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  • 1
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    Congenital heart disease caused by mutations in the transcription factor NKX2-5 (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-07-04
    Description: Mutations in the gene encoding the homeobox transcription factor NKX2-5 were found to cause nonsyndromic, human congenital heart disease. A dominant disease locus associated with cardiac malformations and atrioventricular conduction abnormalities was mapped to chromosome 5q35, where NKX2-5, a Drosophila tinman homolog, is located. Three different NKX2-5 mutations were identified. Two are predicted to impair binding of NKX2-5 to target DNA, resulting in haploinsufficiency, and a third potentially augments target-DNA binding. These data indicate that NKX2-5 is important for regulation of septation during cardiac morphogenesis and for maturation and maintenance of atrioventricular node function throughout life.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schott, J J -- Benson, D W -- Basson, C T -- Pease, W -- Silberbach, G M -- Moak, J P -- Maron, B J -- Seidman, C E -- Seidman, J G -- New York, N.Y. -- Science. 1998 Jul 3;281(5373):108-11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics and Howard Hughes Medical Institute, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9651244" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Atrioventricular Node/physiopathology ; Chromosome Mapping ; Chromosomes, Human, Pair 5 ; Codon ; Female ; Genes, Dominant ; Genetic Linkage ; Heart Block/*genetics/physiopathology ; Heart Septal Defects, Atrial/*genetics/physiopathology ; Homeodomain Proteins/*genetics/metabolism ; Humans ; Male ; Mice ; Molecular Sequence Data ; Mutation ; Pedigree ; Protein Biosynthesis ; Transcription Factors/*genetics/metabolism ; *Xenopus Proteins
    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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    A small, nonpeptidyl mimic of granulocyte-colony-stimulating factor [see commetns] (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-07-10
    Description: A nonpeptidyl small molecule SB 247464, capable of activating granulocyte-colony-stimulating factor (G-CSF) signal transduction pathways, was identified in a high-throughput assay in cultured cells. Like G-CSF, SB 247464 induced tyrosine phosphorylation of multiple signaling proteins and stimulated primary murine bone marrow cells to form granulocytic colonies in vitro. It also elevated peripheral blood neutrophil counts in mice. The extracellular domain of the murine G-CSF receptor was required for the activity of SB 247464, suggesting that the compound acts by oligomerizing receptor chains. The results indicate that a small molecule can activate a receptor that normally binds a relatively large protein ligand.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tian, S S -- Lamb, P -- King, A G -- Miller, S G -- Kessler, L -- Luengo, J I -- Averill, L -- Johnson, R K -- Gleason, J G -- Pelus, L M -- Dillon, S B -- Rosen, J -- New York, N.Y. -- Science. 1998 Jul 10;281(5374):257-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Transcription Research, Ligand Pharmaceuticals, San Diego, CA 92121, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9657720" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Benzimidazoles/chemistry/metabolism/*pharmacology ; Cell Line ; Colony-Forming Units Assay ; DNA-Binding Proteins/metabolism ; Dimerization ; Female ; Granulocyte Colony-Stimulating Factor/metabolism/pharmacology ; Granulocytes/cytology ; Guanidines/chemistry/metabolism/*pharmacology ; Humans ; Janus Kinase 1 ; Janus Kinase 2 ; Leukocyte Count ; Leukopoiesis ; Mice ; Mice, Inbred C57BL ; *Milk Proteins ; Neutrophils/cytology ; Phosphorylation ; Phosphotyrosine/metabolism ; Protein-Tyrosine Kinases/metabolism ; *Proto-Oncogene Proteins ; Receptors, Granulocyte Colony-Stimulating Factor/chemistry/*metabolism ; Recombinant Fusion Proteins/chemistry/metabolism ; STAT3 Transcription Factor ; STAT5 Transcription Factor ; Signal Transduction/drug effects ; Species Specificity ; Trans-Activators/metabolism ; Transfection ; Tumor Cells, Cultured
    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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    A mouse model of familial hypertrophic cardiomyopathy (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-05-03
