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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    International journal of urology 5 (1998), S. 0 
    ISSN: 1442-2042
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background: information concerning the mechanisms underlying recovery from hydronephrosis is limited. The frequency of apoptosis during healing from hydronephrosis was studied using a rat kidney model. Methods: The presence of apoptosis was studied using an in situ DNA 3 end labeling method, electron microscopy, and agarose gel electrophoresis. Results: The degree of apoptosis in both the medulla and cortex gradually increased during ureteral obstruction as shown by in situ DNA 3 end labeling. Release of the ureteral obstruction resulted in a further increase in the degree of apoptosis in the medulla and cortex. The increase in apoptosis in the medulla was transient and lasted for only 4 days following release, while that in the cortex continued for at least 3 weeks. Apoptosis in the glomerulus was not observed. Electron microscopy revealed cells with aggregated chromatin in compact granular masses that abutted the nuclear membrane. Following release of ureteral obstruction, DNA fragmentation characteristic of apoptosis was visible on agarose gel electrophoresis. Conclusion: These results suggest that apoptosis is involved in post-obstructive tubular damage in the rat kidney.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-0533
    Keywords: Key words     Calcium ; Ischemia ; Cerebellum ; Purkinje cell ; Microfluorometry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract      Changes in levels of intracellular calcium ion ([Ca2+]i) induced by in vitro ischemic conditions in gerbil cerebellar and hippocampal slices were investigated using a calcium imaging system and electron microscopy. When the cerebellar slice was perfused with a glucose-free physiological medium equilibrated with a 95% N2/5% CO2 gas mixture (in vitro ischemic medium), a large [Ca2+]i elevation was region-specifically induced in the molecular layer of the cerebellar cortex (a dendritic field of Purkinje cells). When the hippocampal slice was perfused with in vitro ischemic medium, a large [Ca2+]i elevation was region-specifically induced in CA1 field of the hippocampal slices. Electron microscopic examinations showed that the large [Ca2+]i elevations occurred in Purkinje cells and CA1 pyramidal neurons. To isolate Ca2+ release from intracellular Ca2+ store sites, the slices were perfused with Ca2+-free in vitro ischemic medium. The increases in [Ca2+]i in both cerebellar and hippocampal slices were significantly lower than those observed in the slices perfused with the Ca2+-containing in vitro ischemic medium. However, the suppression of the [Ca2+]i elevation in the molecular layer of the cerebellar slices was smaller than that in the CA1 field of the hippocampal slices. These results reinforce the hypothesis that calcium plays a pivotal role in the development of ischemia-induced neuronal death, and suggest that Ca2+ release from intracellular Ca2+ store sites may play an important role in the ischemia-induced [Ca2+]i elevation in Purkinje cells.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-0533
    Keywords: Calcium ; Ischemia ; Cerebellum ; Purkinje cell ; Microfluorometry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Changes in levels of intracellular calcium ion ([Ca2+]i) induced by in vitro ischemic conditions in gerbil cerebellar and hippocampal slices were investigated using a calcium imaging system and electron microscopy. When the cerebellar slice was perfused with a glucose-free physiological medium equilibrated with a 95% N2/5% CO2 gas mixture (in vitro ischemic medium), a large [Ca2+]i elevation was region-specifically induced in the molecular laver of the cerebellar cortex (a dendritic field of Purkinje cells). When the hippocampal slice was perfused with in vitro ischemic medium, a large [Ca2+]i elevation was region-specifically induced in CA1 field of the hippocampal slices. Electron microscopic examinations showed that the large [Ca2+]i elevations occurred in Purkinje cells and CA1 pyramidal neurons. To isolate Ca2+ release from intracellular Ca2+ store sites, the slices were perfused with Ca2+-free in vitro ischemic medium. the increases in [Ca2+]i in both cerebellar and hippocampal slices were significantly lower than those observed in the slices perfused with the Ca2+-containing in vitro ischemic medium. However, the suppression of the [Ca2+]i-elevation in the molecular layer of the cerebellar slices was smaller than that in the CA1 field of the hippocampal slices. These results reinforce the hypothesis that calcium plays a pivotal role in the development of ischemia-induced neuronal death, and suggest that Ca2+ release from intracellular Ca2+ store sites may play an important role in the ischemia-induced [Ca2+]i elevation in Purkinje cells.
    Type of Medium: Electronic Resource
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