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  • Electronic Resource  (3)
  • 1995-1999  (3)
  • 1996  (2)
  • 1995  (1)
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  • Electronic Resource  (3)
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  • 1995-1999  (3)
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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 65 (1995), S. 0 
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Excessive free radical formation or antioxidant enzyme deficiency can result in oxidative stress, a mechanism proposed in the toxicity of MPTP and in the etiology of Parkinson's disease (PD). However, it is unclear if altered antioxidant enzyme activity is sufficient to increase lipid peroxidation in PD. We therefore investigated if MPTP can alter the activity of the antioxidant enzymes, superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-PX) and the level of lipid peroxidation. l-Deprenyl, prior to MPTP administration, is used to inhibit MPP+ formation and its subsequent effect on antioxidant enzymes. MPTP induced a threefold increase in SOD activity in the striatum of C57BL/6 mice. No parallel increase in GSH-PX or CAT activities was observed, while striatal lipid peroxidation decreased. At the level of the substantia nigra (SN), even though increases in CAT activity and reduction in SOD and GSH-PX activities were detected, lipid peroxidation was not altered. Interestingly, l-deprenyl induced similar changes in antioxidant enzymes and lipid peroxidation levels, as did MPTP. Taken together, these results suggest that an alteration in SOD activity, without compensatory increases in CAT or GSH-PX activities, is not sufficient to induce lipid peroxidation.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 777 (1996), S. 0 
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Notes: Apolipoprotein E is a plasma cholesterol and phospholipid transporter which plays a central role in lipoprotein metabolism in the brain. Apolipoprotein E is a polymorphic protein with three common alleles in the general population, designated ε2, ε3 and ε4 coding for proteins ApoE2, ApoE3 and ApoE4, respectively. Recent findings have demonstrated a significant relationship between the ε4 allele and late onset familial and sporadic Alzheimer's disease. We examined several classical neuropathological hallmarks of Alzheimer's disease to determine whether they might be related to apolipoprotein E genotype: the presence of intracellular neurofibrillary tangles, extracellular senile plaques, and the attenuation of choline acetyltransferase activity. Significant correlations were found between ε4 allele copy number and senile plaque density in the frontal, parietal and fusiform cortical areas. Similarly, significant correlations were also found with increased neurofibrillary tangle number in the frontal and fusiform cortex. Interestingly, there was an inverse correlation between the ε4 allele with temporal cortical choline acetyltransferase activity. To further define the specific function of ApoE4, cultured rat hippocampal neurons were used to investigate interactions involving β-amyloid protein. In this model, ApoE4 (but not ApoE2) was able to reverse the neuroprotective effects of β-amyloid. ApoE3 was demonstrated to increase the internalization of β-amyloid peptide into these neurons. Taken together, these results support the involvement of ApoE4 in the pathogenesis of Alzheimer's disease and also provide some explanations for the possible function of this protein.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Physics and chemistry of minerals 23 (1996), S. 337-344 
    ISSN: 1432-2021
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Geosciences , Physics
    Notes: Abstract Dislocation configurations in natural single crystals of CaTiO3 perovskite deformed in high-temperature creep were examined and characterized by transmission electron microscopy. Screw dislocations with Burgers vector [100]pc and [011]pc, dissociated on the $$(01\bar 1)_{{\text{pc}}} $$ plane, form rectangular networks with extended four-fold nodes in the shape of octagons, a configuration never observed in any of the previously investigated perovskites, except CaGeO3. Screw dislocations with Burgers vector [101]pc and $$(\bar 101)_{{\text{pc}}} $$ , on the (010)pc plane, react to form a twist wall; the dislocations with Burgers vector [002] produced by the reaction decompose into two perfect dislocations [001]pc. This results in a new configuration, never observed before, with three-fold nodes at the corners of rectangles. Both the octagonal extended nodes and the junctions decomposed into perfect dislocations are seen in samples deformed indifferently by slip on {100}pc or {110}pc planes, but they seem to appear only above 1520 K, in the cubic phase.
    Type of Medium: Electronic Resource
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