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  • 1
    ISSN: 1471-0528
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Anaesthesia 45 (1990), S. 0 
    ISSN: 1365-2044
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: A case is presented of a severe anaphylactoid reaction to hydroxyethyl starch solution that occurred peri-operatively and required extended intensive management of the resultant bronchospasm and hypotension. Subsequent intradermal injection of hetastarch produced a delayed positive response, suggestive of a complement-mediated mechanism.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    [s.l.] : Nature Publishing Group
    Nature 257 (1975), S. 319-321 
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] There are at least three ways of investigating this problem: (1) by making serial observations during embryogenesis; (2) by studying the effects of selective damage to basement membrane and collagenous elements on myelination; or (3) by studying the mutant dystrophic mouse, in which areas of ...
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Cambridge : Cambridge University Press
    International review of social history 20 (1975), S. 48-60 
    ISSN: 0020-8590
    Source: Cambridge Journals Digital Archives
    Topics: History , Sociology
    Notes: For the historian of modern European society the problem of the extent and nature of unemployment at any particular time and in any particular place is a challenging and even frustrating one. It is clearly an important question to ask and yet, except for very recent times, it is almost impossible to answer satisfactorily. Where there are data they are incomplete and their reliability doubtful. This is true even of such a society as Victorian Britain, which might be thought to have a considerable amount of useful material. The early Victorian social investigators in Britain seldom dealt with the problem of unemployment, preferring to focus on educational, sanitary, and similar elements of working-class living standards. Admittedly, from the middle of the nineteenth century continuous series of unemployment figures become increasingly available relating to particular trades and from these aggregate figures have been calculated.1 But the defects of these returns, made by various trade unions and based upon the numbers receiving unemployment benefit, have been recognized almost from the time that they began to appear. As for official labour statistics in general, those for the period before 1886 have recently been described as “deficient, chaotic, and unmanageable”.2 The unemployment statistics improved little after 1886. They continued to be derived from the same sources as before, though a much greater number of unions made returns. But the very nature of the returns means that they were biassed towards the unionised workers in industries like heavy engineering.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 317 (1979), S. 0 
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 83 (1992), S. 158-169 
    ISSN: 1432-0533
    Keywords: Skeletal muscle ; Muscular dystrophy ; Titin ; Desmin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We have used monoclonal antibodies to desmin and titin, and a combination of immunofluoescence and immunogold labelling to study the disposition of these two proteins in normal human muscle fibres and in fibres at various stages of degeneration in dystrophic muscle. The normal pattern of desmin labelling, in particular the subsarcolemmal labelling, became disrupted at an early stage of fibre breakdown. There was a change from a transverse to a longitudinal orientation of the labelled intermediate filaments as the myofibrils sheared relative to one another. Thus, while it is probable that the desmin filaments are able to play a role in the mechanical integration of the myofibrils in healthy muscle, our results suggest that they cannot withstand the excessive forces generated by the hypercontraction and stretching of dystrophic muscle. However, small accumulations of desmin persisted between the damaged myofibrils until necrosis reached an advanced stage. In general, the degradation of titin appeared to occur before the degradation of desmin, and at the ultrastructural level, labelling with antibodies to epitopes from parts of the titin molecule close to the A-I-band junction was lost before labelling with an antibody to an epitope in the A-band. This suggests that different regions of the titin molecule break down at different stages in the breakdown of the fibre. We propose that lysis of titin in the I-band may underlie ‘slippage’, an abnormality often seen in dystrophic muscle, in which the A-band slips to one pole of the sarcomere such that it abuts onto the Z-line. Breakdown of the A-band section of titin may facilitate the disassembly of the A-filaments.
