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  • 1
    ISSN: 1432-0533
    Keywords: Key words Diabetic neuropathy ; Axonal regeneration ; Nerve growth factor receptors ; Schwann cells ; Basal lamina
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Observations were made on myelinated fibre regeneration in diabetic sensory polyneuropathy assessed in sural nerve biopsy specimens. These confirmed that regenerative clusters initially develop within abnormally persistent Schwann cell basal laminal tubes. The number of regenerating fibres, identified by light microscopy, was found to decline in proportion to the reduction in total myelinated fibre density. The relative number of regenerating fibres was significantly greater in patients with insulin-dependent as compared with those with non-insulin-dependent diabetes after correction for age. There was a slight negative correlation between the relative proportion of regenerating fibres and age, but this was not statistically significant. The progressive reduction in the number of regenerating fibres with declining total fibre density indicates that axonal regeneration fails with advancing neuropathy. The production of nerve growth factor (NGF) and NGF receptors by denervated Schwann cells is likely to be important for axonal regeneration. To investigate whether the failure of axonal regeneration could be related to a lack of NGF receptor production by Schwann cells, we examined the expression of p75 NGF receptors by Büngner bands immunocytochemically. In comparison with other types of peripheral neuropathy, p75 NGF receptor expression appeared to take place normally. It is concluded that failure of axonal regeneration constitutes an important component in diabetic neuropathy. Its explanation requires further investigation.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-0533
    Keywords: Diabetic neuropathy ; Axonal regeneration ; Nerve growth factor receptors ; Schwann cells ; Basal lamina
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Observations were made on myelinated fibre regeneration in diabetic sensory polyneuropathy assessed in sural nerve biopsy specimens. These confirmed that regenerative clusters initially develop within abnormally persistent Schwann cell basal laminal tubes. The number of regenerating fibres, identified by light microscopy, was found to decline in proportion to the reduction in total myelinated fibre density. The relative number of regenerating fibres was significantly greater in patients with insulin-dependent as compared with those with non-insulin-dependent diabetes after correction for age. There was a slight negative correlation between the relative proportion of regenerating fibres and age, but this was not statistically significant. The progressive reduction in the number of regenerating fibres with declining total fibre density indicates that axonal regeneration fails with advancing neuropathy. The production of nerve growth factor (NGF) and NGF receptors by denervated Schwann cells is likely to be important for axonal regeneration. To investigate whether the failure of axonal regeneration could be related to a lack of NGF receptor production by Schwann cells, we examined the expression of p75 NGF receptors by Büngner bands immunocytochemically. In comparison with other types of peripheral neuropathy, p75 NGF receptor expression appeared to take place normally. It is concluded that failure of axonal regeneration constitutes an important component in diabetic neuropathy. Its explanation requires further investigation.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Journal of neurology 246 (1999), S. 107-112 
    ISSN: 1432-1459
    Keywords: Key words Hereditary motor and ; sensory neuropathy ; Axonopathy ; Autosomal recessive inheritance
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract A family is described with presumed autosomal recessive inheritance in which three siblings developed a progressive neuropathy that combined limb weakness and severe distal sensory loss leading to prominent mutilating changes. Electrophysiological and nerve biopsy findings indicated an axonopathy. The disorder is therefore classifiable as type II hereditary motor and sensory neuropathy (HMSN II). The clinical features differ from those reported in previously described cases of autosomal recessive HMSN II. This disorder may therefore represent a new variant.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Journal of neurology 239 (1992), S. 361-362 
    ISSN: 1432-1459
    Keywords: Guillain-Barré syndrome ; Chronic inflammatory demyelinating polyneuropathy ; Demyelination ; Axonopathy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Acute inflammatory demyelinating polyneuropathy or the Guillain-Barré syndrome (GBS) has come to be accepted as a clinical entity, although the boundary between it and chronic inflammatory demyelinating polyneuropathy has given rise to discussion. Recent observations have suggested that the GBS may represent the consequence of more than one pathogenetic mechanism. In most cases the salient pathological change is demyelination. In some this may be mediated predominantly by lymphocytes; in others, where the demyelination is produced primarily by macrophages, the process may be antibody-mediated. Both electrophysiological and pathological evidence indicates that occasional patients with the GBS show extensive axonal degeneration. Although this could represent a “bystander effect” secondary to inflammatory infiltration, at times it may reflect a direct attack on axons. Elucidation of the nature of the pathogenetic mechanisms is essential before rational therapy can be devised.
    Type of Medium: Electronic Resource
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