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  • 1
    Electronic Resource
    Electronic Resource
    ELISA for the neuropeptide degrading endopeptidase 3.4.24.11 in human serum and leukocytes
    Amsterdam : Elsevier
    Peptides 15 (1994), S. 843-848 
    Details
    ISSN: 0196-9781
    Keywords: E.C.3.4.24.11 ; ELISA ; Neutral endopeptidase
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://linkinghub.elsevier.com/retrieve/pii/0196-9781(94)90040-X
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Measurement of Allergen-Specific IgD and Correlation with Allergen-Specific IgE (1994)
    Oxford, UK : Blackwell Publishing Ltd
    Scandinavian journal of immunology 40 (1994), S. 0 
    Details
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: A new method for the measurement of allergen-specific IgD (as-IgD) was developed by modifying the ImmunoCAP assay (Pharmacia), and amplification of the signal with a goat anti-human/rabbit antigoat detection system. The assay was sensitive enough to measure as-IgD in serum samples. The specificity of the assay was examined using inhibition tests with excess corresponding and non-corresponding allergens. For the different allergens inhibition rates between 56% (house dust mite) and 88% (cat) could be achieved. Non-corresponding allergens did not inhibit the as-IgD binding. Total IgE and allergen-specific IgE (as-IgE) was measured using the ImmunoCAP system. Total IgD was measured using a sandwich ELISA. As-IgD was measured in serum samples from 51 atopic and 2.1 non-atopic subjects, and the correlation with as-IgE was examined. As-IgD was detected in both atopies and non-atopies but at higher levels in atopies. As-IgD against birch pollen and timothy pollen allergen was found to be increased in atopies with IgE directed against these allergens compared to atopies without IgE against these allergens (P 〈0.02 and P 〈0.03). As-IgD against birch pollen allergen was higher in atopies with IgE specific to this allergen than in non-atopies (P 〈0.02). In contrast to total IgE and total IgD, significant correlations were observed between as-IgD and as-IgE against timothy pollen (r= 0.34, P 〈0.04), birch pollen (r= 0.38, P 〈0.05) and cat dander allergen (r= 0.52, P 〈0.01). The observed correlations between as-IgD and IgE suggest that IgD and IgE may be similarly regulated, and thus the measurement of as-IgD may give further insight into the regulation of IgE.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-3083.1994.tb03496.x
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Demonstration of the high-affinity IgE receptor (FcɛRI) on Langerhans' cells of diseased nasal mucosa (1997)
    Oxford, UK : Blackwell Publishing Ltd
    Allergy 52 (1997), S. 0 
    Details
    ISSN: 1398-9995
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Haas N, Hamann K, Grabbe J, Niehus J, Kunkel G, Kolde G, Czarnetzki M. Demonstration of the high-affinity IgE receptor (FcɛRI) on Langerhans' cells of diseased nasal mucosa.Langerhans' cells in the skin have recently been shown to bind IgE molecules via the high-affinity IgE receptor (FcɛRI). Using two highly specific antibodies against the antibody-binding α-chain of this receptor, 29C6 and 6F7, we demonstrate by immunohistochemistry and immunoelectron microscopy that Langerhans' cells of diseased nasal mucosa can express the FcɛRI. Tissue sections from hyperplastic nasal conchae and nasal polyps of atopic and nonatopic patients have shown no basic differences in epithelial FcɛRII-bearing cells. Only a few cells expressed the low-affinity IgE receptor (FcɛRII) (Tül antibody) in some sections. These findings suggest that Langerhans' cells play an important role in the induction of transepithelial IgE-mediated allergy and in the mediation of inflammation of the nasal mucosa via their FcɛRI.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1398-9995.1997.tb01025.x
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  • 4
    Electronic Resource
    Electronic Resource
    Morphine induced changes in ethanol-and water-intake are attenuated by the 5-HT3/4 antagonist tropisetron (ICS 205-930) (1995)
    Springer
    Psychopharmacology 119 (1995), S. 186-192 
    Details
    ISSN: 1432-2072
    Keywords: Alcohol ; Ethanol self-administration ; Morphine ; Tropisetron ; Opiate ; 5-HT3 antagonist ; 5-HT4 ; Rats
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The opiate agonist morphine has been shown to increase ethanol intake and mesolimbic dopamine (DA) levels. Conversely, the 5-HT3/4 antagonist tropisetron has been shown to decrease ethanol intake and morphine-induced increases in mesolimbic DA levels. This study was designed to test the effects of acutely administered tropisetron on morphine-induced changes in ethanol (6% v/v) and water intake in a two-bottle test procedure. Ten water restricted male rats were injected with combinations of morphine (0.0, 0.56, 1.0, 1.5, 10.0, and 17.0 mg/kg, SC) and tropisetron (0.0, 1.0, 10.0, and 17.0 mg/kg, SC) prior to test sessions. Morphine (1.0 and 1.5 mg/kg) significantly increased absolute (g/kg) and relative ethanol intake (ethanol/total fluid). Tropisetron alone did not affect ethanol or water intake. When tropisetron (10.0 and 17.0 mg/kg) was administered in combination with morphine (1.5 mg/kg), the increase in ethanol intake induced by morphine was attenuated. Tropisetron (1.0 mg/kg) reversed a decrease in ethanol intake induced by morphine (17.0 mg/kg). The two highest doses of tropisetron partially attenuated a significant decrease in water intake produced by morphine (17.0 mg/kg). These data suggest that opiate and 5-HT3 mechanisms could interact in the regulation of ethanol intake. However, the doses of tropisetron tested were high and, therefore, the potential involvement of 5-HT4 receptors or other neurotransmitter systems in regulating ethanol intake is discussed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02246160
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    Paper (German National Licenses)
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