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  • 1
    ISSN: 1432-0533
    Keywords: Wallerian Degeneration ; Peripheral Nerves ; Macrophages ; Monocytes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The origin of the macrophages in peripheral nerves was investigated in newborn rabbits after labelling the blood monocytes with intravenous carbon suspensions. Carbon labelled lipid macrophages were observed at the site of trauma in the nerves but not in areas of Wallerian degeneration. It is suggested that in Wallerian degeneration, resorption of degenerate tissue is performed by endogenous cells only, while in traumatic lesions part of the phagocytosis is performed by migrated monocytes. The early increase in vascular permeability in traumatic lesions may be a prerequisite for the attraction of the monocytes.
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 54 (1981), S. 143-147 
    ISSN: 1432-0533
    Keywords: Hydrocephalus ; Ependyma
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Obstructive hydrocephalus was produced in 14-day old rabbits by injection of kaolin into the cisterna magna. The ependymal lining was studied by scanning electron microscopy. Marked hydrocephalus was present 1 or 2 weeks after the kaolin injection. The ependymal lining adapted remarkably well to the rapid expansion by increasing the surface area of the ependymal cells. No breaks or denudement of the ependymal lining was observed except at the sites of ruptured ventricular synechiae. Generally, these findings confirm previous light and electron microscopic observations on the same model (Torvik et al. 1976; Torvik and Stenwig 1977). The results are discussed in relation to current theories concerning the pathophysiology of acute hydrocephalus.
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  • 3
    ISSN: 1432-0533
    Keywords: Perinatal hypoxic brain damage ; Pontosubicular necrosis ; Dentate fascia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The dentate fascia of the hippocampus was studied in 25 infants with pontosubicular necrosis and in 21 control cases without hypoxic cerebral lesions. Of the control cases 19 were completely normal and 2 showed one single necrotic cell in the granule cell layer. In contrast 15 of the cases with pontosubicular necrosis showed varying degrees of neuronal karyorrhexis in the dentate fascia. The severity of these changes largely parallelled those in the subiculum but there were exceptions to this rule. It is concluded that the dentate fascia is frequently involved in pontosubicular necrosis.
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 80 (1990), S. 85-87 
    ISSN: 1432-0533
    Keywords: Addison's disease ; Adrenocortical failure ; Neuropathology
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A case of untreated and rapidly progressive Addison's disease in a 23-year old woman showed selective necrosis with karyorhexis of the granule cells in the hippocampus. We suggest that this unique lesion was caused by a severe adrenocortical insufficiency. This explanation is in accordance with a recent report of selective loss of hippocampal granule cells after complete adrenalectomy in rats. No evidence of nerve cell loss was found in three cases of Addison's disease that had received cortisone treatment, which is consistent with the experimental observation that even very low levels of cortisone in adrenalectomized rats are sufficient to prevent granule cell loss.
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 81 (1991), S. 479-485 
    ISSN: 1432-0533
    Keywords: Blood-brain barrier ; Necrotic neurons ; Immunohistocliemical neuronal markers ; Axonal transport
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Preliminary observations on human autopsy material have indicated that damaged neurons may take up plasma proteins early after the injury. These observations prompted an experimental study under controlled conditions. Focal brain lesions were produced in rats by extracranial application of dry ice for 90 s. This caused an immediate disruption of the blood-brain barrier with leakage of plasma components into the tissue and sharply circumscribed areas of necrosis of the underlying cortex. Five minutes after the lesion, uptake of albumin, fibrinogen and fibronectin into damaged neurons was demonstrated by immunostains. These proteins were retained in the injured neurons until they were phagocytized 2–4 days later. In addition, normal neurons whose axons or axon collaterals passed through or terminated in the lesion were labeled. This labeling was generally weaker than in damaged neurons and no labeling of neuronal nuclei was observed in these cells in contrast to those of damaged cells. Apart from nerve cells labeled through retrograde axonal transport, no staining of normal neurons was observed. Intravenous injections of Evans blue, which binds to plasma proteins, confirmed that albumin was taken up into damaged neurons almost immediately after the injury and showed that this uptake continued for at least 20 h. It is concluded that uptake of plasma proteins into damaged neurons may serve as early (and late) markers of neuronal injury.
