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  • 1
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    Congenital nephrotic syndrome in mice lacking CD2-associated protein (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-10-09
    Description: CD2-associated protein (CD2AP) is an 80-kilodalton protein that is critical for stabilizing contacts between T cells and antigen-presenting cells. In CD2AP-deficient mice, immune function was compromised, but the mice died at 6 to 7 weeks of age from renal failure. In the kidney, CD2AP was expressed primarily in glomerular epithelial cells. Knockout mice exhibited defects in epithelial cell foot processes, accompanied by mesangial cell hyperplasia and extracellular matrix deposition. Supporting a role for CD2AP in the specialized cell junction known as the slit diaphragm, CD2AP associated with nephrin, the primary component of the slit diaphragm.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shih, N Y -- Li, J -- Karpitskii, V -- Nguyen, A -- Dustin, M L -- Kanagawa, O -- Miner, J H -- Shaw, A S -- New York, N.Y. -- Science. 1999 Oct 8;286(5438):312-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Immunology and Department of Pathology, Washington University, Saint Louis, MO 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10514378" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; Animals ; Basement Membrane/ultrastructure ; Cytoskeletal Proteins ; Epithelial Cells/metabolism/ultrastructure ; Extracellular Matrix Proteins/metabolism ; Glomerular Mesangium/metabolism/ultrastructure ; Intercellular Junctions/metabolism/ultrastructure ; Kidney Glomerulus/blood supply/*metabolism/*ultrastructure ; Lymphocyte Activation ; Membrane Proteins ; Mice ; Mice, Knockout ; Microscopy, Electron ; Nephrotic Syndrome/*congenital/genetics/metabolism/pathology ; Proteins/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; T-Lymphocytes/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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  • 2
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    Generation of live young from xenografted mouse ovaries (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-09-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Snow, Melanie -- Cox, Shae-Lee -- Jenkin, Graham -- Trounson, Alan -- Shaw, Jillian -- New York, N.Y. -- Science. 2002 Sep 27;297(5590):2227.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, Monash University, Victoria, Australia, 3800.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12351780" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Embryo Loss ; Embryo Transfer ; Embryonic and Fetal Development ; Female ; Fertility ; Fertilization in Vitro ; Gonadotropins, Equine/administration & dosage ; Male ; Mice ; Mice, Inbred Strains ; Mice, Nude ; Oocytes/*physiology ; Ovariectomy ; Ovary/*transplantation ; Pregnancy ; Pregnancy Outcome ; Rats ; *Reproductive Techniques, Assisted ; *Transplantation, Heterologous
    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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    The immunological synapse: a molecular machine controlling T cell activation (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-10
    Description: The specialized junction between a T lymphocyte and an antigen-presenting cell, the immunological synapse, consists of a central cluster of T cell receptors surrounded by a ring of adhesion molecules. Immunological synapse formation is now shown to be an active and dynamic mechanism that allows T cells to distinguish potential antigenic ligands. Initially, T cell receptor ligands were engaged in an outermost ring of the nascent synapse. Transport of these complexes into the central cluster was dependent on T cell receptor-ligand interaction kinetics. Finally, formation of a stable central cluster at the heart of the synapse was a determinative event for T cell proliferation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grakoui, A -- Bromley, S K -- Sumen, C -- Davis, M M -- Shaw, A S -- Allen, P M -- Dustin, M L -- New York, N.Y. -- Science. 1999 Jul 9;285(5425):221-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Immunology and the Department of Pathology, Washington University School of Medicine, 660 South Euclid Avenue, St. Louis, MO 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10398592" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen-Presenting Cells/immunology/metabolism ; Antigens, CD4/immunology/metabolism ; CHO Cells ; Cell Movement ; Cricetinae ; Cytochrome c Group/immunology/metabolism ; Fluorescence ; Histocompatibility Antigens/immunology/*metabolism ; Intercellular Adhesion Molecule-1/immunology/metabolism ; Ligands ; Lipid Bilayers ; *Lymphocyte Activation ; Mice ; Mice, Transgenic ; Microscopy, Interference ; Models, Immunological ; Peptides/immunology/metabolism ; Receptors, Antigen, T-Cell/immunology/*metabolism ; Signal Transduction ; T-Lymphocytes/*immunology/metabolism ; Time Factors
