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  • Atrophic auto-immune thyroiditis  (1)
  • Cloning  (1)
  • Contact hypersensitivity  (1)
  • 1
    Digitale Medien
    Digitale Medien
    Amsterdam : Elsevier
    FEBS Letters 302 (1992), S. 161-165 
    ISSN: 0014-5793
    Schlagwort(e): Cloning ; High-affinity IgE receptor ; Human β subunit ; Polymerase chain reaction ; Polymerase chain reaction walking ; Sequencing
    Quelle: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Thema: Biologie , Chemie und Pharmazie , Physik
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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  • 2
    ISSN: 1432-069X
    Schlagwort(e): 1α,25-Dihydroxyvitamin D3 ; Vitamin D3 ; Contact hypersensitivity
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary Recent evidence indicates that the biologically active metabolite of vitamin D3, 1α,25-dihydroxy-vitamin D3 [1α,25(OH)2D3], has an effect on the regulation of the immune response. We investigated whether topical treatment of mice with 1α,25(OH)2D3 influences the contact hypersensitivity (CHS) response to trinitrochlorobenzene (TNCB). 1α,25(OH)2D3 was applied to the dorsal trunk of A/J mice on days 0–3, and on day 4 topical application of 5% TNCB on the 1α,25(OH)2D3-treated site was performed. The mice were tested for CHS on day 10 by applying 1% TNCB to the ears. No effect on induction of CHS response to TNCB was observed in 1α,25(OH)2D3-treated mice compared with 24,25-dihydroxyvitamin D3[24,25-(OH)2D3]-treated mice as control. In a second experiment, the dorsal trunk of A/J mice was treated with 5% TNCB on day 0. The topical application of 1α,25(OH)2D3 on the ears was performed from days 2 to 5. On day 6, the mice were tested for CHS by applying 1% TNCB to the 1α,25(OH)2D3-treated ears. When 1α,25(OH)2D3 increased their response to TNCB by 40% compared with 24,25(OH)2D3-treated mice as 1α,25(OH)2D3 increased their response to TNCB by 40% compared with 24,25(OH)2D3-treated mice as control (P〈0.01). There were no findings suggesting that the pretreatment of the challenge site with 1α,25(OH)2D3 induced an irritant dermatitis that was superimposed on a subsequent CHS reaction. The 1α,25(OH)2D3 modulation of CHS response to TNCB in mice suggests that the hormone may play a role in the regulation of the immune response in vivo.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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  • 3
    ISSN: 1432-1076
    Schlagwort(e): Atrophic auto-immune thyroiditis ; Goitrous auto-immune thyroiditis ; TSH-binding inhibitor immunoglobulins ; Thyroid stimulation blocking antibodies ; TSH receptor antibodies
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Abstract We studied the clinical features, laboratory and thyroid functions and thyrotropin (TSH)-receptor and thyroid-stimulation antibodies in 21 patients with atrophic auto-immune thyroiditis (AAT) and 48 patients with goitrous auto-immune thyroiditis (GAT) of childhood onset. The clinical features of patient with AAT were cessation of growth and obesity, while asymptomatic enlargement of the thyroid gland was the sole symptom in most patients with GAT. Although the ages at diagnosis were comparable in both groups, the estimated ages at onset were much lower in patients with AAT than in those with GAT. Patients with AAT exhibited more severe hypothyroidism when evaluated by serum thyroxine (T4), tri-iodothyronine (T3), TSH, cholesterol levels and basal metabolic rates. The 24h123I-thyroidal uptake was significantly lower in patients with AAT than in those with GAT. None of the 19 patients with AAT possessed TSH-binding inhibitor immunoglobulins (TBII). On the other hand, 3 of the 32 GAT patients tested, possessed weak to potent TBII activities. Three TBII-positive patients with GAT also possessed thyroid-stimulation blocking antibodies. These findings suggest that: 1. Pathogenesis of AAT in children whose onset of hypothyroidism was before puberty is not due to TSH-receptor blocking antibodies, which are often found in patients with AAT of postpubertal onset. 2. AAT in children is considered not to be due to the later stage of GAT. 3. Some patients with GAT possessed TSH-receptor blocking antibodies. The aetiology and pathogenesis of AAT in children have yet to be elucidated.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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