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  • 1
    Electronic Resource
    Electronic Resource
    Barriers and transport properties of the perineurium (1979)
    Springer
    Acta neuropathologica 47 (1979), S. 139-143 
    Details
    ISSN: 1432-0533
    Keywords: Perineurium ; Permeability ; Peripheral nerve ; Rat ; Ultrastructure ; Autoradiography ; Albumin ; Peroxidase ; Protein deprivation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The permeability properties of the perineurium in sciatic nerves of 12-week-old rats were studied. The penetration of125I-labeled albumin and horseradish peroxidase into the perineurium was investigated electronmicroscopically 10, 30, and 120 min after the local extraneural application of the tracers. The autoradiographic study included age-matched protein-deprived rats. It was concluded that the perineurium acted as a diffusion barrier but also permitted a slow passage of the macromolecules into the endoneurium. The result indicates that this penetration to some extent is due to vesicular transport across the perineurial cells. The significance of these barrier and transport properties of the perineurium is discussed. No obvious differences in perineurial permeability between normal and protein-deprived rats were obtained.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00717037
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  • 2
    Electronic Resource
    Electronic Resource
    The effect of undernutrition on spinal ganglion nerve cell size (1977)
    Springer
    Acta neuropathologica 39 (1977), S. 75-80 
    Details
    ISSN: 1432-0533
    Keywords: Spinal ganglion ; Undernutrition ; Development ; Nerve cell size
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In previous investigations on rat it has been shown that prenatally instituted undernutrition leads to an irreversibly impaired calibre growth in sensory fibres of the peripheral as well as the central nervous system. A study was made on the increase in size of spinal ganglion nerve cells of normal and undernourished rats. Although the undernourished rats weighed only 50% of the controls no differences in spinal ganglion nerve cell size were found in the four age groups examined, i.e. rats 20, 60, 90 and 180 days of age.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00690388
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  • 3
    Electronic Resource
    Electronic Resource
    Paranodal myelin retraction in protein deficient and normal rats (1977)
    Springer
    Acta neuropathologica 40 (1977), S. 249-252 
    Details
    ISSN: 1432-0533
    Keywords: Low-protein diet ; Rat ; Peripheral nerve ; Paranodal area ; Morphometry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Young rats, submitted to severe protein restriction were studied concerning the width of intermyelin gaps at the nodes of Ranvier in peripheral nerve fibres. The results gave no proof of increased paranodal myelin retraction in lumbar spinal roots or the sciatic nerves of low-protein rats. Malnourished rats as well as controls showed great interindividual differences as to the presence of nodes with wide inter-myelin gaps.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00691962
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    Macrophages in peripheral nerves (1980)
    Springer
    Acta neuropathologica 49 (1980), S. 43-49 
    Details
    ISSN: 1432-0533
    Keywords: Rat ; Peripheral nerve ; Macrophage ; Ultrastructure ; Histochemistry ; Acid phosphatase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The cellular content of the endoneurium in peripheral nerves of normal adult rats was studied. Endoneurial cells with high light-microscopical activity of acid phosphatase were usually located close to blood vessels or near the perineurium. Cells with the ultrastructural appearance of macrophages showed the same distribution and accounted for 2–4% of the endoneurial cell nuclei profiles. These cells rapidly endocytosed carbon particles after endoneurial administration of colloidal carbon in vitro.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00692218
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  • 5
    Electronic Resource
    Electronic Resource
    Motor nerve conduction velocity and nerve fibre diameter in experimental protein deprivation (1980)
    Springer
    Acta neuropathologica 51 (1980), S. 215-221 
    Details
    ISSN: 1432-0533
    Keywords: Protein deprivation ; Rats ; Development ; Motor nerve conduction velocity ; Nerve fibre diameter ; Peripheral nerve