    Description: A mouse model of familial hypertrophic cardiomyopathy (FHC) was generated by the introduction of an Arg 403 --〉 Gln mutation into the alpha cardiac myosin heavy chain (MHC) gene. Homozygous alpha MHC 403/403 mice died 7 days after birth, and sedentary heterozygous alpha MHC 403/+ mice survived for 1 year. Cardiac histopathology and dysfunction in the alpha MHC 403/+ mice resembled human FHC. Cardiac dysfunction preceded histopathologic changes, and myocyte disarray, hypertrophy, and fibrosis increased with age. Young male alpha MHC 403/+ mice showed more evidence of disease than did their female counterparts. Preliminary results suggested that exercise capacity may have been compromised in the alpha MHC 403/+ mice. This mouse model may help to define the natural history of FHC.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Geisterfer-Lowrance, A A -- Christe, M -- Conner, D A -- Ingwall, J S -- Schoen, F J -- Seidman, C E -- Seidman, J G -- New York, N.Y. -- Science. 1996 May 3;272(5262):731-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8614836" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cardiac Output ; Cardiomyopathy, Hypertrophic/*genetics/pathology/physiopathology ; *Disease Models, Animal ; Female ; Gene Transfer Techniques ; Heart/*physiopathology ; Heterozygote ; Homozygote ; Humans ; Male ; Mice ; Mice, Mutant Strains ; Molecular Sequence Data ; Mutation ; Myocardium/chemistry/*pathology ; Myosin Heavy Chains/*genetics ; Physical Exertion ; Sex Characteristics ; Ventricular Function, Left
    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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    Tourette syndrome: prediction of phenotypic variation in monozygotic twins by caudate nucleus D2 receptor binding (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-08-30
    Description: Tourette syndrome, a chronic tic disorder with autosomal dominant inheritance, exhibits considerable phenotypic variability even within monozygotic twin pairs. The origins of this variability remain unclear. Recent findings have implicated the caudate nucleus as a locus of pathology, and pharmacological evidence supports dopaminergic involvement. Within monozygotic twins discordant for Tourette syndrome severity, differences in D2 dopamine receptor binding in the head of the caudate nucleus predicted differences in phenotypic severity (r = 0.99); this relation was not observed in putamen. These data may link Tourette syndrome with a spectrum of neuropsychiatric disorders that involve associative striatal circuitry.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wolf, S S -- Jones, D W -- Knable, M B -- Gorey, J G -- Lee, K S -- Hyde, T M -- Coppola, R -- Weinberger, D R -- New York, N.Y. -- Science. 1996 Aug 30;273(5279):1225-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Clinical Brain Disorders Branch, National Institute of Mental Health (NIMH), National Institutes of Health, NIMH Neuroscience Center at St. Elizabeths, 2700 Martin Luther King Jr. Avenue, SE, Washington, DC 200.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8703056" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Benzamides/metabolism ; Caudate Nucleus/*metabolism ; *Diseases in Twins ; Dopamine Antagonists/metabolism ; Female ; Humans ; Male ; Phenotype ; Putamen/metabolism ; Pyrrolidines/metabolism ; Receptors, Dopamine D2/*metabolism ; Tomography, Emission-Computed, Single-Photon ; Tourette Syndrome/genetics/*metabolism ; *Twins, Monozygotic
    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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    Regulation of the proinflammatory effects of Fas ligand (CD95L) (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-11-30
    Description: Fas ligand (CD95L) inhibits T cell function in immune-privileged organs such as the eye and testis, yet in most tissues CD95L expression induces potent inflammatory responses. With a stably transfected colon carcinoma cell line, CT26-CD95L, the molecular basis for these divergent responses was defined. When injected subcutaneously, rejection of CT26-CD95L was caused by neutrophils activated by CD95L. CT26-CD95L survived in the intraocular space because of the presence of transforming growth factor-beta (TGF-beta), which inhibited neutrophil activation. Providing TGF-beta to subcutaneous sites protected against tumor rejection. Thus, these cytokines together generate a microenvironment that promotes immunologic tolerance, which may aid in the amelioration of allograft rejection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, J J -- Sun, Y -- Nabel, G J -- New York, N.Y. -- Science. 1998 Nov 27;282(5394):1714-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, University of Michigan Medical Center, Departments of Internal Medicine and Biological Chemistry, 1150 West Medical Center Drive, 4520 Medical Science Research Building I, Ann Arbor, MI 48109-0650, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9831564" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anterior Chamber ; Apoptosis ; Calcium-Calmodulin-Dependent Protein Kinases/antagonists & inhibitors/metabolism ; Cytotoxicity, Immunologic ; Fas Ligand Protein ; Female ; Graft Rejection ; Humans ; Immune Tolerance ; Inflammation/*immunology ; Jurkat Cells ; Membrane Glycoproteins/*physiology ; Mice ; Mice, Inbred BALB C ; *Mitogen-Activated Protein Kinases ; Neoplasm Transplantation ; Neoplasms, Experimental/*immunology/pathology ; *Neutrophil Activation ; Neutrophils/immunology ; Transfection ; Transforming Growth Factor beta/pharmacology ; Tumor Cells, Cultured ; p38 Mitogen-Activated Protein Kinases
