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  • 1985-1989  (2)
  • 1915-1919
  • anti-IgA antibodies  (1)
  • selectivity  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Haemodynamic, metabolic, and lymphocyte beta2-adrenoceptor changes following chronic beta-adrenoceptor antagonism (1987)
    Springer
    European journal of clinical pharmacology 32 (1987), S. 237-243 
    Details
    ISSN: 1432-1041
    Keywords: beta-antagonists ; beta2-adrenoceptor ; selectivity ; intrinsic sympathomimetic activity ; adrenaline hypokalaemia ; vasidilatation ; receptor up-regulation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary We have examined the effects of 7 days treatment with beta adrenoceptor antagonists in 8 healthy volunteers in a placebo controlled, crossover study. We investigated three beta-adrenoceptor antagonists (atenolol, oxprenolol, and propranolol), which have differing profiles of selectivity and partial agonist properties (intrinsic sympathomimetic activity, ISA). We studied adrenaline-induced hypokalaemia, the vasodilator response to an infusion of adrenaline (0.06 µg·kg−1·min−1 for 90 min), and lymphocyte beta2-adrenoceptor number, determined by (-) [125I]-iodocyanopindolol binding, and measured these variables both before and after 7 days of treatment. The beta2-mediated depressor response to adrenaline infusion was abolished by propranolol and oxprenolol but persisted after atenolol. In contrast, the hypokalaemia induced by adrenaline was abolished by all three beta-blockers. Lymphocyte beta2-adrenoceptor number increased significantly following propranolol treatment, but not after oxprenolol for atenolol. We conclude that up-regulation of lymphocyte beta2-adrenoceptors is dependent on beta2-receptor blockade and is modified by ISA. The reversal of the hypokalaemic response by atenolol suggests that beta1 receptors may contribute to the former effect. Alternatively, since different populations of beta2-adrenoceptors differ in their susceptibility to antagonists there may also be differences in agonist coupling to beta2-responses between tissues.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00607569
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    Anti-IgA antibodies in IgA-deficient children (1988)
    Springer
    Journal of clinical immunology 8 (1988), S. 356-361 
    Details
    ISSN: 1573-2592
    Keywords: IgA deficiency ; anti-IgA antibodies
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract IgG and IgM isotype antibodies to polyclonal human IgA, myeloma IgA1, and myeloma IgA2 were estimated in 38 IgA-deficient children aged between 0.9 and 15 years. All children had IgM anti-IgA antibodies. IgG antibodies against either polyclonal IgA, IgA1, or IgA2 were present in 63% of the IgA-deficient children. IgG anti-IgA antibodies were detected against all three antigens in 8 of 11 severely IgA-deficient children and in 7 of 27 partially IgA-deficient children, but in only 1 of 23 healthy adult controls. The proportion of children with IgG anti-IgA antibodies was significantly greater in the severely IgA-deficient group in comparison with the partially IgA-deficient group and the adult controls (chi-square test,P〈0.01 andP〈0.005, respectively). There was a strong correlation within each IgG subclass between antibody responses toward each of the three IgA antigens. Twenty-four children were followed over a period ranging from 0.9 to 11 years (mean, 2.3 years). Three children who were initially IgG anti-IgA antibody negative became antibody positive and three who were antibody positive became antibody negative. Five children with severe IgA deficiency remained severely IgA deficient and IgG antibodies to IgA persisted in all five at follow-up. The presence of IgG anti-IgA antibodies did not influence the normalization of serum IgA at follow-up in 14 of 19 children who were initially partially IgA deficient.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00917151
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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