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  • 2000-2004  (2)
  • 1980-1984
  • 1960-1964
  • 2001  (2)
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  • 2000-2004  (2)
  • 1980-1984
  • 1960-1964
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  • 1
    ISSN: 1365-2044
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: We have used the up-and-down allocation technique to assess the relative analgesic potencies of epidural ropivacaine alone and ropivacaine combined with sufentanil 0.75 µg.ml−1 in 42 women requesting epidural analgesia in the first stage of labour. Parturients were randomly allocated to one of the two epidural solutions in a double-blind manner. The concentration of local anaesthetic was determined by the response of the previous parturient: an effective concentration (pain ≤ 10 mm on a 10-cm visual analogue pain score within 30 min) resulted in a 0.01% decrease in the concentration of ropivacaine for the next parturient, an ineffective concentration resulted in a 0.01% increase. Minimum local analgesic concentration of ropivacaine alone was 0.13% (95% CI 0.12–0.13%) compared with 0.09% (95% CI 0.08–0.1%) for ropivacaine with sufentanil (p 〈 0.00001).
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Copenhagen : Munksgaard International Publishers
    Experimental dermatology 10 (2001), S. 0 
    ISSN: 1600-0625
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Sunburn cell (SBC) formation in the epidermis is a characteristic consequence of ultraviolet radiation (UVR) exposure at doses around or above the minimum erythema dose. SBC have been identified morphologically and biologically as keratinocytes undergoing apoptosis. There is evidence that SBC formation is a protective mechanism to eliminate cells at risk of malignant transformation. The level of DNA photodamage is a major determinant of SBC induction by a process controlled by the tumor suppressor gene p53. However, extra-nuclear events also contribute to SBC formation, such as the activation of death receptors including CD95/Fas. UVR triggers death receptors either by direct activation of these surface molecules or by inducing the release of their ligands such as CD95 ligand or tumor necrosis factor. Oxidative stress also appears to be involved, probably via mitochondrial pathways, resulting in the release of cytochrome C. Pathways which modify SBC formation are now extensively studied given the importance of apoptosis in eliminating irreparably damaged cells. A greater understanding of the mechanisms that induce and prevent UVR-induced apoptosis will contribute to our understanding of mechanisms relevant in genomic integrity.
    Type of Medium: Electronic Resource
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