    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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    Frameshift mutants of beta amyloid precursor protein and ubiquitin-B in Alzheimer's and Down patients (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-01-31
    Description: The cerebral cortex of Alzheimer's and Down syndrome patients is characterized by the presence of protein deposits in neurofibrillary tangles, neuritic plaques, and neuropil threads. These structures were shown to contain forms of beta amyloid precursor protein and ubiquitin-B that are aberrant (+1 proteins) in the carboxyl terminus. The +1 proteins were not found in young control patients, whereas the presence of ubiquitin-B+1 in elderly control patients may indicate early stages of neurodegeneration. The two species of +1 proteins displayed cellular colocalization, suggesting a common origin, operating at the transcriptional level or by posttranscriptional editing of RNA. This type of transcript mutation is likely an important factor in the widely occurring nonfamilial early- and late-onset forms of Alzheimer's disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉van Leeuwen, F W -- de Kleijn, D P -- van den Hurk, H H -- Neubauer, A -- Sonnemans, M A -- Sluijs, J A -- Koycu, S -- Ramdjielal, R D -- Salehi, A -- Martens, G J -- Grosveld, F G -- Peter, J -- Burbach, H -- Hol, E M -- New York, N.Y. -- Science. 1998 Jan 9;279(5348):242-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Graduate School for Neurosciences Amsterdam, Netherlands Institute for Brain Research, 1105 AZ Amsterdam, The Netherlands. f.van.leeuwen@nih.knaw.nl〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9422699" target="_blank"〉PubMed〈/a〉
    Keywords: Aged ; Aging/genetics ; Alzheimer Disease/*genetics/metabolism/pathology ; Amino Acid Sequence ; Amyloid beta-Protein Precursor/analysis/chemistry/*genetics ; Base Sequence ; *Brain Chemistry ; Cerebral Cortex/chemistry/pathology ; Cloning, Molecular ; Down Syndrome/*genetics/metabolism/pathology ; Female ; *Frameshift Mutation ; Hippocampus/chemistry/pathology ; Humans ; Male ; Molecular Sequence Data ; Neurites/chemistry ; Neurofibrillary Tangles/chemistry ; Neuropil/chemistry ; Polymerase Chain Reaction ; RNA Editing ; Repetitive Sequences, Nucleic Acid ; Sequence Deletion ; Transcription, Genetic ; Ubiquitins/analysis/chemistry/*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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  • 7
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    T cell awareness of paternal alloantigens during pregnancy (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-10-27
    Description: During pregnancy a semiallogeneic fetus survives despite the presence of maternal T cells specific for paternally inherited histocompatibility antigens. A mouse transgenic for a T cell receptor recognizing the major histocompatibility (MHC) antigen H-2Kb was used to follow the fate of T cells reactive to paternal alloantigens. In contrast to syngeneic and third-party allogeneic pregnancies, mice bearing a Kb-positive conceptus had reduced numbers of Kb-reactive T cells and accepted Kb-positive tumor grafts. T cell phenotype and responsiveness were restored after delivery. Thus, during pregnancy maternal T cells acquire a transient state of tolerance specific for paternal alloantigens.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tafuri, A -- Alferink, J -- Moller, P -- Hammerling, G J -- Arnold, B -- New York, N.Y. -- Science. 1995 Oct 27;270(5236):630-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Tumor Immunology Program, Deutsches Krebsforschungszentrum (DKFZ), Heidelberg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7570020" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CD4-Positive T-Lymphocytes/immunology ; CD8-Positive T-Lymphocytes/immunology ; Fathers ; Female ; Fetus/*immunology ; Graft Rejection ; H-2 Antigens/*immunology ; *Immune Tolerance ; Male ; Mice ; Mice, Inbred C57BL ; Mice, SCID ; Mice, Transgenic ; Neoplasm Transplantation ; Phenotype ; Placenta/immunology ; Pregnancy ; Pregnancy, Animal/*immunology ; Receptors, Antigen, T-Cell/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
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  • 8
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    Immunostimulatory DNA sequences necessary for effective intradermal gene immunization (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-07-19
