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  • 1
    Electronic Resource
    Electronic Resource
    Allergens from fish and egg (2001)
    Copenhagen : Munksgaard International Publishers
    Allergy 56 (2001), S. 0 
    Details
    ISSN: 1398-9995
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Allergens from fish and egg belong to some of the most frequent causes of food allergic reactions reported in the literature. Egg allergens have been described in both white and yolk, and the egg white proteins ovomucoid, ovalbumin, ovotransferrin and lysozyme have been adopted in the allergen nomenclature as Gal d1–d4. The most reported allergen from egg yolk seems to be alpha-livitin. In fish, the dominating allergen is the homologues of Gad c1 from cod, formerly described as protein M. A close cross-reactivity exists within different species of fish between this calcium-binding protein family, denominated the parvalbumins. This cross-reactivity has been indicated to be of clinical relevance for several species, since patients with a positive double-blind, placebo-controlled food challenge to cod will also react with other fish species, such as herring, plaice and mackerel. In spite of the importance of these two allergen systems, only a few studies have been performed, and the scarcity of cloned allergens from both of the systems is emphasized.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1034/j.1398-9995.2001.00912.x
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  • 2
    Electronic Resource
    Electronic Resource
    Analysis of an Escherichia coli mutant strain resistant to the cell-killing function encoded by the gef gene family (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Molecular microbiology 6 (1992), S. 0 
    Details
    ISSN: 1365-2958
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology , Medicine
    Notes: The chromosomal genes gef and relF from Escherichia coli and the plasmid-encoded genes hok, flmA, srnB, and pndA constitute the gef qene family, which encodes a cell-killing function. In order to investigate the mechanism of cell killing we have isolated an E. coli mutant strain that is resistant to the overexpression of the toxic proteins encoded by the gef gene family. This phenotype requires at least two mutations, one of which has been mapped to 55.2 minutes. This mutation was sequenced and shown to represent a single base substitution in an open reading frame (ORF178) encoding a putative membrane protein having a molecular mass of 20.1 kDa. ORF178 and an upstream frame, ORF190, probably constitute an operon.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2958.1992.tb01540.x
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  • 3
    Electronic Resource
    Electronic Resource
    Nickel-induced cytokine production from mononuclear cells in nickel-sensitive individuals and controls (2000)
    Springer
    Archives of dermatological research 292 (2000), S. 285-291 
    Details
    ISSN: 1432-069X
    Keywords: Key words Nickel ; Allergic contact dermatitis ; T cells ; IL-4 ; IL-5
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Exposure to nickel is a major cause of allergic contact dermatitis which is considered to be an inflammatory response induced by antigen-specific T cells. Here we describe the in vitro analysis of the nickel-specific T-cell-derived cytokine response of peripheral blood mononuclear cells from 35 nickel-allergic and 30 non-nickel-allergic individuals. Peripheral blood mononuclear cells were stimulated with 10–4 and 10–5 mol/l NiSO4 for 6 days and then additionally with ionomycin and phorbol myristate acetate for 24 h. Culture supernatants were analysed for interleukin-4 (IL-4), IL-5, interferon-γ (IFN-γ) and tumour necrosis factor-α (TNF-α) by quantitative ELISA. The analysis showed that the synthesis of IL-4 and IL-5 but not of IFN-γ or TNF-α was significantly higher in the nickel-allergic individuals. The finding of preferential synthesis of Th2 cytokines was somewhat of a surprise, since previous studies have suggested a Th1 response in nickel-mediated allergic contact dermatitis. Subsequently, the nickel-allergic individuals were randomized to experimental exposure to nickel or vehicle in a double-blind design. A daily 10-min exposure of one finger to 10 ppm nickel solution for 1 week followed by 100 ppm for an additional week evoked a clinical response of hand eczema in the nickel-exposed group. Blood samples were drawn on days 7 and 14 after the start of this exposure to occupationally relevant concentrations of nickel. No statistically significant differences were observed in the nickel-induced in vitro cytokine response during the exposure period. Our results indicate the possibility that IL-4 and IL-5 are involved in the pathogenesis of nickel-mediated contact dermatitis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004030000129
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