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Motor nerve conduction velocity (MCV) and nerve fibre calibre spectra of peripheral nerves were determined at different ages, during development in normal and protein-deprived rats. The protein deprivation was achieved by feeding female rats a protein deficient diet, given ad lib from 2 weeks before conception and onwards. After weaning, the offspring were fed the same protein-deficient diet. Compared to control rats which were given a balanced diet, the protein-deprived rats showed considerably reduced body weights but moderately reduced values of albumin and total protein in serum at 6 and 15 weeks of age. Although essentially the same, the mean nerve fibre diameter of the studied dorsal tail nerve was slightly larger in the protein-deprived rats at 6 weeks of age than in controls, while the inverse relationship was found at 15 weeks of age. The increase of MCV in normal and protein-deprived rats followed essentially the same curve during the period from 5–30 weeks of age. The results indicate that the MCV and nerve fibre diameter during development are correlated to chronological age and not to body size, although protein deprivation may, to a minor extent, influence nerve fibre calibre growth.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00687388
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  • 6
    Electronic Resource
    Electronic Resource
    Fatal mitochondrial myopathy, lactic acidosis, and complex I deficiency associated with a heteroplasmic A→G mutation at position 3251 in the mitochondrial tRNALeu(UUR) gene (1996)
    Springer
    Human genetics 〈Berlin〉 97 (1996), S. 269-273 
    Details
    ISSN: 1432-1203
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract A girl, who died at 14 years of age from a rapidly progressive mitochondrial myopathy, was found to be heteroplasmic for a mutation in the mitochondrial tRNALeu(UUR) gene at position 3251. A large proportion of muscle fibres contained accumulations of abnormal mitochondria but no cytochrome c oxidase deficient fibres were present. Polarographic and enzymatic measurements on isolated muscle mitochondria revealed a profound isolated complex I deficiency. A high percentage of mutant mtDNA was found in muscle (94%), fibroblasts (93%), brain (90%), liver (80%), and heart (79%). The family was not available for investigation. For genotype to phenotype correlation studies, we investigated the proportion of mutated mtDNA in single muscle fibres of normal appearance and muscle fibres with accumulations of mitochondria. The proportion of mutant mtDNA was 28% (range 〈 0.3%–86%) in normal-appearing fibres and 61% (range 15%–88%) in abnormal fibres. The difference in the proportion of mutant mtDNA was highly significant (P 〈 0.001) between the two groups of fibres.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02185750
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  • 7
    Electronic Resource
    Electronic Resource
    De novo mutation in the mitochondrial ATP synthase subunit 6 gene (T8993G) with rapid segregation resulting in Leigh syndrome in the offspring (1995)
    Springer
    Human genetics 〈Berlin〉 96 (1995), S. 290-294 
    Details
    ISSN: 1432-1203
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract The mutation in the mitochondrial ATP synthase subunit 6 gene (ATP6 T8993G) was identified in a male infant who died at age 15 months of Leigh syndrome. He had 94% mutated mitochondrial DNA (mtDNA) in muscle and 92% in lymphocytes. His mother was healthy but had 37% mutated mtDNA in muscle and 38% in lymphocytes. The proband's brother, who was also healthy, had 44% mutated mtDNA in lymphocytes. No mutated mtDNA was detected in muscle and lymphocytes from the maternal grandmother of the proband or in lymphocytes from 15 other maternal relatives, showing that the first carrier of the ATP6 T8993G mutation in this family was the mother of the proband. This study shows that this point mutation may occur at substantial levels in a carrier of a de novo mutation and rapid segregation with high levels of mutated mtDNA causing neurodegenerative disease may occur in the second generation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00210409
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  • 8
    Electronic Resource
    Electronic Resource
    Fatal mitochondrial myopathy, lactic acidosis, and complex I deficiency associated with a heteroplasmic A→G mutation at position 3251 in the mitochondrial tRNALeu(UUR) gene (1996)
    Springer
    Human genetics 〈Berlin〉 97 (1996), S. 269-273 
    Details
    ISSN: 1432-1203
