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  • 1990-1994  (1)
  • 1985-1989  (1)
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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of oral pathology & medicine 17 (1988), S. 0 
    ISSN: 1600-0714
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The purpose of the present report was to document the stress response produced by physical and chemical abuses to human periodontal ligament cells, and to review some of the known functions of stress response proteins produced as a result of such treatments. For these studies human PDL cells were exposed to sublethal challenges of 43°C heat, sodium arsenite and the amino acid analog L-azetidine-2-carboxylic acid (AZC). The cells were labelled with [35S]-methionine and the proteins produced were examined by autofluorography of SDS-PAGE gels. Heat challenges were shown to induce hsps with an apparent mol. wts. of 90K, 68-72K, 41–47K, and 36 K. Arsenite-treated cells produced similar hsps including a 30k protein not produced by other forms of stress. AZC treatment resulted in the production of apparent functionless hsps with apparent molecular weights of 90,000, 72,000, 68,000 and 36,000. The function of these proteins and their possible role in periodontal disease is discussed.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-0428
    Keywords: Diabetic embryopathy ; myo-inositol ; prostaglandins ; neural tube ; mouse embryos
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Neural tube defects in infants of diabetic mothers constitute an important and frequent cause of neonatal mortality/morbidity and long-term chronic handicaps. The mechanism by which normal neural tube fusion occurs is not known. The failure of rostral neural tube fusion seen in mouse embryos incubated in the presence of excess-D-glucose can be significantly prevented by the supplementation of myo-inositol to the culture medium. This protective effect of myo-inositol is reversed by indomethacin, an inhibitor of arachidonic acid metabolism leading to prostaglandin synthesis. Prostaglandin E2 added to the culture medium completely protects against the glucose-induced neural tube defect. These data suggest that the failure of neural tube fusion seen in diabetic embryopathy is mediated through a mechanism involving abnormalities in both the myo-inositol and arachidonic acid pathways, resulting in a functional deficiency of prostaglandins at a critical time of neural tube fusion.
    Type of Medium: Electronic Resource
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