enterocytes/enzymology/metabolism ; Enzyme Induction ; Ferric Compounds/*metabolism ; *Intestinal Absorption ; Intestinal Mucosa/enzymology/*metabolism ; Iron, Dietary/administration & dosage/*metabolism ; Male ; Mice ; Microvilli/enzymology/metabolism ; Molecular Sequence Data ; Nitroblue Tetrazolium/metabolism ; Oocytes ; Oxidation-Reduction ; Oxidoreductases/chemistry/genetics/*metabolism ; RNA, Messenger/genetics/metabolism ; Tetrazolium Salts/metabolism ; Thiazoles/metabolism ; *Transfection ; Up-Regulation ; Xenopus
    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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  • 2
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    Monoallelic expression of the interleukin-2 locus (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-04-16
    Description: The lymphokine interleukin-2 (IL-2) is responsible for autocrine cell cycle progression and regulation of immune responses. Uncontrolled secretion of IL-2 results in adverse reactions ranging from anergy, to aberrant T cell activation, to autoimmunity. With the use of fluorescent in situ hybridization and single-cell polymerase chain reaction in cells with different IL-2 alleles, IL-2 expression in mature thymocytes and T cells was found to be tightly controlled by monoallelic expression. Because IL-2 is encoded at a nonimprinted autosomal locus, this result represents an unusual regulatory mode for controlling the precise expression of a single gene.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hollander, G A -- Zuklys, S -- Morel, C -- Mizoguchi, E -- Mobisson, K -- Simpson, S -- Terhorst, C -- Wishart, W -- Golan, D E -- Bhan, A K -- Burakoff, S J -- P01 CA39542-09/CA/NCI NIH HHS/ -- R01 AI17258-18/AI/NIAID NIH HHS/ -- R01 DK47677/DK/NIDDK NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1998 Mar 27;279(5359):2118-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Pediatric Immunology, Department of Research and Children's Hospital, Basel University Medical School, 4031 Basel, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9516115" target="_blank"〉PubMed〈/a〉
    Keywords: *Alleles ; Animals ; CD4-Positive T-Lymphocytes/cytology/*immunology ; Concanavalin A/pharmacology ; DNA Replication ; Female ; Flow Cytometry ; *Gene Expression Regulation ; Heterozygote ; In Situ Hybridization, Fluorescence ; Interleukin-2/biosynthesis/*genetics ; Lymphocyte Activation ; Male ; Mice ; Mice, Inbred C57BL ; Muridae ; Mutation ; Polymerase Chain Reaction ; S Phase ; 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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  • 3
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    Transient regenerative potential of the neonatal mouse heart (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-02-26
    Description: Certain fish and amphibians retain a robust capacity for cardiac regeneration throughout life, but the same is not true of the adult mammalian heart. Whether the capacity for cardiac regeneration is absent in mammals or whether it exists and is switched off early after birth has been unclear. We found that the hearts of 1-day-old neonatal mice can regenerate after partial surgical resection, but this capacity is lost by 7 days of age. This regenerative response in 1-day-old mice was characterized by cardiomyocyte proliferation with minimal hypertrophy or fibrosis, thereby distinguishing it from repair processes. Genetic fate mapping indicated that the majority of cardiomyocytes within the regenerated tissue originated from preexisting cardiomyocytes. Echocardiography performed 2 months after surgery revealed that the regenerated ventricular apex had normal systolic function. Thus, for a brief period after birth, the mammalian heart appears to have the capacity to regenerate.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3099478/" 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/PMC3099478/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Porrello, Enzo R -- Mahmoud, Ahmed I -- Simpson, Emma -- Hill, Joseph A -- Richardson, James A -- Olson, Eric N -- Sadek, Hesham A -- HL100401-01/HL/NHLBI NIH HHS/ -- R01 HL077439/HL/NHLBI NIH HHS/ -- R01 HL077439-06/HL/NHLBI NIH HHS/ -- R01 HL077439-06W1/HL/NHLBI NIH HHS/ -- R01 HL077439-07/HL/NHLBI NIH HHS/ -- R01 HL077439-08/HL/NHLBI NIH HHS/ -- R01 HL093039/HL/NHLBI NIH HHS/ -- R01 HL093039-01A1/HL/NHLBI NIH HHS/ -- R01 HL093039-01A1W1/HL/NHLBI NIH HHS/ -- R01 HL093039-02/HL/NHLBI NIH HHS/ -- R01 HL093039-03/HL/NHLBI NIH HHS/ -- R01 HL115275/HL/NHLBI NIH HHS/ -- R37 HL053351/HL/NHLBI NIH HHS/ -- R37 HL053351-12/HL/NHLBI NIH HHS/ -- R37 HL053351-13/HL/NHLBI NIH HHS/ -- R37 HL053351-14/HL/NHLBI NIH HHS/ -- R37 HL053351-15/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2011 Feb 25;331(6020):1078-80. doi: 10.1126/science.1200708.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21350179" target="_blank"〉PubMed〈/a〉