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1432-0533
    Keywords: Key words: Dystrophin – Dystrophin-associated proteins – Skeletal muscle – Duchenne muscular dystrophy – Dystroglycan
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. Immunofluorescence and immunogold labelling were used to localise the 43-kDa dystrophin-associated glycoprotein (43DAG) of the dystrophinglycoprotein complex in control and Duchenne muscular dystrophy (DMD) biopsies. In control muscle 43DAG was localised by immunofluorescence to the periphery of the fibre and, by immunogold, was further delimited to the plasma membrane. The labelling was indistinguishable from that previously reported for the dystrophin C terminus [5]. Moreover, the distance separating adjacent 43DAG labelling sites (120 nm mode) closely matched that separating dystrophin C-terminal sites. This is strong evidence supporting Ervasti & Campbell's model in which the DAG complex is bound close to the C terminus of dystrophin and in which the DAG complexes are separated by approximately the length of the dystrophin rod [7, 12]. In DMD, where there is a 80 – 90% reduction in the glycoprotein complex [16], a faint or locally patchy distribution of 43DAG was seen by immunofluorescence. Measurement of nearest-neighbour distances after immunogold labelling showed that in DMD the 43DAG was more dispersed, which is further evidence that dystrophin is normally involved in anchoring the DAGs in the plasma membrane. This is significant because the potential success of dystrophin gene therapy could depend not only on restoring dystrophin but also on restoring the lost DAGs.
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 54 (1981), S. 329-330 
    ISSN: 1432-0533
    Keywords: Muscular dystrophy, Duchenne type ; Ultrastructure ; Satellite cell
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A new organelle found in a case of Duchenne muscular dystrophy is described. It was located at the periphery of a regenerated myofibre close to a satellite cell. It was roughly sperical in shape and 0.30–0.35 μm in diameter. Its internal structure was examined in serial and tilted sections, and consisted of parallel arrays of laminae or, possibly, filaments. The nature of the organelle is briefly discussed.
    Type of Medium: Electronic Resource
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  • 9
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 77 (1988), S. 69-81 
    ISSN: 1432-0533
    Keywords: mdx Mouse ; Muscle pathology ; Regeneration ; Duchenne muscular dystrophy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Ultrastructurally there are some clear differences in the pathology of muscle in X chromosomelinked muscular dystrophy of the mouse (mdx) and Duchenne muscular dystrophy (DMD). In particular the mouse muscle does not become infiltrated by large aggregations of connective tissue. It has been proposed that the differences are due to secondary biochemical changes consequent on the absence of dystrophin in both conditions. If this is the case, attention should be directed to the earliest ultrastructural changes held in common by both disorders. The most conspicuous of these, preceding myofibril breakdown, is dilation of the sarcoplasmic reticulum. Any physiological link between this and the absence of dystrophin remains to be determined. We suggest that in themdx mouse, the widespread myofibre necrosis occurring at 3–4 weeks is triggered by increased mechanical demands causing the lack of dystrophin to become critical at this time. Subsequent regeneration of the myofibres appears to be almost completely successful. The ultimate failure of regeneration in DMD, in contrast, may be due to an additional factors acting in DMD exacerbating the lack of dystrophin. This additional factor may be associated with the plasma membrane lesions (not seen inmdx). Alternatively there may be factors present in the mouse that compensate for the lack of dystrophin. It is pointed out that to understand better the different processes occurring inmdx and DMD we need to learn more about the factors which control the balance between the growth of muscle and the growth of connective tissue in both normal and pathological human and mouse muscle.
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 84 (1992), S. 278-288 
    ISSN: 1432-0533
    Keywords: Desmin ; Titin ; Muscle degeneration ; Muscle regeneration ; Snake venom
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We studied the fate of desmin and titin in rat skeletal muscle during a cycle of degeneration and regeneration induced in vivo by the inoculation of a snake venom. Cryosections of muscle were labelled using antibodies to the two proteins, and examined at fixed time points after venom injection. Early pathological changes in the muscle, such as hypercontraction, preceded the loss of desmin. Immunolabelling using anti-desmin antibodies showed that desmin bridges were still intact when adjacent myofibrils were no longer aligned. The results suggested that although the hydrolysis of desmin is not necessary for the hypercontraction of muscle fibres, it probably contributes to complete fibre breakdown. Titin, or at least the part which lies close to the M-line, remained intact longer than desmin, but was also hydrolysed prior to complete disintegration of the fibres. Both desmin and titin were re-expressed in the regenerating myotubes by 2 days after venom inoculation, and became well organised even before the myofibrils became aligned. We conclude that desmin and titin are involved in both establishing and maintaining the structural integrity of the muscle fibres.
    Type of Medium: Electronic Resource
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