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract A girl, who died at 14 years of age from a rapidly progressive mitochondrial myopathy, was found to be heteroplasmic for a mutation in the mitochondrial tRNALeu(UUR) gene at position 3251. A large proportion of muscle fibres contained accumulations of abnormal mitochondria but no cytochrome c oxidase deficient fibres were present. Polarographic and enzymatic measurements on isolated muscle mitochondria revealed a profound isolated complex I deficiency. A high percentage of mutant mtDNA was found in muscle (94%), fibroblasts (93%), brain (90%), liver (80%), and heart (79%). The family was not available for investigation. For genotype to phenotype correlation studies, we investigated the proportion of mutated mtDNA in single muscle fibres of normal appearance and muscle fibres with accumulations of mitochondria. The proportion of mutant mtDNA was 28% (range 〈 0.3%–86%) in normal-appearing fibres and 61% (range 15%–88%) in abnormal fibres. The difference in the proportion of mutant mtDNA was highly significant (P 〈 0.001) between the two groups of fibres.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02185750
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    Paper (German National Licenses)
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  • 9
    Electronic Resource
    Electronic Resource
    Atypical presentation of multisystem disorders in two girls with mitochondrial DNA deletions (1994)
    Springer
    European journal of pediatrics 154 (1994), S. 35-42 
    Details
    ISSN: 1432-1076
    Keywords: Key words     Mitochondrial DNA ; Renal tubular disease ; Hypoparathyroidism ; Diabetes ; mellitus ; Liver disease
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract      We describe two girls with atypical presentations of multisystem disorders due to deletions in mitochondrial DNA (mtDNA). One presented with painful carpopedal spasms due to hypoparathyroidism at the age of 4 years. The disease was rapidly progressive with development of truncal and limb ataxia, spastic paraparesis, muscle weakness and wasting, pigmentary retinal degeneration and sensorineural hearing loss. She had short stature and vitiligo patches, hirsutism, anaemia, diabetes mellitus and exocrine pancreatic dysfunction. The other girl presented at the age of 6 years with polydipsia, polyuria and fatigue due to renal tubular dysfunction. The disease was insidiously progressive with poor growth and development of sensorineural hearing loss, muscle weakness and truncal and limb ataxia. Morphological, enzyme histochemical and biochemical investigations indicated mitochondrial dysfunction of skeletal muscle, liver and kidney in one patient and of skeletal muscle and liver in the other. Both patients had large proportions of mtDNA molecules with deletion in liver, kidney, skeletal muscle and blood cells. Conclusion     It may be concluded that symptoms from several different organs may be the first manifestation of a mtDNA deletion disorder.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01972970
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  • 10
    Electronic Resource
    Electronic Resource
    Atypical presentation of multisystem disorders in two girls with mitochondrial DNA deletions (1995)
    Springer
    European journal of pediatrics 154 (1995), S. 35-42 
    Details
    ISSN: 1432-1076
    Keywords: Mitochondrial DNA ; Renal tubular disease ; Hypoparathyroidism ; Diabetes mellitus ; Liver disease
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We describe two girls with atypical presentations of multisystem disorders due to deletions in mitochondrial DNA (mtDNA). One presented with painful carpopedal spasms due to hypoparathyroidism at the age of 4 years. The disease was rapidly progressive with development of truncal and limb ataxia, spastic paraparesis, muscle weakness and wasting, pigmentary retinal degeneration and sensorineural hearing loss. She had short stature and vitiligo patches, hirsutism, anaemia, diabetes mellitus and exocrine pancreatic dysfunction. The other girl presented at the age of 6 years with polydipsia, polyuria and fatigue due to renal tubular dysfunction. The disease was insidiously progressive with poor growth and development of sensorineural hearing loss, muscle weakness and truncal and limb ataxia. Morphological, enzyme histochemical and biochemical investigations indicated mitochondrial dysfunction of skeletal muscle, liver and kidney in one patient and of skeletal muscle and liver in the other. Both patients had large proportions of mtDNA molecules with deletion in liver, kidney, skeletal muscle and blood cells. Conclusion It may be concluded that symptoms from several different organs may be the first manifestation of a mtDNA deletion disorder.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01972970
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    Paper (German National Licenses)
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