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  • 1
    Electronic Resource
    Electronic Resource
    Nickel dermatitis from a dental prosthesis without buccal involvement (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Contact dermatitis 21 (1989), S. 0 
    Details
    ISSN: 1600-0536
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1600-0536.1989.tb04687.x
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Correlation of morphologic brain lesions with physiologic alterations and blood-brain barrier impairment in 3-intropropionic acid toxicity in rats (1987)
    Springer
    Acta neuropathologica 74 (1987), S. 67-74 
    Details
    ISSN: 1432-0533
    Keywords: 3-Nitropropionic acid ; Cerebral hypoxia ; Blood pressure determination ; Blood gas analysis ; Blood-brain barrier
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 3-Nitropropionic acid (NPA), a toxin which irreversibly inhibits the Krebs cycle enzyme succinate dehydrogenase, causes severe neurologic disease and a specific pattern of morphologic brain damage when given subcutaneously to rats. To determine whether hypotension or hypoxemia were necessary for development of morphologic brain lesions in NPA neurotoxicity, systemic blood pressure and arterial blood gases were measured in NPA-intoxicated rats. The extent and distribution of albumin extravasation was examined by immunohistochemistry, and was compared to the extent and severity of morphological injury in the caudate-putamen. Neither hypotension nor hypoxemia were necessary for the development of morphologic injury in the brains of NPA-intoxicated rats. In fact, intoxicated rats had significantly higher systolic blood pressure and arterial blood oxygen than did controls. Arterial bicarbonate and pH were significantly lower in intoxicated rats than controls, however, suggesting that acidosis may be involved in the pathogenesis of NPA toxicity. When morphologic injury was severe, albumin extravasation was extensive occupying approximately 30%–80% of the lesion area in the caudate-putamen of NPA-intoxicated rats. When morphologic injury was mild, albumin extravasation was absent, or limited to small cuffs around individual capillaries (〈1% of the lesion area). There was no leakage of albumin in the cerebral cortex, which was resistant to morphologic injury. It was concluded that leakage of protein-rich fluid into cerebral parenchyma from blood-brain barrier impairment is not responsible for the initiation of morphologic injury in NPA toxicity, but may contribute to the severity of injury later in the evolution of brain lesions.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00688340
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Nature and distribution of brain lesions in rats intoxicated with 3-nitropropionic acid: A type of hypoxic (energy deficient) brain damage (1987)
    Springer
    Acta neuropathologica 72 (1987), S. 286-297 
    Details
    ISSN: 1432-0533
    Keywords: 3-Nitropropionic acid ; Cerebral hypoxia ; Brain injury ; Microscopy ; Rats
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The clinical signs and morphological brain lesions associated with histotoxic hypoxia induced by subcutaneous injection of 3-nitropropionic acid (NPA) in rats are described, and compared to hypoxic brain damage from other causes including ischemia and hypoglycemia. The brains were perfusion-fixed with paraformaldehyde/glutaraldehyde fixative, and examined by light and electron microscopy. Intoxicated rats developed severe neurological disease characterized by somnolence, uncoordinated gait with stereotypical paddling movements, and ventral or lateral recumbency. Recumbent rats had a selective, bilaterally symmetrical pattern of severe morphological injury in the caudate-putamen, hippocampus, and thalamus. Recumbency was a consistent indicator of the development of morphological brain lesions. In contrast to reports describing rat models of ischemia and hypoglycemia, morphological injury was not seen in the cerebral and cerebellar cortices of NPA-intoxicated rats. Ultrastructurally, neuronal alterations ranged from chromatin clumping with increased cytoplasmic lucency to severe cellular shrinkage or swelling with marked mitochondrial swelling (high amplitude swelling). White matter alterations included axonal swelling and adaxonal splitting of myelin lamellae. Vascular changes included perivascular deposits of proteinaceous material presumably from leakage of serum proteins, variable electron lucency of endothelial cell cytoplasm, an apparent increase in pinocytotic vesicles, rare platelet thrombosis of capillaries, and rare intravascular blebs of luminal plasma membrane. As a model of brain damage following energy deficiency, NPA intoxication has the advantages of producing morphological brain injury in a highly predictable anatomical pattern, and at a time paralleling the onset of clinical recumbency.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00691103
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    Paper (German National Licenses)
    Fulltext
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