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  • Articles: DFG German National Licenses  (20)
  • 1995-1999  (10)
  • 1980-1984  (10)
  • 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
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 62 (1984), S. 316-323 
    ISSN: 1432-0533
    Keywords: Experimental allergic neuritis ; Macrophage function ; Silica blockade
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The selective toxicity of silica dust for macrophages has been used to assess the role of these cells in experimental allergic neuritis (EAN). Inbred Lewis rats were inoculated with bovine dorsal roots in Freund's complete adjuvant (day 0). In two experiments, animals received 200 mg of silica dust in 1 cm3 of saline intraperitoneally (IP) at days 8 and 16. In another two experiments, animals received IP silica at days 3, 7, and 11. Control animals received 1 cm3 saline IP at corresponding times. Regular clinical assessment showed that in animals treated on days 8 and 16 there was a significant delay in the time taken to reach their maximum degree of illness. This delay was not seen in the animals treated on days 3, 7, and 11. Neither of the injection regimes reduced the final maximum severity of the disease. In three experiments recovery of the treated and control animals occurred concurrently, hence the duration of the disease was reduced in the animals treated at days 8 and 16. However, in one group of animals given silica at days 3, 7 and 11, there was a delay in the time taken to recover from the most severe phase of the disease but thereafter the treated animals improved more quickly to reach their best grade at the same time as the controls. If the silica blockade of macrophages is to be effective in delaying the onset of EAN, the timing of injections is critical.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 59 (1983), S. 262-268 
    ISSN: 1432-0533
    Keywords: Experimental allergic neuritis ; Cyclosporin-A
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Experimental allergic neuritis (EAN) was induced in guinea pigs and rats and treated with Cyclosporin-A (Cy-A). When Cy-A was given prophylactically for 1 month from the time of induction of the disease, it prevented the development of EAN during the course of its administration. When Cy-A was given therapeutically after the onset of neurological signs, it effectively prevented further deterioration. This effect was more marked after 3 weeks' treatment than after only 1 week's treatment. In both regimens, when dosing with Cy-A ceased there was a latent period before clinical signs of EAN developed. This latent period is similar to that seen in the development of EAN in normal control animals and is probably due to the continued presence of antigen at the injection sites. After primary treatment of EAN with Cy-A, animals that relapsed did not respond to further treatment with Cy-A. Histological examination revealed that the nature of the EAN lesions in both groups of animals given Cy-A were not as severe as those seen in control animals. Despite these observations, there was no statistically significant difference between the maximum clinical grades reached by animals in any one group. These experiments suggest that T-cells are important in the development of EAN and that Cy-A interferes with this process by suppressing T-helper cells. They also show that it is possible to influence favourably the course of immune mediated neurological disease.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 53 (1981), S. 257-265 
    ISSN: 1432-0533
    Keywords: Experimental diabetes ; Skeletal growth ; Nerve fibre maturation ; Diabetic neuropathy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Observations were made between the ages of 2 and 12 months on rats made diabetic with streptozotocin at the age of 1 month, and compared with the findings in age-matched controls. Tibial length and body weight in the control animals increased progressively over the period examined, the growth rate being more rapid in the initial stages. Both of these parameters were consistently less in the diabetic animals over the whole of the observation period. Myelinated fibre numbers and diameters were measured in the tibial and plantar nerves. In the tibial nerve, fibre diameter did not differ between the diabetic and control animals up until 4 months of age; thereafter it changed little in the diabetic animals, but continued to increase in the controls. The findings in the medial plantar nerve were more difficult to analyse but showed comparable although less pronounced changes; fibre diameter may be have diminished in the diabetic nerves after 6 months. Teased fibre studies demonstrated few abnormalities in the tibial nerve, either in the control or the diabetic rats. In the lateral plantar nerves, there was a significant excess of axonal degeneration and regeneration in the diabetic nerves. It was concluded that diabetes impairs growth in nerve fibre diameter, but only after 4 months of age. Before then, no growth retardation is obvious, despite the fact that tibial length and body weight are less. This suggests that the peripheral nervous system may be protected against growth retardation during the early part of the postnatal growth period. The significance of the axonal degeneration in the plantar nerves is uncertain, but it may represent either an increased vulnerability of diabetic nerve to compression injury or, less probably, a distal axonopathy related to the diabetic state.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1432-0533