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 84 (1992), S. 234-237 
    ISSN: 1432-0533
    Keywords: Cerebral contusions ; Plasma proteins ; Immunohistochemistry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Twenty-five cases of cerebral contusions of varions age were examined immunohistochemically for neuronal uptake of albumin and fibrinogen. The neurons in the damaged areas were heavily stained in all cases, even in those of only a few minutes' survival, and they remained positive for serum proteins until they disappeared from the lesions. In hematoxylin and eosinstained sections, neuronal changes were observed from the first minutes after the lesion but they were indistinguishable from the shrunken “dark” neurons that occur as artifacts in poorly fixed material. However, in contrast to the artificially changed cells, the truely damaged ones took up serum proteins. It is concluded that staining with antisera against serum proteins may serve as early markers for neuronal injury before reliable histological changes have developed.
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  • 7
    ISSN: 1432-0533
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Die retrograden Zellveränderungen im Facialiskern der Maus wurden nach intracerebraler Injektion von Actinomycin D untersucht. Normalerweise zeigen diese Neurone erhöhte Basophilie des Cytoplasmas und abnehmende Größe der Nissl-Schollen während der ersten Tage nach Durchtrennung des Nerven. Der Nervenzelldurchmesser nimmt während des 2.–4. Tages nach der Nervendurchtrennung zu. Nach intracerebraler Injektion von Actinomycin D kommt es zur raschen Desintegration der Nucleoli sämtlicher Neurone, während das Cytoplasma nur geringe Veränderungen aufweist. Die Nissl-Substanz der normalen Neurone erscheint 2 Tage nach der Behandlung gut erhalten. Wird Actinomycin zum Zeitpunkt der Durchtrennung des N. facialis verabreicht, so sind alle Veränderungen der retrograden Zellveränderung während der folgenden 48 Std blockiert. Diese Befunde weisen darauf hin, daß die Auflösung der Nissl-Substanz im Rahmen der retrograden Zellreaktion durch eine induzierte Enzymsynthese vermittelt wird. Wird die erste Actinomycin-Injektion 2 Tage nach der Nervendurchtrennung verabreicht, so zeigen die Neurone der durchtrennten Seite nach 2 Tagen extreme Chromatolyse. Das könnte auf eine raschere Übertragungsrate von RNS auf die fein verteilten basophilen Partikeln des Cytoplasmas als auf die großen Nissl-Granula der normalen Neurone hinweisen.
    Notes: Summary The retrograde reaction in the facial nucleus of mice has been studied after intracerebral injection of actinomycin D. Normally these neurons show increasing cytoplasmic basophilia and decreasing size of the Nissl granules during the first days after section of the facial nerve. The nerve cell diameter increases between the 2nd and 4th day after section of the nerve. After intracerebral injection of actinomycin D the nucleolus of all neurons disintegrates rapidly while the cytoplasm shows only slight changes. The Nissl substance of normal neurons appears well preserved after 2 days' treatment. When actinomycin is given at the time of section of the facial nerve, all aspects of retrograde reaction is blocked during the next 48 hours. The findings suggest that the dispersion of the Nissl substance during retrograde reaction is mediated through induced enzyme synthesis. When the first injection of actinomycin is given 2 days after section of the nerve the neurons on the operated side show extreme chromatolysis 2 days later. This may indicate a more rapid turnover rate of the RNA of the finely dispersed cytoplasmic basophilic particles than of the large Nissl granules of normal neurons.
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  • 8
    ISSN: 1432-0533
    Keywords: Metabolic Encephalopathy ; Cerebral Degeneration ; Alpers' Disease
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The clinical and pathological features of a case with primary progressive degeneration of the cerebral cortex are presented. Two siblings had nearly identical clinical histories. All three children were born microcephalic and they died at the age of 7, 10 and 18 months, respectively. All showed progressive mental and motor deterioration. Myoclonus and attacks of opisthotonus were prominent features. Postmortem examination was performed in the third child, who died at the age of 10 months. The brain weight was 310 g. The cerebral cortex was severely atrophic, with extensive laminar neuronal loss. The cerebellum was normal. The optic tracts were atrophic. Neuronal loss was observed also in a few other systems but their relation to the primary disease is uncertain. The basal ganglia were normal and the hippocampus showed only slight nerve cell loss. The case is considered to belong to a small group of cases with primary progressive cortical degeneration described by Laurence and Cavanagh (1968). This group should be distinguished from cases with secondary cortical degeneration caused by anoxic damage from recurrent epileptic attacks. The primary cortical degeneration may start shortly before birth, or after a brief periood of normal postnatal development. A positive family history has been reported in most cases, suggesting an inherited metabolic defect as cause of the disease.
