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  • Endonuclease  (1)
  • Insulin receptors, myotonic dystrophy  (1)
  • 1
    ISSN: 0014-5793
    Keywords: Apoptosis ; Chromatin ; Endonuclease ; Liver nuclei ; Protease
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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  • 2
    ISSN: 1590-3478
    Keywords: Insulin receptors, myotonic dystrophy ; serum insulin ; mononuclear leucocytes ; erythrocytes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Sommario Gli autori hanno valutato l'attività dei recettori insulinici nei leucociti mononucleari e negli eritrociti di 9 pazienti affetti di distrofia miotonica e in 9 controlli. I risultati documentano che nella distrofia miotonica si verifica: 1. L'attività dei recettori risulta danneggiare notevolmente (p〈0,01) per la riduzione di numero dei recettori ad alta e a bassa affinità 2. la costante di affinità non è compromessa in modo significativo 3. non vi è correlazione tra attività dei recettori, comportamento insulinico e tolleranza al glucosio. Questi dati ottenuti in 2 differenti sistemi cellulari suggeriscono che la costante riduzione numerica dei recettori insulinici è probabilmente dovuta a un difetto sistemico di membrana come è tipico della distrofia miotonica.
    Notes: Abstract We evaluated insulin receptor activity on mononuclear leucocytes and erythrocytes in 9 patients with myotonic dystrophy and in 9 controls. The results demonstrated that in myotonic dystrophy: 1. insulin binding to specific receptors was significantly impaired (P 〈 0.01) because of a reduction in the number of high and low affinity receptors. 2. the affinity constants were not significantly affected 3. there was no correlation between receptor activity, insulin behaviour and glucose tolerance. These data obtained in two different cellular systems suggest that the constant numerical reduction of insulin receptors was probably due to a systemic membrane defect, typical of myotonic dystrophy.
    Type of Medium: Electronic Resource
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