    Keywords: Key words Diabetic polyneuropathy ; Nodes of ; Ranvier ; Paranodes ; Axoglial dysjunction
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Observations have been made on the structure of the paranodal region at nodes of Ranvier in the sural nerve of patients with diabetic sensory polyneuropathy. The structure of the paranodes was examined with particular attention to the definition and assessment of axoglial dysjunction, which has been claimed to be a characteristic feature of both human and experimental diabetic neuropathy and which has been related to paranodal swelling. In the present series of cases it was not possible to confirm that axoglial dysjunction is a distinctive feature of diabetic polyneuropathy in fibres not undergoing active demyelination or wallerian-type degeneration, neither was excessive paranodal enlargement found.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1432-0533
    Keywords: Key words Peripheral neuropathy ; Hypomyelination ; Dysmorphism ; Cataracts
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Observations have been made on the peripheral nerve changes in four patients, ranging in age from 4 to 32 years, with the congenital cataracts facial dysmorphism neuropathy syndrome. Myelinated fibre density was within normal limits. The salient abnormality was diffuse hypomyelination which, in the older patients, was associated with demyelination and then axonal degeneration. These findings could be correlated with the relative preservation of sensory action potential amplitude despite markedly reduced nerve conduction velocity. Unmyelinated axon density was preserved. The morphological observations suggest the operation of a developmental process affecting myelination with a later superimposed degenerative disorder.
    Type of Medium: Electronic Resource
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  • 7
    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
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  • 8
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 63 (1984), S. 319-329 
    ISSN: 1432-0533
    Keywords: Peripheral nerve myelin ; Myelin periodicity ; Myelin structure
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The occurrence of myelin with an unusually large periodicity has been noted in a variety of human and animal diseases by many authors. It has also proved possible to create regular alterations in periodicity by various treatments of fresh unfixed nerve. We have quantified the changes found in material from a variety of sources and conclude that they are compatible with the occurrence of physicochemical changes in the myelin membranes, leading to overhydration.
    Type of Medium: Electronic Resource
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  • 9
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 52 (1980), S. 1-6 
    ISSN: 1432-0533
    Keywords: Peripheral nerves ; Aging ; Pressure neuropathy ; Axonal glycogen bodies ; Polyglucosan bodies ; Hirano bodies
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Ultrastructural observations have been made on the tibial and plantar nerves of Wistar rats aged 18–24 months. Changes indicative of segmental demyelination and remyelination and axonal degeneration and regeneration were prominent in the plantar nerves. Both in the plantar and tibial nerves, but particularly in the former, axonal abnormalities were frequent. These included the occurrence of multiple intra-axonal vacuoles containing glycogen and polyglucosan bodies. Axonal sequestration by adaxonal Schwann cell processes was also increased. The Schwann cell cytoplasm in relation to this activity contained bundles of filaments with the ultrastructural features of Hirano bodies. The changes in the plantar nerves probably indicate a pressure neuropathy, but the possibility of a superimposed distal axonal degeneration related to aging cannot be excluded on the present evidence. Such changes must be taken into consideration in experimental studies performed on rats of this age.
    Type of Medium: Electronic Resource
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  • 10
    ISSN: 1432-0533
    Keywords: Experimental allergic neuritis ; Suppression ; Bovine dorsal root ; Lewis rat ; Resistance to reinduction
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The injection of bovine dorsal root antigen in complete Freund's adjuvant can be used to produce experimental allergic neuritis (EAN) in rats. In this study attempts were made to prevent the development of the disease by prior injections of antigen. It was found that eight intradermal (i.d.) injections of antigen in either incomplete Freund's adjuvant or in saline failed to suppress EAN. A single intraperitoneal (i.p.) injection of antigen in saline produced only minimal protection against the disease. However, it was found that rats which had been given a primary course of EAN were subsequently completely unresponsive to a second injection of antigen.
    Type of Medium: Electronic Resource
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