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  • 1
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    Inner radiation belt particle acceleration and energy structuring by drift resonance with ULF waves during geomagnetic storms (2013)
    Wiley
    Details
    Publication Date: 2013-01-20
    Description: [1]  Geomagnetic storms are frequently associated with the formation of multiple bands of energetic electrons inside the inner radiation belt at L = 1.1-1.9 and with prominent energy structures of protons inside the slot region at L = 2.2–3.5. These structures typically from 100 keV up to the MeV range result from coherent interactions of energetic particles with quasi- monochromatic Ultra Low Frequency waves (ULF). These waves are induced by magnetospheric changes due to the arrival of dense solar material and related nightside injections of particles from the outer magnetosphere that destabilize field lines in the inner magnetosphere down to L = 1.1. Using low-altitude data from the polar orbiting Demeter spacecraft, we perform case and statistical studies of these structures. We show that with such a spacecraft, these structures are best seen near the South Atlantic Anomaly because of lowering of the belt particle mirror point. As evidenced from ground measurements, energy bands are associated with quasi-sinusoidal ULF Pc5 and Pc4 waves with periods in the 1000 second range for L = 1.1–1.9 and in the 60 second range for L = 2.2–3.5. Numerical simulations of the coherent drift resonance of energetic particles with Ultra Low Frequency waves show how the particles are accelerated and how the observed structures build up.
    Print ISSN: 0148-0227
    Topics: Geosciences , Physics
    Published by Wiley on behalf of American Geophysical Union (AGU).
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  • 2
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    An activating Fgfr3 mutation affects trabecular bone formation via a paracrine mechanism during growth (2012)
    Oxford University Press
    Details
    Publication Date: 2012-05-11
    Description: The fibroblast growth factor receptor 3 (FGFR3) plays a critical role in the regulation of endochondral ossification. Fgfr3 gain-of-function mutations cause achondroplasia, the most common form of dwarfism, and a spectrum of chondrodysplasias. Despite a significant number of studies on the role of FGFR3 in cartilage, to date, none has investigated the influence of Fgfr3-mediated effects of the growth plate on bone formation. We studied three mouse models, each expressing Fgfr3 mutation either ubiquitously (C MV-Fgfr3 Y367C/+ ), in chondrocytes ( Col II-Fgfr3 Y367C/+ ) or in mature osteoblasts ( Col I-Fgfr3 Y367C/+ ). Interestingly, we demonstrated that dwarfism with a significant defect in bone formation during growth was only observed in mouse models expressing mutant Fgfr3 in the cartilage. We observed a dramatic reduction in cartilage matrix mineralization and a strong defect of primary spongiosa. Anomalies of primary spongiosa were associated with an increase in osteoclast recruitment and a defect of osteoblasts at the mineralization front. A significant decrease in bone volume, trabecular thickness and number was also observed in the trabecular bone. Interestingly, no anomalies in proliferation and differentiation of primary osteoblasts from C MV-Fgfr3 Y367C/+ mice were observed. Based on these data, we excluded a potential function of Fgfr3 directly on osteoblasts at 3 weeks of age and we obtained evidence that the disorganization of the growth plate is responsible for the anomalies of the trabecular bone during bone formation. Herein, we propose that impaired FGFR3 signaling pathways may affect trabecular bone formation via a paracrine mechanism during growth. These results redefine our understanding of endochondral ossification in FGFR3-related chondrodysplasias.
    Print ISSN: 0964-6906
    Electronic ISSN: 1460-2083
    Topics: Biology , Medicine
    Published by Oxford University Press
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  • 3
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    Arthritis provoked by linked T and B cell recognition of a glycolytic enzyme (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-27
    Description: The hallmark of rheumatoid arthritis (RA) is specific destruction of the synovial joints. In a mouse line that spontaneously develops a disorder with many of the features of human RA, disease is initiated by T cell recognition of a ubiquitously expressed self-antigen; once initiated, pathology is driven almost entirely by immunoglobulins. In this study, the target of both the initiating T cells and pathogenic immunoglobulins was identified as glucose-6-phosphate isomerase, a glycolytic enzyme. Thus, some forms of RA or related arthritides may develop by a mechanism fundamentally different from the currently popular paradigm of a joint-specific T cell response.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Matsumoto, I -- Staub, A -- Benoist, C -- Mathis, D -- New York, N.Y. -- Science. 1999 Nov 26;286(5445):1732-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut de Genetique et de Biologie Moleculaire et Cellulaire (CNRS/INSERM/ULP), BP 163, 67404 Illkirch, C.U. de Strasbourg, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10576739" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen Presentation ; Antigen-Antibody Complex/immunology/metabolism ; Arthritis, Rheumatoid/*immunology ; Autoantibodies/*immunology ; Autoantigens/*immunology ; B-Lymphocytes/*immunology ; Cross Reactions ; Disease Models, Animal ; Glucose-6-Phosphate Isomerase/chemistry/*immunology ; Humans ; Immunoglobulins/immunology ; Joints/immunology ; Mice ; Mice, Inbred C57BL ; Mice, Inbred NOD ; Mice, Transgenic ; Recombinant Fusion Proteins/immunology ; T-Lymphocytes/*immunology