    Keywords: Aging ; Animals ; Animals, Newborn ; Cardiomegaly ; Cell Lineage ; Cell Proliferation ; Echocardiography ; Fibrosis ; Heart/*physiology ; Heart Ventricles/surgery ; Mice ; Myocardial Contraction ; Myocardium/pathology ; Myocytes, Cardiac/*physiology ; *Regeneration ; Sarcomeres/ultrastructure ; Stroke Volume
    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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    Repeated cortico-striatal stimulation generates persistent OCD-like behavior (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-06-08
    Description: Although cortico-striato-thalamo-cortical (CSTC) circuit dysregulation is correlated with obsessive compulsive disorder (OCD), causation cannot be tested in humans. We used optogenetics in mice to simulate CSTC hyperactivation observed in OCD patients. Whereas acute orbitofrontal cortex (OFC)-ventromedial striatum (VMS) stimulation did not produce repetitive behaviors, repeated hyperactivation over multiple days generated a progressive increase in grooming, a mouse behavior related to OCD. Increased grooming persisted for 2 weeks after stimulation cessation. The grooming increase was temporally coupled with a progressive increase in light-evoked firing of postsynaptic VMS cells. Both increased grooming and evoked firing were reversed by chronic fluoxetine, a first-line OCD treatment. Brief but repeated episodes of abnormal circuit activity may thus set the stage for the development of persistent psychopathology.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3954809/" 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/PMC3954809/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ahmari, Susanne E -- Spellman, Timothy -- Douglass, Neria L -- Kheirbek, Mazen A -- Simpson, H Blair -- Deisseroth, Karl -- Gordon, Joshua A -- Hen, Rene -- K01 MH099371/MH/NIMH NIH HHS/ -- K01MH099371/MH/NIMH NIH HHS/ -- K08 MH087718/MH/NIMH NIH HHS/ -- K08MH087718/MH/NIMH NIH HHS/ -- K24 MH091555/MH/NIMH NIH HHS/ -- R01 MH096274/MH/NIMH NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2013 Jun 7;340(6137):1234-9. doi: 10.1126/science.1234733.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychiatry, Columbia University College of Physicians and Surgeons, New York, NY 10032, USA. sea2103@columbia.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23744948" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoviridae ; Animals ; Artificial Gene Fusion ; Bacterial Proteins/genetics ; Behavior, Animal ; Corpus Striatum/drug effects/*physiopathology ; Electric Stimulation ; Fluoxetine/pharmacology ; Frontal Lobe/drug effects/*physiopathology ; Luminescent Proteins/genetics ; Male ; Mice ; Obsessive-Compulsive Disorder/*physiopathology/*psychology ; Optogenetics ; Rhodopsin/biosynthesis/genetics ; Serotonin Uptake Inhibitors/pharmacology ; Thalamus/drug effects/*physiopathology
    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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    Intestinal inflammation targets cancer-inducing activity of the microbiota (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-08-21
    Description: Inflammation alters host physiology to promote cancer, as seen in colitis-associated colorectal cancer (CRC). Here, we identify the intestinal microbiota as a target of inflammation that affects the progression of CRC. High-throughput sequencing revealed that inflammation modifies gut microbial composition in colitis-susceptible interleukin-10-deficient (Il10(-/-)) mice. Monocolonization with the commensal Escherichia coli NC101 promoted invasive carcinoma in azoxymethane (AOM)-treated Il10(-/-) mice. Deletion of the polyketide synthase (pks) genotoxic island from E. coli NC101 decreased tumor multiplicity and invasion in AOM/Il10(-/-) mice, without altering intestinal inflammation. Mucosa-associated pks(+) E. coli were found in a significantly high percentage of inflammatory bowel disease and CRC patients. This suggests that in mice, colitis can promote tumorigenesis by altering microbial composition and inducing the expansion of microorganisms with genotoxic capabilities.