    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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    T cell receptor signaling precedes immunological synapse formation (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-02-23
    Description: The area of contact between a T cell and an antigen-presenting cell (APC) is known as the immunological synapse. Although its exact function is unknown, one model suggests that it allows for T cell receptor (TCR) clustering and for sustained signaling in T cells for many hours. Here we demonstrate that TCR-mediated tyrosine kinase signaling in naive T cells occurred primarily at the periphery of the synapse and was largely abated before mature immunological synapses had formed. These data suggest that many hours of TCR signaling are not required for T cell activation. These observations challenge current ideas about the role of immunological synapses in T cell activation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, Kyeong-Hee -- Holdorf, Amy D -- Dustin, Michael L -- Chan, Andrew C -- Allen, Paul M -- Shaw, Andrey S -- New York, N.Y. -- Science. 2002 Feb 22;295(5559):1539-42.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and Immunology, Washington University School of Medicine, 660 South Euclid, Box 8118, Saint Louis, MO 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11859198" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen-Presenting Cells/*immunology ; Cell Division ; Cells, Cultured ; Down-Regulation ; Endocytosis ; Enzyme Activation ; Image Processing, Computer-Assisted ; Intercellular Junctions/*immunology/metabolism ; *Lymphocyte Activation ; Lymphocyte Function-Associated Antigen-1/metabolism ; Lymphocyte Specific Protein Tyrosine Kinase p56(lck)/metabolism ; Mice ; Mice, Transgenic ; Peptides/immunology ; Protein-Tyrosine Kinases/metabolism ; Receptor Aggregation ; Receptors, Antigen, T-Cell/immunology/*metabolism ; *Signal Transduction ; T-Lymphocytes/*immunology/metabolism ; Time Factors ; ZAP-70 Protein-Tyrosine Kinase
    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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    The after-hours mutant reveals a role for Fbxl3 in determining mammalian circadian period (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-04-28
    Description: By screening N-ethyl-N-nitrosourea-mutagenized animals for alterations in rhythms of wheel-running activity, we identified a mouse mutation, after hours (Afh). The mutation, a Cys(358)Ser substitution in Fbxl3, an F-box protein with leucine-rich repeats, results in long free-running rhythms of about 27 hours in homozygotes. Circadian transcriptional and translational oscillations are attenuated in Afh mice. The Afh allele significantly affected Per2 expression and delayed the rate of Cry protein degradation in Per2::Luciferase tissue slices. Our in vivo and in vitro studies reveal a central role for Fbxl3 in mammalian circadian timekeeping.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Godinho, Sofia I H -- Maywood, Elizabeth S -- Shaw, Linda -- Tucci, Valter -- Barnard, Alun R -- Busino, Luca -- Pagano, Michele -- Kendall, Rachel -- Quwailid, Mohamed M -- Romero, M Rosario -- O'neill, John -- Chesham, Johanna E -- Brooker, Debra -- Lalanne, Zuzanna -- Hastings, Michael H -- Nolan, Patrick M -- MC_U105170643/Medical Research Council/United Kingdom -- MC_U142684172/Medical Research Council/United Kingdom -- MC_U142684173/Medical Research Council/United Kingdom -- MC_U142684175/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2007 May 11;316(5826):897-900. Epub 2007 Apr 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council (MRC) Mammalian Genetics Unit, Harwell, Oxfordshire OX11 0RD, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17463252" target="_blank"〉PubMed〈/a〉
    Keywords: ARNTL Transcription Factors ; Amino Acid Sequence ; Amino Acid Substitution ; Animals ; Basic Helix-Loop-Helix Transcription Factors/genetics/metabolism ; CLOCK Proteins ; COS Cells ; Cell Cycle Proteins/genetics/metabolism ; Cercopithecus aethiops ; *Circadian Rhythm/genetics ; Crosses, Genetic ; Cryptochromes ; F-Box Proteins/*genetics/*physiology ; Female ; Flavoproteins/genetics/metabolism ; Gene Expression Regulation ; Liver/metabolism ; Lung/metabolism ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C3H ; Molecular Sequence Data ; Nuclear Proteins/genetics/metabolism ; Period Circadian Proteins ; *Point Mutation ; Suprachiasmatic Nucleus/metabolism ; Trans-Activators/genetics/metabolism ; Transcription Factors/genetics/metabolism ; 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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  • 6
