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  • 1
    Electronic Resource
    Electronic Resource
    Ca2+ and Reactive Oxygen Species in Staurosporine-Induced Neuronal Apoptosis (1997)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 68 (1997), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Staurosporine (0.03–0.5 µM) induced a dose-dependent, apoptotic degeneration in cultured rat hippocampal neurons that was sensitive to 24-h pretreatments with the protein synthesis inhibitor cycloheximide (1 µM) or the cell cycle inhibitor mimosine (100 µM). To investigate the role of Ca2+ and reactive oxygen species in staurosporine-induced neuronal apoptosis, we overexpressed calbindin D28K, a Ca2+ binding protein, and Cu/Zn superoxide dismutase, an antioxidative enzyme, in the hippocampal neurons using adenovirus-mediated gene transfer. Infection of the cultures with the recombinant adenoviruses (100 multiplicity of infection) resulted in a stable expression of the respective proteins assessed 48 h later. Overexpression of both calbindin D28K and Cu/Zn superoxide dismutase significantly reduced staurosporine neurotoxicity compared with control cultures infected with a β-galactosidase overexpressing adenovirus. Staurosporine-induced neuronal apoptosis was also significantly reduced when the culture medium was supplemented with 10 or 30 mM K+, suggesting that Ca2+ influx via voltage-sensitive Ca2+ channels reduces this apoptotic cell death. In contrast, neither the glutamate receptor agonist NMDA (1–10 µM) nor the NMDA receptor antagonist dizocilpine (MK-801; 1 µM) was able to reduce staurosporine neurotoxicity. Cultures treated with the antioxidants U-74500A (1–10 µM) and N-acetylcysteine (100 µM) also demonstrated reduced staurosporine neurotoxicity. These results suggest a fundamental role for both Ca2+ and reactive oxygen species in staurosporine-induced neuronal apoptosis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.1997.68041679.x
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  • 2
    Electronic Resource
    Electronic Resource
    No correlation between aggregates of Cu/Zn superoxide dismutase and cell death in familial amyotrophic lateral sclerosis (2002)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 82 (2002), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Aggregates of Cu/Zn superoxide dismutase (SOD) have been demonstrated in familial amyotrophic lateral sclerosis (FALS) and other neurodegenerative diseases; however, their role in disease pathogenesis is unclear. In this study, we investigated the presence of SOD aggregates in nerve growth factor (NGF)-differentiated PC12 cells and cell viability following: (i) transduction with replication-deficient recombinant adenoviruses (AdVs) expressing wild-type SOD (SODWT) or mutant SOD (SODMT, V148G or A4V); (ii) transfection of yellow fluorescent protein-tagged SODWT (SODWT-YFP) or SODMT (SODA4V-YFP, SODV148G-YFP). SOD aggregates were more prominent in cells following transduction of AdSODMT than AdSODWT and following treatment with H2O2, suggesting that mutant SOD leads to oxidation of cellular components. In addition, cells expressing SODMT-YFP yielded SOD aggregates that were significantly larger and more frequent than SOD aggregates in cells expressing SODWT-YFP. Proteasome inhibitors, but not cathepsin B inhibitors, increased aggregate formation but did not increase cell death. In addition, treatments that increased cell viability did not significantly decrease SOD aggregates. Taken together, our data demonstrate that there is no association between SOD aggregates and cell death in FALS.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.2002.01056.x
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  • 3
    Electronic Resource
    Electronic Resource
    Non-productive paramyxovirus infection: Nariva virus infection in hamsters (1979)
    Springer
    Archives of virology 62 (1979), S. 229-240 
    Details
    ISSN: 1432-8798
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The pathogenesis of infection with Nariva virus (NV)—recently classified as a paramyxovirus—was studied in the hamster, an animal closely related to the natural host. Intracranial inoculation of suckling hamsters produces an acute necrotizing encephalitis with large amounts of infectious virus and virus antigen in the brain. In contrast, weanling hamsters have only small amounts of infectious virus and only early in the disease, when they are well; later, when clinically ill, they have a non-productive infection with continuing evidence of viral antigen, but no detectable infectious virus. Weanlings die later than sucklings with less cerebral parenchymal necrosis. The integrity of the immune system affects the expression of NV since brain tissue from anti-lymphocyte serum (ALS) treated infected weanling hamsters have more infectious virus, and for longer periods, than brain tissue from untreated infected weanling hamsters. Changing susceptibility of the host's neural cells may also be involved in determining the course of the illness and expression of the virus since: 1) ALS treatment does not influence the clinical course of the disease or pathology, 2) ALS treated weanlings still have much lower levels of infectious virus than sucklings, 3) infected weanling and suckling hamsters have a similar time course of development of NV neutralizing antibody.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01317555
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  • 4
    Electronic Resource
    Electronic Resource
    Neuropathy accompanying IgMλ monoclonal gammopathy (1983)
    Springer
    Acta neuropathologica 59 (1983), S. 255-261 
    Details
    ISSN: 1432-0533
    Keywords: IgM monoclonal gammopathy ; Neuropathy ; Myelin-associated glycoprotein
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A set of observations made on a patient with IgMλ monoclonal gammopathy and neuropathy implicate humoral immunity in the pathogenesis of the neuropathy. A sural nerve biopsy from the patient showed a characteristic increase in the width of the intraperiod lines. Deposits of μ-heavy chains and λ-light chains were found in myelin sheaths of the nerve biopsy. Immunohistochemically, it was demonstrated that μ-heavy chains and λ-light chains from the patient's serum bound to myelin sheaths of normal peripheral nerves and to a lesser extent to myelin sheaths in the central nervous system (CNS). By immunoblots it was demonstrated that μ-heavy chains and λ-light chains from the patient's serum bound to myelin associated glycoprotein but to no other antigens from the peripheral and central nervous systems. γ and α heavy chains and ϰ light chains from the patient's serum were also shown to bind to myelin-associated glycoprotein but not as distinctly as the μ and λ chains. It is postulated that the monoclonal gammopathy may have arisen on the background of polyclonal autoimmune attack directed against myelin-assoiated glycoprotein.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00691490
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    Paper (German National Licenses)
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