    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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  • 4
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    Mast cells: a cellular link between autoantibodies and inflammatory arthritis (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-09-07
    Description: Previous studies have revealed that autoantibodies, complement components, and Fc receptors each participate in the pathogenesis of erosive arthritis in K/BxN mice. However, it is not known which cellular populations are responsive to these inflammatory signals. We find that two strains of mice deficient in mast cells, W/Wv and Sl/Sld, were resistant to development of joint inflammation and that susceptibility was restored in the W/Wv strain by mast cell engraftment. Thus, mast cells may function as a cellular link between autoantibodies, soluble mediators, and other effector populations in inflammatory arthritis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, David M -- Friend, Daniel S -- Gurish, Michael F -- Benoist, Christophe -- Mathis, Diane -- Brenner, Michael B -- 1R01 AR/AI46580-01/AR/NIAMS NIH HHS/ -- New York, N.Y. -- Science. 2002 Sep 6;297(5587):1689-92.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12215644" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arthritis/*immunology/pathology ; Autoantibodies/*immunology ; Blood Transfusion ; Bone Marrow Transplantation ; Cell Degranulation ; Joints/*immunology/pathology ; Male ; Mast Cells/*immunology/transplantation ; Mice ; Mice, Inbred C57BL
    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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  • 5
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    MHC-linked protection from diabetes dissociated from clonal deletion of T cells (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-07-20
    Description: The I-E molecule of the major histocompatibility complex (MHC) can prevent the spontaneous development of diabetes in nonobese diabetic (NOD) mice. The mechanism of this protection has been investigated by breeding wild-type and promoter-mutated E kappa alpha transgenes onto the NOD genetic background. Animals carrying the various mutated transgenes expressed I-E on different subsets of immunocompetent cells, and thus cells important for the I-E protective effect could be identified. Although the wild-type transgene prevented the infiltration of lymphocytes into pancreatic islets, none of the mutants did. However, all of the transgenes could mediate the intrathymic elimination of T cells bearing antigen receptors with variable regions that recognize I-E. Thus, the I-E molecule does not protect NOD mice from diabetes simply by inducing the deletion of self-reactive T cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bohme, J -- Schuhbaur, B -- Kanagawa, O -- Benoist, C -- Mathis, D -- New York, N.Y. -- Science. 1990 Jul 20;249(4966):293-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratoire de Genetique Moleculaire des Eucaryotes du CNRS, Faculte de Medecine, Strasbourg, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2115690" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Clone Cells ; Crosses, Genetic ; Diabetes Mellitus, Experimental/*immunology/prevention & control ; Genes, MHC Class II ; Histocompatibility Antigens Class II/genetics/*immunology ; Islets of Langerhans/immunology ; *Major Histocompatibility Complex ; Mice ; Mice, Mutant Strains ; Mice, Transgenic ; Mutation ; Promoter Regions, Genetic ; Receptors, Antigen, T-Cell/genetics ; T-Lymphocytes/*immunology ; Thymus Gland/immunology
    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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  • 6
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    Immunology. Flow cytometry, amped up (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-05-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Benoist, Christophe -- Hacohen, Nir -- New York, N.Y. -- Science. 2011 May 6;332(6030):677-8. doi: 10.1126/science.1206351.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Harvard Medical School, Boston, MA 02115, USA. cb@hms.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21551055" target="_blank"〉PubMed〈/a〉
    Keywords: Bone Marrow Cells/*cytology/*metabolism ; Flow Cytometry/*methods ; Humans ; Lymphocyte Subsets/*cytology/*metabolism ; Mass Spectrometry/*methods ; Metabolic Networks and Pathways ; Metals, Rare Earth ; Signal Transduction ; Single-Cell Analysis/*methods ; Software
    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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  • 7
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    Positive selection of T cells induced by viral delivery of neopeptides to the thymus (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-01-31
