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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 40 (1977), S. 259-268 
    ISSN: 1432-0533
    Keywords: Lead encephalopathy ; Neuronal development
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Developmental changes in the cerebellum of neonatal Long-Evans rats with lead encephalopathy were studied by Golgi technique and by light and electron microscopy. Lead encephalopathy was produced by administering daily doses of lead acetate (600 mg of lead acetate/kg of body weight) through an esophageal catheter. Histopathologic changes were observed at 3, 5, 8, 10, 13, and 15 days of age. Matrix cells and neuroblasts of the external granular layer were minimally altered prior to day 8 but thereafter the number of mitotic figures per folium decreased moderately and the number of pyknotic cells increased markedly. The thickness of the molecular layer in lead poisoned animals persistently lagged behind that of control animals after 3 days. Purkinje cells survived the cerebellar alterations of lead encephalopathy very well for the first 5–8 days. However, the rate of Purkinje cell maturation dropped off and at 10 days many still possessed the “mitre” of reticular cytoplasm and the perisomatic processes that are so characteristic of 5–8-day old Purkinje cells. This was particularly true for Purkinje cells located superficial to the “edematous cavities” produced by lead intoxication. The perisomatic processes of these Purkinje cells maintained synaptic contact with climbing fibers, whereas the climbing fibers of control animals had formed asymmetric synapses in the lower dendritic field and the cell soma had symmetric basket fiber synapses. A great variation existed in dendritic growth. Morphologically the neurons were minimally altered by lead intoxication until late in the disease process. The observed neuronal damage supports the suggestion that it is secondary to vascular disruption.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1546-1718
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Medicine
    Notes: [Auszug] Although the link between the BRCA1 tumour–suppressor gene and hereditary breast and ovarian cancer is established, the role, if any, of BRCA1 in non–familial cancers is unclear. BRCA1 mutations are rare in sporadic cancers, but loss of BRCA1 resulting from reduced expression or ...
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  • 3
    ISSN: 1432-1335
    Keywords: p53 ; Tumor-suppressor gene ; Ovarian carcinoma ; Immunohistochemistry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Objective: The objective of this study was to analyze the incidence of immunohistochemically detectable p53 protein accumulation in epithelial ovarian carcinomas and to correlate these data with the clinical outcome so as to clarify further the role of p53 mutations in prognosis with these patients.Methods: Tumor tissues from 179 patients with epithelial ovarian carcinoma were used for immuno-histochemical analysis with monoclonal antibody DO1 and BP 53-12-1 on formalin-fixed, paraffin-embedded tissue.Results: A total of 78 cases (44%) showed positive nuclear p53 staining. The p53-positive cases were found in all histological types of epithelial ovarian tumors. p53 staining was found in tumors of all stages with a higher percentage of positive cases in stage IV ovarian carcinomas (not significant). Poorly differentiated carcinomas showed a significantly higher percentage of p53 protein expression than did highly differentiated tumors (P=0.0002). Clinical follow-up of up to 14 years (median 25 months) showed a slightly but not significantly shortened disease-free and overall survival time for patients with p53-positive epithelial ovarian carcinomas.Conclusions: We conclude from our data that p53 expression in ovarian carcinoma is associated with poor differentiation but not with the disease being in an advanced stage. There was a tendency for shortened disease-free and overall survival for patients with p53-positive tumors.
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