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  • 1
    ISSN: 1432-0428
    Schlagwort(e): Human ; insulin-dependent ; diabetes mellitus ; complement ; antibody-dependent cell cytotoxicity ; auto-antibodies ; antigens ; surface ; Islands of Langerhans
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary The role of complement in the pathogenesis of diabetes was studied in 31 Type 1 (insulin-dependent) diabetic children by assaying serum islet cell surface antibody, C3, C4 and serum complement-dependent antibody-mediated cytotoxicity. Nine of 21 islet cell surface antibody-positive children were within 5 months of disease onset and showed significantly lower serum C3 and C4 levels than either 1 year later or the remainder of the islet cell surface antibody-positive children at 6–12 months after disease onset. The overall trend of all islet cell surface antibody-positive diabetic children within 1 year of disease onset was toward increased serum C3 and C4 levels as the disease progressed. Serum C4 concentration and complement-dependent antibody-mediated cytotoxicity which showed an initial negative correlation were uncorrelated 1 year later. Four children who were initially strongly islet cell surface antibody-positive but negative 1 year later also exhibited significantly higher (p〈0.05) mean serum C4levels after 1 year. There was a significant decrease in complement-dependent antibody-mediated cytotoxicity when sera from the diabetic children were treated with either ethylene glycol tetra-acetic acid or ethylene diamine tetra-acetic acid. These data strongly suggest that complement-dependent antibody-mediated cytotoxicity induced by the classical complement pathway involving an islet cell surface antibody may play an important role in the pathogenesis of Type 1 diabetes.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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  • 2
    Digitale Medien
    Digitale Medien
    Springer
    Diabetologia 37 (1994), S. 225-231 
    ISSN: 1432-0428
    Schlagwort(e): Osmotic diuresis ; urea ; renal hypertrophy ; glomerular hyperfiltration ; diabetes ; rat
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary To study the effects of chronic osmotic diuresis which were not associated with hyperglycaemia on the rat kidney, osmotic diuresis was induced by i. v. infusion of urea. A 5 mol/l urea solution was continuously infused at a rate of 100 ml · kg−1 · day−1 on the basis of body weight on day 0. Duration of infusion was 2, 6, 10 or 14 days. Control rats received continuously infused Ringer's solution. Urea-treated groups developed osmotic diuresis (urine flow = about 0.04 ml · min −1 · 100 g body weight−1) comparable to that in rats with experimental diabetes mellitus induced by i. v. streptozotocin (55 mg/kg), however urea-induced osmotic diuresis was not associated with blood glucose level increases. Compared with their controls, rats receiving urea for 2–14 days had markedly increased kidney weight. Rats receiving urea for 10 days showed greatest kidney weight increase, 0.565 ± 0.044 g/100 g body weight (mean ± SD), representing a 53% increase compared with the control (0.369 ± 0.034 g/100 g body weight). Kidney weight was associated with increases in kidney protein content. In contrast, none of control kidney weight values differed significantly from day 0 values (=normal rats; 0.387 ± 0.028 g/100 g body weight). Creatinine clearance values in urea-treated groups were also higher than those in controls. The maximum value, 0.65 ± 0.17.ml · min−1 · 100 g body weight−1, was recorded in the 14-day group and was significantly higher than the corresponding control value (0.34 ± 0.07 ml · min−1 · 100 g body weight−1) (p 〈0.001). Urea clearance values were also significantly higher in urea-treated groups than in respective controls. This study suggests that osmotic diuresis may induce renal hypertrophy/hyperplasia and glomerular hyperfiltration immediately after development of diabetes.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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