    Description: Vaccination with naked DNA elicits cellular and humoral immune responses that have a T helper cell type 1 bias. However, plasmid vectors expressing large amounts of gene product do not necessarily induce immune responses to the encoded antigens. Instead, the immunogenicity of plasmid DNA (pDNA) requires short immunostimulatory DNA sequences (ISS) that contain a CpG dinucleotide in a particular base context. Human monocytes transfected with pDNA or double-stranded oligonucleotides containing the ISS, but not those transfected with ISS-deficient pDNA or oligonucleotides, transcribed large amounts of interferon-alpha, interferon-beta, and interleukin-12. Although ISS are necessary for gene vaccination, they down-regulate gene expression and thus may interfere with gene replacement therapy by inducing proinflammatory cytokines.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sato, Y -- Roman, M -- Tighe, H -- Lee, D -- Corr, M -- Nguyen, M D -- Silverman, G J -- Lotz, M -- Carson, D A -- Raz, E -- AI36214/AI/NIAID NIH HHS/ -- AI37305/AI/NIAID NIH HHS/ -- AR41897/AR/NIAMS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1996 Jul 19;273(5273):352-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine and The Sam and Rose Stein Institute for Research on Aging, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0663, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8662521" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Ampicillin Resistance/*genetics ; Animals ; *Antibody Formation ; Base Sequence ; CpG Islands ; Cytokines/*biosynthesis ; DNA/chemistry/genetics/*immunology ; Female ; Gene Expression Regulation ; Genetic Vectors ; Humans ; Injections, Intradermal ; Interferons/biosynthesis ; Interleukin-12/biosynthesis ; Mice ; Mice, Inbred BALB C ; Molecular Sequence Data ; Monocytes/immunology ; Plasmids/genetics/*immunology ; Th1 Cells/immunology ; Transfection ; *Vaccination ; beta-Galactosidase/*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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    Impaired energy homeostasis in C/EBP alpha knockout mice (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-08-25
    Description: Mice homozygous for the targeted deletion of the c/ebp alpha gene, which expresses the CCAAT/enhancer-binding protein alpha (C/EBP alpha), did not store hepatic glycogen and died from hypoglycemia within 8 hours after birth. In these mutant mice, the amounts of glycogen synthase messenger RNA were 50 to 70 percent of normal and the transcriptional induction of the genes for two gluconeogenic enzymes, phosphoenolpyruvate carboxykinase and glucose-6-phosphatase, was delayed. The hepatocytes and adipocytes of the mutant mice failed to accumulate lipid and the expression of the gene for uncoupling protein, the defining marker of brown adipose tissue, was reduced. This study demonstrates that C/EBP alpha is critical for the establishment and maintenance of energy homeostasis in neonates.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, N D -- Finegold, M J -- Bradley, A -- Ou, C N -- Abdelsayed, S V -- Wilde, M D -- Taylor, L R -- Wilson, D R -- Darlington, G J -- DK 45285/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1995 Aug 25;269(5227):1108-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, 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/7652557" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue/metabolism ; Adipose Tissue, Brown/metabolism ; Animals ; Animals, Newborn ; Blood Glucose/metabolism ; CCAAT-Enhancer-Binding Proteins ; Carrier Proteins/genetics ; DNA-Binding Proteins/genetics/*physiology ; *Energy Metabolism ; Female ; Gene Expression Regulation ; Glucose-6-Phosphatase/genetics ; Glycogen Synthase/genetics/metabolism ; Homeostasis ; Humans ; Ion Channels ; Lipid Metabolism ; Liver/metabolism ; Liver Glycogen/metabolism ; Male ; Membrane Proteins/genetics ; Mice ; Mice, Knockout ; Mitochondrial Proteins ; Nuclear Proteins/genetics/*physiology ; Phosphoenolpyruvate Carboxykinase (GTP)/genetics ; RNA, Messenger/metabolism ; Serum Albumin/genetics
    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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  • 10
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    Extragalactic diffuse (C II) emission (1995)
    In:  Other Sources
    Details
    Publication Date: 2013-08-29
    Description: The 158 micro m (CII) line has been mapped in the galaxies Centaurus A, M83, NGC 6946, and NGC 891. The emission exists over very large scales, peaking in the nuclei and extending beyond the spiral arms and molecular disks. While most of the (CII) emission from the nuclei and spiral arms originates in photodissociated gas, the diffuse atomic gas can account for much of the (CII) emission in the extended regions.
    Keywords: SPACE RADIATION
    Type: Astronomical Society of the Pacific, Airborne Astronomy Symposium on the Galactic Ecosystem: From Gas to Stars to Dust, Volume 73; p 181-184
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