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  • 1
    ISSN: 1438-2199
    Keywords: Keywords: Amino acids ; Kainic acid ; Neurodegeneration ; Excitotoxicity ; Poly(ADP-ribose) polymerase ; PARP ; In vivo
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary. Poly(ADP-ribose) polymerase (PARP) is activated in glutamate-induced toxicity of neurons in culture (Cosi et al., 1994). Since injection of the excitatory amino acid, kainic acid (KA) into the rat striatum induces a delayed neuronal death, the effects of this in vivo excitotoxin lesioning procedure on striatal PARP activity was investigated. PARP activity was measured in striatal extracts both in the absence ("endogenous" activity) and presence ("total" activity) of exogenously-added fragmented DNA. KA (5 nmols/1 μl) produced significant and time-dependent changes in striatal PARP activity, compared to saline-injected control animals: no changes at 6 h after intrastriatal KA, a 68% and 48% decrease in endogenous and total PARP activity respectively at 12 h, a doubling in endogenous PARP activity at 24 h, and a 382% and 60% increase in endogenous and total activities at 1 week after KA. PARP cleavage was not detected at any time point. These results suggest a participation of PARP in KA-induced toxicity in the brain in vivo.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    International journal of clinical oncology 5 (2000), S. 345-354 
    ISSN: 1437-7772
    Keywords: Key words Prostate cancer ; Chromosome ; Loss of heterozygosity ; Tumor suppressor gene ; Metastasis suppressor gene
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Cytogenetic, molecular cytogenetic, and molecular studies of prostate cancer have produced a large volume of data about chromosomal loci that are aberrant in prostate cancer. The cumulative data on prostate cancer reveal allelic losses on chromosome arms 2q, 3p, 5q, 6q, 7q, 8p, 9p, 10p, 10q, 11p, 11q, 12p, 13q, 16q, 17p, 17q, 18q, and 21q, but there is a great deal of variability between studies. In most cases, the frequency of allelic loss is higher in metastatic tissues or hormone-refractory tumors than in primary tumors. There also seem to be discrepancies in the genetic findings depending on methods employed. Molecular genetic studies, using polymerase chain reaction (PCR) analysis of microsatellite markers, demonstrated allelic loss at 7q31.1, whereas fluorescence in situ hybridization analysis showed a gain at the same region. Com-mon sites of allelic loss that are consistently observed by various methods seem to exist on chromosome arms 8p, 10q, 13q, and 16q. PTEN/MMAC1 has been identified on 10q23.3 and was found to be frequently mutated in advanced prostate cancer. Other regions are also considered to harbor genes associated with the development and progression of prostate cancer, and these could be included in the diagnostic methods for the substaging of prostate cancer.
    Type of Medium: Electronic Resource
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