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  • Cytochrome c oxidase deficiency  (2)
  • 1,3-Dibutyl-l-nitrosourea  (1)
  • Acute autonomic and sensory neuropathy  (1)
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  • 1
    Digitale Medien
    Digitale Medien
    Mammary tumorigenic effect of a new nitrosourea, 1,3-dibutyl-l-nitrosourea (B-BNU), in female Donryu rats (1980)
    Springer
    Journal of cancer research and clinical oncology 96 (1980), S. 35-41 
    Details
    ISSN: 1432-1335
    Schlagwort(e): Mammary tumor ; Nitrosourea ; 1,3-Dibutyl-l-nitrosourea ; Donryu rat
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary Four groups (groups 1-4) of female Donryu rats were given continuously 400, 200, 100, or 0 ppm solution of 1,3-dibutyl-1-nitrosourea (B-BNU) as their drinking water, and were studied for the development of tumors. The incidence of mammary tumors was 15/19 (79%), 20/24 (83%), 21/26 (81%), and 8/25 (32%) in groups 1, 2, 3, and 4, respectively. In addition, hematopoietic neoplasms, uterine tumors, and vaginal tumors developed in 13, 11, and six rats, respectively in 69 treated rats. Other tumors were infrequent.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/BF00412895
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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  • 2
    Digitale Medien
    Digitale Medien
    Quantitative evaluation of electron transport system proteins in mitochondrial encephalomyopathy (1993)
    Springer
    Acta neuropathologica 85 (1993), S. 370-377 
    Details
    ISSN: 1432-0533
    Schlagwort(e): Mitochondrial myopathy ; Cytochrome c oxidase deficiency ; Immunoelectron microscopy ; In situ hybridization
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary The levels of mitochondrial electron transport system proteins cytochrome c oxidase (COX) and complex III were measured in muscle fibers of patients with mitochondrial encephalomyopathy using quantitative immunoelectron microscopy. In a patient with Leigh's encephalopathy, immunoreactive COX protein was decreased to 20% of the normal mean value in all muscle fibers examined, while the amount of complex III was within the normal range. In a patient with fatal infantile COX deficiency, the level of COX protein was found to be decreased to 27–40% of the normal value in all muscle fibers examined. In patients with mitochondrial myopathy, encephalopathy, lactic acidosis associated with stroke-like episodes (MELAS) and chronic progressive external ophthalmoplegia (CPEO), COX protein levels were decreased to 20% of normal in muscle fibers lacking COX activity. In normal fibers, however, COX protein levels were also normal. The amount of complex III protein was normal in COX-deficient muscle fibers. In two patients, in situ hybridization was performed for detection of mitochondrial mRNA. Mitochondrial mRNAs were found to be abundant in muscle fibers with decreased COX protein, suggesting a defect at the mitochondrial protein-synthesis level in a COX-deficient muscle fiber.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/BF00334446
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  • 3
    Digitale Medien
    Digitale Medien
    Biochemical study in 28 children with lactic acidosis, in relation to Leigh's encephalomyelopathy (1985)
    Springer
    European journal of pediatrics 143 (1985), S. 278-283 
    Details
    ISSN: 1432-1076
    Schlagwort(e): Lactic acidosis ; Pyruvate decarboxylase deficiency ; Subacute necrotizing encephalomyelopathy ; Cytochrome c oxidase deficiency
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Abstract An enzymatic study of cultured skin fibroblasts was made in 28 patients with lactic acidosis. In three of these patients a diagnosis of Leigh's encephalomyelopathy was established from autopsy findings. Pyruvate decarboxylase (PDC) deficiency was found in four patients. In two of them, in whom Leigh's encephalomyelopathy was proved by autopsy, PDC activity was lower than 10% of the normal. The other two living patients, who showed 22%–25% of the normal activity, had clinical symptoms and courses different from Leigh's disease. These findings suggest that the patients with severe PDC deficiency develop Leigh's disease but those with mild deficiency may not. A deficiency of cytochrome c oxidase was found in two siblings. One of them, who was diagnosed as having Leigh's encephalomyelopathy by postmortem examination, showed a reduction of cytochrome c oxidase in the liver and brain. In the other sibling, who is living, the reduction of cytochrome c oxidase was demonstrated in the cultured skin fibroblasts and biopsied muscle. In an electron-microscopic study of biopsied muscle, two patients with mitochondrial myopathy were found. Their fundamental enzymatic defects were unclear. In two patients, in whom Leigh's disease was suspected following a brain CT, the production of 14CO2 from [3-14C] pyruvate was found to be low; suggesting a reduced activity of the TCA cycle. In another 18 patients, the fundamental defect was not clear.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/BF00442301
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  • 4
    Digitale Medien
    Digitale Medien
    Acute autonomic and sensory neuropathy: a case report (1990)
    Springer
    Journal of neurology 237 (1990), S. 42-44 
    Details
    ISSN: 1432-1459
    Schlagwort(e): Acute autonomic and sensory neuropathy ; Epstein-Barr virus ; Orthostatic hypotension ; Peripheral neuropathy ; l-Threo-2,3.-dihydroxyphenylserine
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary A female patient with acute autonomic and sensory neuropathy is described. Urinary disturbance developed rapidly and was followed by orthostatic syncope, absence of lacrimation, salivation and sweating, and sensory impairment. Muscle strength had been consistently normal despite diffuse muscular atrophy. Marked decrease in the number of small myelinated and unmyelinated fibres was revealed in biopsied sural nerve. Eighteen months after the onset, her autonomic symptoms have partially improved.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/BF00319667
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