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  • Frontiers Media SA  (4)
  • 2000-2004  (4)
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  • Frontiers Media SA  (4)
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  • 2000-2004  (4)
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  • 1
    Online Resource
    Online Resource
    Frontiers Media SA ; 2003
    In:  British Journal of Biomedical Science Vol. 60, No. 1 ( 2003-01), p. 22-25
    In: British Journal of Biomedical Science, Frontiers Media SA, Vol. 60, No. 1 ( 2003-01), p. 22-25
    Type of Medium: Online Resource
    ISSN: 0967-4845
    Language: English
    Publisher: Frontiers Media SA
    Publication Date: 2003
    detail.hit.zdb_id: 1152119-3
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  • 2
    Online Resource
    Online Resource
    Frontiers Media SA ; 2002
    In:  British Journal of Biomedical Science Vol. 59, No. 2 ( 2002-01), p. 112-113
    In: British Journal of Biomedical Science, Frontiers Media SA, Vol. 59, No. 2 ( 2002-01), p. 112-113
    Type of Medium: Online Resource
    ISSN: 0967-4845
    Language: English
    Publisher: Frontiers Media SA
    Publication Date: 2002
    detail.hit.zdb_id: 1152119-3
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  • 3
    Online Resource
    Online Resource
    Frontiers Media SA ; 2001
    In:  Experimental Biology and Medicine Vol. 226, No. 10 ( 2001-10), p. 927-933
    In: Experimental Biology and Medicine, Frontiers Media SA, Vol. 226, No. 10 ( 2001-10), p. 927-933
    Abstract: Activation of p38 kinase by osmotic stress has been documented in many cells; however, no report has distinguished the effects of cell volume on p38 activity from the effects of the altered osmotic condition per se. Here we report asymmetrical activation of astrocyte p38 mitogen-activated protein (MAP) kinase in response to volume increases and volume decreases. We separate effects of cell volume changes from the effects of osmotic exposure on p38 activation. Exposure to 400, 500, or 600 mOsm phosphate-buffered saline (PBS) caused cell shrinkage and an osmolality-dependent increase in p38 activity to 175%, 409%, or 518%, respectively, compared with cells maintained in control conditions (290 mOsm). Likewise, hyposmotic conditions ranging from 250 to 57 mOsm PBS caused the same activation of p38 (approximately 300% of the control value within 10 min). The activity in hyposmotic conditions did not diminish over 30 min despite cell volume recovery, indicating a dependence of extracellular osmolality or ionic strength rather than cell volume. Cells that were returned to isosmotic conditions following 30 min in 250, 150, or 57 mOsm PBS shrunk to 73%, 39%, or 26% of the control cell volume, respectively. In these cells, the activity of p38 increased further from approximately 300% of the control values in each hyposmotic condition to as much as 500% of the control activity as a function of the degree of cell shrinkage. Thus, p38 may be activated by cell shrinkage in hyperosmotic or in isoosmotic conditions, indicating reduced cell volume is a more important determinant of this enzyme activity than extracellular osmolality. Our results indicate distinct mechanisms of p38 activation in astrocytes exposed to hyperosmotic or hyposmotic PBS.
    Type of Medium: Online Resource
    ISSN: 1535-3702 , 1535-3699
    Language: English
    Publisher: Frontiers Media SA
    Publication Date: 2001
    detail.hit.zdb_id: 2031237-4
    detail.hit.zdb_id: 2020856-X
    SSG: 12
    Location Call Number Limitation Availability
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  • 4
    Online Resource
    Online Resource
    Frontiers Media SA ; 2003
    In:  Experimental Biology and Medicine Vol. 228, No. 4 ( 2003-04), p. 413-423
    In: Experimental Biology and Medicine, Frontiers Media SA, Vol. 228, No. 4 ( 2003-04), p. 413-423
    Abstract: Humic acid (HA) has been implicated as an etiological factor of Blackfoot disease endemic in the southwest coast of Taiwan. Dysfunction of endothelial cells and vasculopathy have been proposed to explain the onset of ulcerous changes at extremities. However, little is known about the effect of HA on activities of cells in these nonhealing wounds. In the present study, we demonstrate that HA adversely affects the growth properties of fibroblasts, one of the key players in wound repair. HA treatment caused growth arrest and apoptosis in human foreskin fibroblasts (HFF). This was accompanied by a significant increase in the level of 8-hydroxy-2′-deoxyguanosine (8-OHdG) in cellular DNA. The increased fluorescence in dichlorofluorescin (H 2 DCF)-stained and HA-treated cells suggests the involvement of reactive oxygen species (ROS) in HA-induced biological effects. Conversely, vitamin E pretreatment, which significantly reduced the 8-OHdG formation in HA-treated cells, alleviated the growth-inhibitory and apoptosis-inducing effects of HA. These results indicate that HA initiates oxidative damages to fibroblasts, and leads to their dwindling growth potential and survival. The present study suggests that HA-induced growth retardation and apoptosis of fibroblasts may play a role in the pathogenesis of Blackfoot disease.
    Type of Medium: Online Resource
    ISSN: 1535-3702 , 1535-3699
    Language: English
    Publisher: Frontiers Media SA
    Publication Date: 2003
    detail.hit.zdb_id: 2031237-4
    detail.hit.zdb_id: 2020856-X
    SSG: 12
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
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