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  • 1
    ISSN: 1432-2277
    Keywords: Key words Geranylgeranylacetone ; Heat-shock protein 72 ; Liver transplantation ; Warm ischemic injury ; Ischemia reperfusion injury
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract It is well known that heat-shock proteins (HSPs) have a cytoprotective function as “molecular chaperones” when cells are exposed to several stress conditions. Geranylgeranylacetone (GGA) is an antiulcer drug that was developed in Japan and it has recently been reported to induce HSP72 in rat gastric mucosa. In this experiment, we investigated the induction of HSP72 in rat liver in response to oral administration of GGA and assessed its ability to induce tolerance to warm ischemic injury by this approach. We prepared donor rats by orally administering GGA to them and compared HSP72 expression in graft liver, survival rates, and serum TNF-α concentrations after liver transplantation with the findings in controls. The survival rates were significantly increased when the livers were obtained from donor rats given GGA. Western blotting revealed expression of HSP72 in graft livers given GGA, and the serum TNF-α levels were significantly suppressed in the rats given GGA. Oral administration of GGA induced HSP72 in graft livers, and they were better able to tolerate warm ischemic injury. Oral administration of GGA appears to provide a promising new strategy for preventing ischemia-reperfusion injury.
    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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