Search Results - (Author, Cooperation:L. S. Birnbaum)

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  1. 1
    Staff View
    Publication Date:
    2016-03-26
    Publisher:
    American Association for the Advancement of Science (AAAS)
    Print ISSN:
    0036-8075
    Electronic ISSN:
    1095-9203
    Topics:
    Biology
    Chemistry and Pharmacology
    Computer Science
    Medicine
    Natural Sciences in General
    Physics
    Keywords:
    Animals ; Biomedical Research/*economics ; Humans ; National Institutes of Health (U.S.)/*economics
    Published by:
    Latest Papers from Table of Contents or Articles in Press
  2. 2
    P. J. Landrigan ; R. O. Wright ; L. S. Birnbaum
    American Association for the Advancement of Science (AAAS)
    Published 2013
    Staff View
    Publication Date:
    2013-12-21
    Publisher:
    American Association for the Advancement of Science (AAAS)
    Print ISSN:
    0036-8075
    Electronic ISSN:
    1095-9203
    Topics:
    Biology
    Chemistry and Pharmacology
    Computer Science
    Medicine
    Natural Sciences in General
    Physics
    Keywords:
    Animals ; Environmental Pollutants/*toxicity ; Environmental Pollution/*prevention & control ; Humans ; *International Cooperation ; Mercury Poisoning/*prevention & control ; Methylmercury Compounds/*toxicity
    Published by:
    Latest Papers from Table of Contents or Articles in Press
  3. 3
    Weber, H. ; Birnbaum, L. S.
    Springer
    Published 1985
    Staff View
    ISSN:
    1432-0738
    Keywords:
    Cleft palate ; TCDD ; TCDF ; Distribution and excretion in pregnant mice
    Source:
    Springer Online Journal Archives 1860-2000
    Topics:
    Medicine
    Notes:
    Abstract The distribution and excretion of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and 2,3,7,8-tetrachlordibenzofuran (TCDF) were studied in pregnant C57BL/6N mice following an oral dose of 30 μg/kg 14C-TCDD and 800 μg/kg 14C-TCDF on gestation day 11. The distribution in maternal blood and liver and excretion in urine and feces was similar to that previously reported in males of the same strain. However, the rates of elimination were more rapid in pregnant females for both chemicals. This was more pronounced for TCDD than for TCDF. At all time points examined, the levels of radioactivity in the individual embryos were below 0.5% of the total TCDD dose and below 0.05% of the total TCDF dose. Assuming that all radioactive material found in embryos was unmetabolized compound, no more than 2.6 ng (8 pmoles) TCDD and 6.4 ng (21 pmoles) TCDF per g tissue were detected. In light of recent findings which strongly suggest a direct effect of TCDD and related compounds on embryonic palatal tissue, our data clearly support the potent teratogenic effect of TCDD and TCDF on the development of the secondary palate.
    Type of Medium:
    Electronic Resource
    URL:
    Articles: DFG German National Licenses
  4. 4
    Abbott, B. D. ; Birnbaum, L. S. ; Perdew, G. H.

    New York, NY [u.a.] : Wiley-Blackwell
    Published 1995
    Staff View
    ISSN:
    1058-8388
    Keywords:
    Aryl hydrocarbon receptor ; Aryl hydrocarbon nuclear translocator ; Dioxin ; Life and Medical Sciences ; Cell & Developmental Biology
    Source:
    Wiley InterScience Backfile Collection 1832-2000
    Topics:
    Medicine
    Notes:
    The aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor with a basic region/helix-loop-helix (bHLH) motif. AhR has been sequenced and the functional domains defined and there is information on the formation of complexes with other peptides and interactions with DNA, although these areas continue to be investigated. AhR mediates many biological effects such as developmental toxicity, including induction of cleft palate and hydronephrosis. This regulatory protein is expressed in embryonic liver and has been immunohistochemically localized in cells of human and mouse secondary palate. The expression of AhR in embryonic tissues and its ability to disrupt development suggests a significant role for this protein in development. The present study examines the pattern of AhR expression in the C57BL/6N mouse embryo from gestation days (GD) 10-16, using in situ hybridization and immunohistochemical analysis. AhR mRNA was localized with 35S-RNA antisense riboprobe (cAh1 probe, 1.8 Kb amino terminal DNA). AhR protein was localized with purified monoclonal antibody (RPT-9) raised against the N-terminal peptide sequence. AhR mRNA and protein were expressed in GD 10-13 neuroepithelium, and as development progressed the levels in brain decreased. GD 10-12 embryos also showed AhR in branchial arches, heart, somites, and liver. AhR protein and mRNA in heart were highest at GD 10-11 and decreased with age. In liver, AhR mRNA and protein levels increased and nuclear localization became more pronounced with gestational age. In GD 14-16 embryos levels in liver and adrenal were highest, but AhR was present in ectoderm, bone, and muscle. AhR expression was specific for both cell type, organ/tissue, and developmental stage, suggesting that this novel ligand-activated transcriptional regulator may be important in normal embryonic development. © 1995 wiley-Liss, Inc.This article is a US Government work and, as such, is in the public domain in the United States of America.
    Additional Material:
    5 Ill.
    Type of Medium:
    Electronic Resource
    URL:
    Articles: DFG German National Licenses