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  • Selective vulnerability  (2)
  • AIDS-Cerebral toxoplasmosis  (1)
  • 1
    ISSN: 1432-0533
    Schlagwort(e): AIDS-Cerebral toxoplasmosis
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary Frequency, pathogenesis and morphological features of toxoplasmosis were assessed in a consecutive autopsy study. Among 204 patients who died from AIDS in Zurich during 1981–1990, 46 (23%) showed morphological evidence of cerebral toxoplasmosis. In 38 out of 46 cases (83%), toxoplasmosis was restricted to the central nervous system (CNS) and, therefore, pathogenetically classified as reactivation of a latent infection. Acute, systemic toxoplasmosis most frequently involved heart and lungs in addition to the CNS and was observed in 7 cases (15%). These patients probably acquired the infection during HIV-induced immunosuppression. Latent infection with intracerebral tissue cysts but no inflammatory response was present in only one case. Diffuse, necrotizing toxoplasma encephalitis with widespread, confluent areas of necrosis was mainly observed during the early period of the AIDS epidemic and restricted to 6 patients (13%) who did not receive chemotherapy. The majority of patients (83%) had multiple, macroscopically well-circumscribed abscesses with preferential location in the cerebral hemispheres. Of all CNS regions, the rostral basal ganglia were most frequently affected (78% of cases). Since 1989, chronic, burnt-out lesions were observed. These were mainly composed of lipid-laden macrophages and immunocyto-chemistry for Toxoplasma gondii usually failed to detect the parasite. This changing pattern of CNS lesions probably reflects improved clinical management of patients with AIDS.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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  • 2
    ISSN: 1432-0533
    Schlagwort(e): Gerbil ; Ischemia ; Selective vulnerability ; Protein synthesis ; Autoradiography
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary Regional cerebral protein synthesis was investigated in the Mongolian gerbil during recovery from forebrain ischemia produced by bilateral common carotid artery occlusion for 5 min. At various recirculation periods up to 72 h animals received a single dose ofl-(3,5-3H)tyrosine and were killed 30 min later. Brains were processed for autoradiography using the stripping film technique. During the initial 30 min of recirculation autoradiographs revealed an almost complete inhibition of protein synthesis in all forebrain structures with the exception of the medio-dorsal thalamic nuclei. Between 30 min and 12 h of recirculation amino acid incorporation was completely restored in neurons of the cerebral cortex, basal ganglia, hippocampal CA3 and CA4 zones and the dentate gyrus. In CA1, early (90-min postischemia) and progressive recovery of a few irregularly dispersed neurons was observed, but the vast majority of pyramidal cells never regained their normal biosynthetic activity. Between 3 and 6 h of recirculation CA1 neurons showed faint labeling, followed by a secondary deterioration resulting in complete lack of incorporation within 12 h after restoration of blood flow. Autoradiographs at all subsequent time points exhibited persistent inhibition of protein synthesis in CA1 until neuronal necrosis occurred 2–3 days later. Thus, in contrast to ischemia-resistant cell populations with rapid progressive and complete restoration of protein synthesis, hippocampal neurons undergoing delayed necrosis are characterized by an early incomplete recovery immediately followed by a secondary persistent inhibition.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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  • 3
    Digitale Medien
    Digitale Medien
    Springer
    Acta neuropathologica 72 (1986), S. 23-28 
    ISSN: 1432-0533
    Schlagwort(e): Hypoglycemia ; Cerebellum ; Selective vulnerability ; Neural grafts ; Protein synthesis
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary Prolonged insulin-induced hypoglycemia causes widespread loss of neurons and permanent brain damage with irreversible coma. Although the deprivation of carbohydrate stores affects all brain regions, the breakdown of energy metabolism and cessation of protein synthesis occur predominantly in the cerebral cortex, caudoputamen and hippocampus. The cerebellum, brain stem and hypothalamus are largely resistant. Following transplantation of the cerebellar anlage of rat fetuses (day 15 of gestation) into the caudoputamen of adult rats, the grafts were allowed to differentiate for a period of 8 weeks. The host animals were then subjected to 30 min of severe hypoglycemia with isoelectric EEG (‘coma’). In contrast to the surrounding vulnerable brain structures, protein synthesis was fully preserved within the cerebellar transplant. Grafting of fetal forebrain cortex to the same location did not result in escape from hypoglycemic cell injury. This indicates that resistance to hypoglycemia is part of the programmed differentiation of the cerebellum and develops irrespective of its location and functional integration within the nervous system.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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