Search Results - (Author, Cooperation:S. C. Phillips)

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  1. 1
    Staff View
    Publication Date:
    2015-07-25
    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:
    Aquatic Organisms/*classification/genetics/metabolism ; Archaea/*classification/genetics/metabolism ; Bacteria/*classification/genetics/metabolism ; Biomarkers/metabolism ; Carbon Dioxide/metabolism ; Coal/*microbiology ; Geologic Sediments/*microbiology ; Japan ; Methane/metabolism ; Methanococcus/classification/genetics/metabolism ; Methanosarcina barkeri/classification/genetics/metabolism ; *Microbial Consortia ; Pacific Ocean ; Seawater/*microbiology
    Published by:
    http://www.aaas.org/

    Latest Papers from Table of Contents or Articles in Press
  2. 2
    Phillips, S. C. ; Cragg, B. G.
    Springer
    Published 1984
    Staff View
    ISSN:
    1432-0533
    Keywords:
    Thiamine deficiency ; Alcohol ; Brain pathology ; Blood-brain barrier ; Rats
    Source:
    Springer Online Journal Archives 1860-2000
    Topics:
    Medicine
    Notes:
    Summary Rats maintained on a thiamine-deficient diet for 38 days lost weight and showed neurological symptoms. The PA value, representing the permeability of the blood-brain barrier to14C-sucrose, was significantly increased whether urethane or ethanol was used as anaesthetic. This increase was prevented by giving rats on the same diet injections of thiamine twice weekly. Barrier function was normalised by injecting thiamine into deficient rats for just 3 days before biopsy. The brains of the thiamine-deficient rats were stained by the Fink-Heimer method but showed no degenerating axons except for silver grains in the glomeruli of the olfactory bulb. Other rats were maintained on the same diet for 38 days and additionally exposed to ethanol vapour for 16 h per day. This resulted in a similar loss of weight but a greater leakage of the blood-brain barrier. The latter was normalised by a thiamine injection only 24 h before biopsy, but was not reduced by withdrawal of ethanol for 3 days before biopsy. Axonal degeneration was present in the olfactory glomeruli. However, no lesions or extravasated blood cells were seen in any brains, there was no change in brain water indicative of oedema and no degeneration in retina, distal peripheral nerves or leg muscles. The relation of these and other experimental findings to alcohol-related brain damage is considered.
    Type of Medium:
    Electronic Resource
    URL:
    http://dx.doi.org/10.1007/BF00691858

    Articles: DFG German National Licenses
  3. 3
    Phillips, S. C.
    Springer
    Published 1987
    Staff View
    ISSN:
    1432-0533
    Keywords:
    Thiamine deficiency ; Ethanol ; Neural degeneration ; Mice
    Source:
    Springer Online Journal Archives 1860-2000
    Topics:
    Medicine
    Notes:
    Summary Groups of adult male mice were either fed a thiamine-deficient diet for 10 weeks and thereafter treated with ethanol by making them inhale vapourized cane spirit for 10 weeks, or given both treatments simultaneously. The brains of these mice were then searched for degeneration using both light and electron microscopy. No degenerating nerve cells were observed in any animal in the cerebral cortex, hippocampus, cerebellum, olfactory bulbs, midbrain or hindbrain. However, axon terminal degeneration was seen in the olfactory bulbs and deep cerebellar nuclei in mice given the combined treatment. No cerebellar degeneration was found and only little degeneration was present in the olfactory bulbs of mice given the two treatments at different times. Thus, the combined treatment of alcohol and thiamine deficiency produced more brain damage than the sum of that produced by the two treatments given separately. This represents the first experimental in vivo demonstration of a biochemical interaction between these two factors in alcohol-related brain damage. The findings of long-term animal treatment with models using thiamine antagonists are compared.
    Type of Medium:
    Electronic Resource
    URL:
    http://dx.doi.org/10.1007/BF00693784

    Articles: DFG German National Licenses