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  • Muscular dystrophy  (3)
  • 72.55.+S  (1)
  • 1
    Electronic Resource
    Electronic Resource
    2,4-dinitrophenol, lysosomal breakdown and rapid myofilament degradation in vertebrate skeletal muscle (1980)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 315 (1980), S. 77-82 
    Details
    ISSN: 1432-1912
    Keywords: Muscle ; Lysosomes ; Calcium ; Muscular dystrophy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 1. The possibility that rapid Ca2+-uptake by skeletal muscle mitochondria may cause local reductions in pH i (by H+/Ca2+ exchange) and so promote lysosomal breakdown has been explored using amphibian and mammalian preparations. Recent studies suggested that such a sequence of events is possible in cardiac muscle. 2. However, extensive muscle damage can still be initiated in skeletal muscle when the mitochondria are uncoupled so that Ca2+-uptake is prevented. 3. DNP alone induces extensive myofilament degradation which is similar to that produced by A 23187 and caffeine and described previously. 4. It is suggested that (a) the known action of DNP in promoting lysosomal labilization in living cells is produced by mitochondrial uncoupling and the release of stored Ca2+, (b) raised [Ca2+] i promotes lysosomal breakdown in skeletal muscle, so that the hydrolases released effect myofilament dissolution rapidly. 5. DNP also rapidly causes septation and division of the mitochondria in mammalian skeletal muscle.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00504233
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    The action of caffeine in promoting ultrastructural damage in frog skeletal muscle fibres (1978)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 305 (1978), S. 159-166 
    Details
    ISSN: 1432-1912
    Keywords: Caffeine ; Muscle ; Muscular dystrophy ; Calcium ; A23187
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 1. Caffeine at concentrations above 5 mM was shown to cause rapidly extensive ultrastructural damage to the myofibrils of frog skeletal muscle. 2. The effect was promoted at lower temperatures, whereas the myofibrils were protected by prior exposure to procaine. 3. It is argued that caffeine causes a Ca2+-induced release of Ca2+ (the CROC) from the S.R. and that the consequent rise in [Ca2+]i promotes the ultrastructural damage observed. 4. Myofibril degradation is also produced by treatment of the muscle with the divalent cation ionophore A23187; this effect is not protected by either procaine or Dantrolene sodium. 5. It is suggested that A23187 causes the release of Ca2+ from the S.R. by a mechanism that differs from both excitation and the CROC; the resultant rise in [Ca2+]i again causes myofibril degradation. 6. The ways in which a marked rise in [Ca2+]i could cause muscle damage and the possible relevance of these findings to the sequence of events in the development of myopathies of human skeletal muscle are discussed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00508287
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    The effect of the ionophore A23187 on the ultrastructure and electrophysiological properties of frog skeletal muscle (1976)
    Springer
    Cell & tissue research 173 (1976), S. 193-209 
    Details
    ISSN: 1432-0878
    Keywords: Muscle ; Ionophore A23187 ; Calcium ; Muscular dystrophy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary The divalent cation ionophore A23187 has three major effects on the thin cutaneous pectoris muscle of frog: (1) The membrane potential is depolarized, an action that is found only when the [Ca2+] of the bathing saline is very low. (2) It causes an increase in resting tension and the development of contraction. This action is produced at both normal and low values of [Ca2+]o and is, therefore, independent of Ca2+ entry and of changes in Em. The ionophore is believed to act primarily by releasing Ca2+ from intracellular stores. (3) It causes major ultrastructural damage to the muscle filaments. It is believed that this damage is the result of the action of A23187 on the sarcoplasmic reticulum and the elevation of [Ca2+]i and we suggest that the action of this ionophore may serve as a useful model for the study of certain myopathies.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00221375
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    Comment on the observation of magnetoacoustic quantum oscillations in UBe13 (1993)
    Springer
    The European physical journal 91 (1993), S. 135-137 
    Details
    ISSN: 1434-6036
    Keywords: 72.55.+S
    Source: Springer Online Journal Archives 1860-2000
    Topics: Physics
    Notes: Abstract The origin of previously reported magnetic quantum oscillations in UBe13 is possibly due to Al inclusions. New measurements of the a.c. susceptibility show Al inclusions which result from the method of crystal growth using aluminium as flux. We discuss the distribution and form of the inclusions and compare our dHvA measurements with those of the γ-orbits of Al.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01315226
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    Paper (German National Licenses)
    Fulltext
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