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  • 9
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 38 (1977), S. 21-26 
    ISSN: 1432-0533
    Keywords: Hydrocephalus ; Ependyma
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Obstructive hydrocephalus was produced in 10–14 day-old rabbits by injection of kaolin into the cisterna magna and the ependyma and subependymal tissue was studied by electron microscopy. Generally, the study confirmed recent light microscopic observations on similar models (Torvik et al., 1976). In contrast to most previous reports,it was found that the ependyma adapted remarkably well to ventricular dilatation. No true ependymal defects occurred even in extensive hydrocephalus except at the sites of the ventricular synechiae which sometimes ruptured. The specialized ependymal junctions remained intact but outside the junctions the intercellular clefts were widened, particularly along the lateral wall of the lateral ventricle. The density of the microvilli and cilia decreased, probably because of the increase in the surface area of the ependyma. Dense bundles of filaments developed in the ependymal cells of the hydrocephalic animals. The extracellular space of the subependymal white matter appeared increased but there was no evidence of destruction of fibres or cells. Thus, the reduction of the cerebral mantle thickness was probably mainly caused by pressure atrophy.
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  • 10
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 14 (1969), S. 62-71 
    ISSN: 1432-0533
    Keywords: Nerve Cell ; Actinomycin D ; Retrograde Reaction ; Reticular Formation ; Facial Nucleus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Die retrograde Zellreaktion wurde an Neuronen der Formatio reticularis und des Facialiskernes von Mäusen nach intracerebraler Injektion von Actinomycin D untersucht. Gewöhnlich zeigen die retikulären Neurone den klassischen Typ der retrograden Reaktion mit Dispersion der Nissl-Substanz und zentraler Chromatolyse. Die Neurone des Facialiskernes zeigen gleichfalls Dispersion der Nissl-Granula, aber leichte Zunahme der Cytoplasma-Basophilie statt Chromatolyse. Diese Neuronentypen zeigen demnach etwas differente Arten der retrograden Reaktion. Actinomycin verhindert das Auftreten retrograder Reaktion im Facialiskern, wenn die Substanz z. Z. der Operation injiziert wird (Torvik u.Heding, 1967). Die vorliegende Studie zeigt, daß Actinomycin auch die retrograde Reaktion in der Formatio reticularis bei Verabreichung 2 Std vor Durchtrennung der reticulospinalen Fasern hemmt. Wird die Substanz 12 Std nach Durchtrennung der reticulospinalen Fasern verabreicht, so entwickelt sich die retrograde Degeneration in üblicher Weise in der Formatio reticularis, obwohl die Neurone zur Zeit der Injektion normal waren. Im Facialiskern wird die retrograde Reaktion durch Gabe der Substanz 9 Std nach der Operation, nicht aber nach 15 Std, blockiert. Die Befunde lassen vermuten, daß den morphologischen Nervenzellveränderungen nach Axonläsion die Synthese neuer Enzyme in den geschädigten Zellen vorausght, die irgendwie für die folgende Dispersion der Nissl-Substanz erforderlich sind.
    Notes: Summary The retrograde nerve cell reaction was studied in the neurons of the reticular formation and in the facial nucleus of mice after intracerebral injections of actinomycin D. Normally the reticular neurons show a classical type of retrograde reaction with dispersion of the Nissl substance and central chromatolysis. The facial neurons also show a dispersion of the Nissl granules but there is an early increase in the cytoplasmic basophilia instead of chromatolysis. The two types of neurons thus show somewhat different patterns of retrograde reaction. It was shown previously that actinomycin prevented the appearance of retrograde reaction in the facial nucleus when the drug was injected at the time of operation (Torvik andHeding, 1967). The present study showed that actinomycin blocked the retrograde reaction also in the reticular formation when it was given 2 h before the reticulospinal fibers were cut. When the drug was given 12 h after section of the reticulospinal fibers, the retrograde reaction developed normally in the reticular formation, although the neurons were morphologically normal at the time of injection. In the facial nucleus the retrograde reaction was blocked when the drug was given 9 h after the operation but not by 15 h. The findings suggest that the morphological nerve cell changes after axon lesions are preceded by the synthesis of new enzymes in the injured cells, which in some way are necessary for the ensuing dispersion of the Nissl substance.
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