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    Immunology. CAR'ing for the skin (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-09-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shaw, Andrey S -- Huang, Yina -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Sep 3;329(5996):1154-5. doi: 10.1126/science.1195337.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and Immunology and Howard Hughes Medical Institute, Washington University School of Medicine, St. Louis, MO 63110, USA. shaw@pathology.wustl.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20813941" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Adhesion Molecules/chemistry/*metabolism ; Coxsackie and Adenovirus Receptor-Like Membrane Protein ; Crystallization ; Epidermis/*immunology/metabolism/ultrastructure ; Hydrogen Bonding ; Ligands ; Lymphocyte Activation ; Mice ; Phosphatidylinositol 3-Kinases/metabolism ; Protein Binding ; Protein Interaction Domains and Motifs ; Protein Multimerization ; Receptors, Antigen, T-Cell, gamma-delta/*immunology/metabolism ; Receptors, Virus/chemistry/*metabolism ; Signal Transduction ; T-Lymphocyte Subsets/*immunology/*metabolism ; Tight Junctions/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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  • 7
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    Exercise and genetic rescue of SCA1 via the transcriptional repressor Capicua (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-11-05
    Description: Spinocerebellar ataxia type 1 (SCA1) is a fatal neurodegenerative disease caused by expansion of a translated CAG repeat in Ataxin-1 (ATXN1). To determine the long-term effects of exercise, we implemented a mild exercise regimen in a mouse model of SCA1 and found a considerable improvement in survival accompanied by up-regulation of epidermal growth factor and consequential down-regulation of Capicua, which is an ATXN1 interactor. Offspring of Capicua mutant mice bred to SCA1 mice showed significant improvement of all disease phenotypes. Although polyglutamine-expanded Atxn1 caused some loss of Capicua function, further reduction of Capicua levels--either genetically or by exercise--mitigated the disease phenotypes by dampening the toxic gain of function. Thus, exercise might have long-term beneficial effects in other ataxias and neurodegenerative diseases.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3232424/" 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/PMC3232424/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fryer, John D -- Yu, Peng -- Kang, Hyojin -- Mandel-Brehm, Caleigh -- Carter, Angela N -- Crespo-Barreto, Juan -- Gao, Yan -- Flora, Adriano -- Shaw, Chad -- Orr, Harry T -- Zoghbi, Huda Y -- 1F32NS055545/NS/NINDS NIH HHS/ -- HD24064/HD/NICHD NIH HHS/ -- NS022920/NS/NINDS NIH HHS/ -- NS045667/NS/NINDS NIH HHS/ -- NS27699/NS/NINDS NIH HHS/ -- NS27699-20S1/NS/NINDS NIH HHS/ -- P30 HD024064/HD/NICHD NIH HHS/ -- P30 HD024064-22/HD/NICHD NIH HHS/ -- P30 HD024064-23/HD/NICHD NIH HHS/ -- R01 NS027699/NS/NINDS NIH HHS/ -- R01 NS027699-20S1/NS/NINDS NIH HHS/ -- R01 NS027699-21/NS/NINDS NIH HHS/ -- R01 NS027699-22/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2011 Nov 4;334(6056):690-3. doi: 10.1126/science.1212673.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22053053" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Ataxin-1 ; Ataxins ; Cerebellum/metabolism ; Disease Models, Animal ; *Exercise Therapy ; Gene Knock-In Techniques ; Mice ; Mice, Inbred C57BL ; Mice, Mutant Strains ; Nerve Tissue Proteins/genetics ; Nuclear Proteins/genetics ; Repressor Proteins/genetics/*physiology ; Spinocerebellar Ataxias/genetics/*therapy
    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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    A secreted PTEN phosphatase that enters cells to alter signaling and survival (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-06-08