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3645302/" 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/PMC3645302/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Arthur, Janelle C -- Perez-Chanona, Ernesto -- Muhlbauer, Marcus -- Tomkovich, Sarah -- Uronis, Joshua M -- Fan, Ting-Jia -- Campbell, Barry J -- Abujamel, Turki -- Dogan, Belgin -- Rogers, Arlin B -- Rhodes, Jonathan M -- Stintzi, Alain -- Simpson, Kenneth W -- Hansen, Jonathan J -- Keku, Temitope O -- Fodor, Anthony A -- Jobin, Christian -- MOP114872/Canadian Institutes of Health Research/Canada -- P30 CA016086/CA/NCI NIH HHS/ -- P30 DK034987/DK/NIDDK NIH HHS/ -- P40 R018603/PHS HHS/ -- R01 CA136887/CA/NCI NIH HHS/ -- R01 DK047700/DK/NIDDK NIH HHS/ -- R01 DK073338/DK/NIDDK NIH HHS/ -- R01 DK47700/DK/NIDDK NIH HHS/ -- R01 DK53347-11/DK/NIDDK NIH HHS/ -- R01 DK73338/DK/NIDDK NIH HHS/ -- T32 DK007737/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2012 Oct 5;338(6103):120-3. doi: 10.1126/science.1224820. Epub 2012 Aug 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Pharmacology and Immunology-Microbiology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22903521" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Azoxymethane/toxicity ; Carcinogens/toxicity ; Carcinoma/chemically induced/*microbiology/pathology ; Cell Transformation, Neoplastic/genetics/pathology ; Colitis/*complications/genetics ; Colorectal Neoplasms/chemically induced/*microbiology/pathology ; *DNA Damage ; Escherichia coli/genetics/pathogenicity ; Interleukin-10/genetics ; Intestines/*microbiology/pathology ; Metagenome/genetics/*physiology ; Mice ; Mice, Mutant Strains ; Polyketide Synthases/genetics ; Sequence Deletion
    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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    Permeability of the cell-to-cell membrane channels in mammalian cell juncton (1979)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1979-07-27
    Description: The channels in the junctions of various mammalian cell types--primary cultures and lines--were probed with a series of linear fluorescent amino acid and peptide molecules of different size and charge. Permeability is limited by probe size and electronegativity, these two factors apparently being related reciprocally. In respect to both factors, mammalian junctional channels are more restrictive than insect channels; hence the mammalian channels are narrower, more polar, or both. The channels of the various mammalian cell types differed slightly from each other; in some types the serum of the culture medium affected the channel permeability.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Flagg-Newton, J -- Simpson, I -- Loewenstein, W R -- New York, N.Y. -- Science. 1979 Jul 27;205(4404):404-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/377490" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cell Membrane/physiology ; *Cell Membrane Permeability ; Cells, Cultured ; Cricetinae ; Fluorescent Antibody Technique ; Kidney ; Mice ; Mice, Inbred BALB C ; Species Specificity
    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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    Association of parvoviruses with rheumatoid arthritis of humans (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-03-30
    Description: A small virus resembling parvoviruses in its morphological and physicochemical properties was derived from synovial tissue of a patient with severe rheumatoid arthritis. This virus, designated RA-1, elicits a syndrome in neonatal mice that includes neurological disturbances, permanent crippling of limbs, dwarfism, alopecia, blepharitis, "masking," and a rigid curvature of the thoracic spine. Polyclonal antibodies against RA-1 display high virus neutralizing activity and in immunoassays detect reactive antigen in synovial cells from different rheumatoid arthritis patients but not persons with osteoarthritis. Putative parvoviruses isolated from several other rheumatoid arthritis patients are only weakly pathogenic for newborn mice but can generate RA-1 virus-specific antigens in tissues of these animals. It has not been established that RA-1 and existing parvoviruses of mammalian species are related.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Simpson, R W -- McGinty, L -- Simon, L -- Smith, C A -- Godzeski, C W -- Boyd, R J -- AI-14359/AI/NIAID NIH HHS/ -- AI-17262/AI/NIAID NIH HHS/ -- AM-15796/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1984 Mar 30;223(4643):1425-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6701529" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn/microbiology ; Antibodies, Viral/immunology ; Arthritis, Rheumatoid/*microbiology ; Cells, Cultured ; Enzyme-Linked Immunosorbent Assay ; Humans ; Mice ; Microscopy, Electron ; Osteoarthritis/microbiology ; Parvoviridae/immunology/*isolation & purification/ultrastructure ; Rabbits ; Synovial Fluid/cytology/microbiology
    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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