    Description: The relation between an antigenic peptide that can stimulate a mature T cell and the natural peptide that promoted selection of this cell in the thymus is still unknown. An experimental system was devised to address this issue in vivo-mice expressing neopeptides in thymic stromal cells after adenovirus-mediated delivery of invariant chain-peptide fusion proteins. In this system, selection of T cells capable of responding to a given antigenic peptide could be promoted by the peptide itself, by closely related analogs lacking agonist and antagonist activity, or by ostensibly unrelated peptides. However, the precise repertoire of T cells selected was dictated by the particular neopeptide expressed.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nakano, N -- Rooke, R -- Benoist, C -- Mathis, D -- New York, N.Y. -- Science. 1997 Jan 31;275(5300):678-83.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut de Genetique et de Biologie Moleculaire et Cellulaire (INSERM, CNRS, Universite Louis Pasteur), 1 rue Laurent Fries, 67404 Illkirch, C.U. de Strasbourg, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9005856" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoviridae/genetics ; Amino Acid Sequence ; Animals ; Antigen-Presenting Cells/immunology ; Antigens, Differentiation, B-Lymphocyte/genetics ; Cells, Cultured ; Cloning, Molecular ; Cross Reactions ; Cytochrome c Group/immunology ; DNA, Complementary/genetics ; Genetic Vectors ; Histocompatibility Antigens Class II/genetics ; Hybridomas ; Interleukin-2/biosynthesis ; *Lymphocyte Activation ; Mice ; Molecular Sequence Data ; Peptides/chemistry/*immunology ; Receptors, Antigen, T-Cell/*immunology ; Recombinant Fusion Proteins ; T-Lymphocytes/*immunology ; Thymus Gland/cytology/*immunology
    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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  • 8
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    Selection for survival? (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-06-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Benoist, C -- Mathis, D -- New York, N.Y. -- Science. 1997 Jun 27;276(5321):2000-1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut de Genetique et de Biologie Moleculaire et Cellulaire (INSERM, CNRS, ULP), 1 rue Laurent Fries, 6704 Illkirch, C.U. de Strasbourg, France. cb@titus.u-strasbg.fr〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9221508" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CD8-Positive T-Lymphocytes/cytology/*immunology ; Cell Division ; Cell Survival ; Female ; H-2 Antigens/immunology ; H-Y Antigen/immunology ; Histocompatibility Antigen H-2D ; Humans ; *Immunologic Memory ; Lymphocyte Activation ; Male ; Mice ; Mice, Transgenic ; Receptors, Antigen, T-Cell/immunology ; T-Lymphocyte Subsets/cytology/*immunology
    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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  • 9
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    Projection of an immunological self shadow within the thymus by the aire protein (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-10-12
    Description: Humans expressing a defective form of the transcription factor AIRE (autoimmune regulator) develop multiorgan autoimmune disease. We used aire- deficient mice to test the hypothesis that this transcription factor regulates autoimmunity by promoting the ectopic expression of peripheral tissue- restricted antigens in medullary epithelial cells of the thymus. This hypothesis proved correct. The mutant animals exhibited a defined profile of autoimmune diseases that depended on the absence of aire in stromal cells of the thymus. Aire-deficient thymic medullary epithelial cells showed a specific reduction in ectopic transcription of genes encoding peripheral antigens. These findings highlight the importance of thymically imposed "central" tolerance in controlling autoimmunity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Anderson, Mark S -- Venanzi, Emily S -- Klein, Ludger -- Chen, Zhibin -- Berzins, Stuart P -- Turley, Shannon J -- von Boehmer, Harald -- Bronson, Roderick -- Dierich, Andree -- Benoist, Christophe -- Mathis, Diane -- 2 P30 DK36836-16/DK/NIDDK NIH HHS/ -- 2T32 DK07260-26/DK/NIDDK NIH HHS/ -- KO8-DK59958-01A1/DK/NIDDK NIH HHS/ -- R01 DK60027-01/DK/NIDDK NIH HHS/ -- T32CA70083-05/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2002 Nov 15;298(5597):1395-401. Epub 2002 Oct 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section on Immunology and Immunogenetics, Joslin Diabetes Center; Department of Medicine, Brigham and Women's Hospital; Harvard Medical School, 1 Joslin Place, Boston, MA 02215, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12376594" target="_blank"〉PubMed〈/a〉
    Keywords: Aging ; Animals ; Autoantibodies/analysis/blood ; Autoantigens/biosynthesis/genetics ; Autoimmune Diseases/genetics/immunology/metabolism ; Autoimmunity ; Epithelial Cells/physiology ; Female ; Gene Expression Profiling ; Gene Expression Regulation ; Gene Targeting ; Humans ; Lymphocytes/immunology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Polyendocrinopathies, Autoimmune/genetics/immunology/metabolism ; Radiation Chimera ; Reverse Transcriptase Polymerase Chain Reaction ; *Self Tolerance ; Stromal Cells/immunology/metabolism ; T-Lymphocytes/*immunology ; Thymus Gland/cytology/*immunology/*metabolism ; Transcription Factors/genetics/*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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    Nobels: Toll pioneers deserve recognition (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-11-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Allison, James P -- Benoist, Christophe -- Chervonsky, Alexander V -- England -- Nature. 2011 Nov 9;479(7372):178. doi: 10.1038/479178a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22071753" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptive Immunity/immunology ; History, 20th Century ; Immunity, Innate/immunology ; Models, Immunological ; *Nobel Prize ; Toll-Like Receptors/*history/immunology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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