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  • American Physiological Society  (2)
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  • American Physiological Society  (2)
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  • 1
    Online Resource
    Online Resource
    American Physiological Society ; 1999
    In:  Journal of Applied Physiology Vol. 87, No. 1 ( 1999-07-01), p. 10-14
    In: Journal of Applied Physiology, American Physiological Society, Vol. 87, No. 1 ( 1999-07-01), p. 10-14
    Abstract: Obstructive sleep apnea syndrome (OSAS) may be one of the most important risk factors of cardiovascular disorders, although the exact mechanism remains to be elucidated. In the present study, we hypothesized that OSAS-induced hypoxic stress might be involved in the etiology of cardiovascular disorders by activating adhesion molecules, including intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), and L-selectin. To examine this hypothesis, we measured circulating ICAM-1, VCAM-1, and L-selectin levels before and after sleep in OSAS patients and age-matched controls. The circulating ICAM-1, VCAM-1, and L-selectin levels increased in the OSAS patients before sleep compared with the normal subjects (ICAM-1: 392.9 ± 48.5 vs. 201.2 ± 55.0 ng/ml, P 〈 0.05; VCAM-1: 811.0 ± 87.8 vs. 574.2 ± 42.7 ng/ml, P 〈 0.05; L-selectin: 1,386.6 ± 77.9 vs. 1,038.8 ± 78.6 ng/ml, P 〈 0.01, respectively). After sleep, significantly greater levels of ICAM-1 and L-selectin, but not VCAM-1, were observed in the OSAS group. These observations suggest that OSAS-induced hypoxia activates adhesion molecules, resulting in the important risk factor of cardiovascular disorders. Treatment of OSAS can be, therefore, a potential approach to prevention of cardiovascular events.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    RVK:
    RVK:
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1999
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
    Location Call Number Limitation Availability
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  • 2
    Online Resource
    Online Resource
    American Physiological Society ; 2001
    In:  American Journal of Physiology-Lung Cellular and Molecular Physiology Vol. 280, No. 6 ( 2001-06-01), p. L1189-L1195
    In: American Journal of Physiology-Lung Cellular and Molecular Physiology, American Physiological Society, Vol. 280, No. 6 ( 2001-06-01), p. L1189-L1195
    Abstract: Cigarette smoking is thought to be a major risk factor in various lung diseases including lung cancer and emphysema. However, the direct effect of cigarette smoke on the viability of lung-derived cells has not been fully elucidated. In this study, we investigated the viability of human lung fibroblast-derived (HFL1) cells to different concentrations of cigarette smoke extract (CSE). CSE induced apoptosis at lower concentrations (10–25%) and necrosis at higher concentrations (50–100%). We also examined the effects of glutathione S-transferase P1 (GSTP1), one of the xenobiotic metabolizing and antioxidant enzymes in the lung, against the cytotoxicity of CSE. Our results indicated that the level of HFL1 cell death was decreased by transfection with a GSTP1 expression vector and was increased by GSTP1 antisense vector transfection. Therefore, transient overexpression and underexpression of GSTP1 appeared to inhibit and enhance the cytotoxic effects of CSE on HFL1 cells, suggesting that GSTP1 may have protective effects against cigarette smoke in the airway cells.
    Type of Medium: Online Resource
    ISSN: 1040-0605 , 1522-1504
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2001
    detail.hit.zdb_id: 1477300-4
    SSG: 12
    Location Call Number Limitation Availability
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