    Description: Phosphatase and tensin homolog on chromosome ten (PTEN) is a tumor suppressor and an antagonist of the phosphoinositide-3 kinase (PI3K) pathway. We identified a 576-amino acid translational variant of PTEN, termed PTEN-Long, that arises from an alternative translation start site 519 base pairs upstream of the ATG initiation sequence, adding 173 N-terminal amino acids to the normal PTEN open reading frame. PTEN-Long is a membrane-permeable lipid phosphatase that is secreted from cells and can enter other cells. As an exogenous agent, PTEN-Long antagonized PI3K signaling and induced tumor cell death in vitro and in vivo. By providing a means to restore a functional tumor-suppressor protein to tumor cells, PTEN-Long may have therapeutic uses.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3935617/" 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/PMC3935617/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hopkins, Benjamin D -- Fine, Barry -- Steinbach, Nicole -- Dendy, Meaghan -- Rapp, Zachary -- Shaw, Jacquelyn -- Pappas, Kyrie -- Yu, Jennifer S -- Hodakoski, Cindy -- Mense, Sarah -- Klein, Joshua -- Pegno, Sarah -- Sulis, Maria-Luisa -- Goldstein, Hannah -- Amendolara, Benjamin -- Lei, Liang -- Maurer, Matthew -- Bruce, Jeffrey -- Canoll, Peter -- Hibshoosh, Hanina -- Parsons, Ramon -- 2T32 CA09503/CA/NCI NIH HHS/ -- CA082783/CA/NCI NIH HHS/ -- CA097403/CA/NCI NIH HHS/ -- P01 CA097403/CA/NCI NIH HHS/ -- R01 CA082783/CA/NCI NIH HHS/ -- R01 CA155117/CA/NCI NIH HHS/ -- R01 NS066955/NS/NINDS NIH HHS/ -- R01 NS073610/NS/NINDS NIH HHS/ -- R01NS066955/NS/NINDS NIH HHS/ -- T32 CA009503/CA/NCI NIH HHS/ -- T32 GM008224/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2013 Jul 26;341(6144):399-402. doi: 10.1126/science.1234907. Epub 2013 Jun 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Oncological Sciences, Icahn School of Medicine at Mount Sinai, 1470 Madison Avenue, New York, NY 10029, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23744781" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cell Line, Tumor ; *Cell Survival ; Embryonic Stem Cells ; Glioblastoma/drug therapy/metabolism/pathology ; HEK293 Cells ; Humans ; Mice ; Mice, Nude ; Molecular Sequence Data ; Mutation ; PTEN Phosphohydrolase/*chemistry/genetics/*metabolism/pharmacology ; Peptide Chain Initiation, Translational ; Phosphatidylinositol 3-Kinase/*metabolism ; Phosphorylation ; Proto-Oncogene Proteins c-akt/metabolism ; RNA, Messenger/genetics/metabolism ; *Signal Transduction/drug effects ; Xenograft Model Antitumor Assays
    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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    Cleavage of fibrinogen by proteinases elicits allergic responses through Toll-like receptor 4 (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    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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  • 10
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    Outbreak of poliomyelitis in Hispaniola associated with circulating type 1 vaccine-derived poliovirus (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-03-16
    Description: An outbreak of paralytic poliomyelitis occurred in the Dominican Republic (13 confirmed cases) and Haiti (8 confirmed cases, including 2 fatal cases) during 2000-2001. All but one of the patients were either unvaccinated or incompletely vaccinated children, and cases occurred in communities with very low (7 to 40%) rates of coverage with oral poliovirus vaccine (OPV). The outbreak was associated with the circulation of a derivative of the type 1 OPV strain, probably originating from a single OPV dose given in 1998-1999. The vaccine-derived poliovirus associated with the outbreak had biological properties indistinguishable from those of wild poliovirus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kew, Olen -- Morris-Glasgow, Victoria -- Landaverde, Mauricio -- Burns, Cara -- Shaw, Jing -- Garib, Zacarias -- Andre, Jean -- Blackman, Elizabeth -- Freeman, C Jason -- Jorba, Jaume -- Sutter, Roland -- Tambini, Gina -- Venczel, Linda -- Pedreira, Cristina -- Laender, Fernando -- Shimizu, Hiroyuki -- Yoneyama, Tetsuo -- Miyamura, Tatsuo -- van Der Avoort, Harrie -- Oberste, M Steven -- Kilpatrick, David -- Cochi, Stephen -- Pallansch, Mark -- de Quadros, Ciro -- New York, N.Y. -- Science. 2002 Apr 12;296(5566):356-9. Epub 2002 Mar 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Viral and Rickettsial Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention (CDC), 1600 Clifton Road, Atlanta, GA 30333, USA. okew@cdc.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11896235" target="_blank"〉PubMed〈/a〉
    Keywords: 5' Untranslated Regions ; Adolescent ; Animals ; Capsid/genetics ; Capsid Proteins ; Child ; Child, Preschool ; *Disease Outbreaks ; Dominican Republic/epidemiology ; Female ; Genes, Viral ; Haiti/epidemiology ; Humans ; Immunization Programs ; Infant ; Male ; Mice ; Molecular Sequence Data ; Point Mutation ; Poliomyelitis/*epidemiology/prevention & control/transmission/*virology ; Poliovirus/classification/*genetics/isolation & purification/*pathogenicity ; Poliovirus Vaccine, Oral/*adverse effects ; Population Surveillance ; Recombination, Genetic ; Vaccination ; Virulence
    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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