Library

feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    ISSN: 1432-0533
    Keywords: Key words Tumor necrosis factor-α ; Lymphotoxin ; Interferon-γ ; Glia ; Cerebrovascular disease
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We examined the immunohistochemical localization of the proinflammatory cytokines tumor necrosis factor-α, lymphotoxin and interferon-γ in 22 autopsy brains of patients with either cerebrovascular disease (CVD) or other neurological diseases as well as 2 non-neurological control brains. These cytokines were coexpressed mostly in the microglia/macrophages and in a few astroglia in the brains with acute cerebral infarction and cerebral hemorrhage. In cases with cerebral infarction, they were observed as early as 33 h after the onset of the illness and persisted for up to 40 days after the onset. In one patient with cerebral hemorrhage who survived for 4 h, the cytokine-immunoreactive glial cells were confined to the margins of the hematoma. In contrast, the cytokine-immunoreactive glia were distributed diffusely in one patient with cerebral hemorrhage who died 12 days after the onset of the illness. Labeling for these cytokines was weak in the glial cells of control brains and those with neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease and multiple system atrophy, in so far as there were no concomitant acute CVD foci. The present results indicate that proinflammatory cytokines are up-regulated in the brains of patients with acute stroke, and suggest an early inflammatory response in human CVD.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 2
    ISSN: 1432-0533
    Keywords: Key words White matter lesions ; Clasmatodendrosis ; Astroglia ; Cerebrovascular disease ; Alzheimer’s disease
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The pathogenesis of white matter lesions, which are frequently found in ischemic cerebrovascular disease and Alzheimer’s disease, remains unclear. Using light and electron microscopic immunohistochemistry for glial fibrillary acidic protein (GFAP) as a marker, the present study focused on the role of astroglia which show characteristic morphological alterations. Of 29 brains of patients with cerebrovascular disease and Alzheimer’s disease, 4 brains showed extensive swelling and vacuolation of white matter astroglia with their processes disintegrated and beaded (termed clasmatodendrosis). No such cells were observed in 6 control patients. Clasmatodendritic astroglia were not intensely eosinophilic using hematoxylin and eosin staining and included large lipophilic granules in their perikarya. These astroglia were immunoreactive for serum proteins such as immunoglobulins, fibrinogen and complement C3, C1q and C3d, as well as for proteins which are known to increase in reactive astroglia, such as vimentin, α-B crystallin, apolipoprotein-E and laminin. Double labeling for GFAP and microglial cell markers indicated that these cells were of astroglial lineage. Immunoelectron microscopy for GFAP revealed that clasmatodendritic astroglia had condensed chromatin, lysosomes and large membrane-bound osmiophilic cytoplasmic inclusions, which corresponded to the lipophilic granules observed with light microscopy. These cytochemical features collectively suggest that clasmatodendritic astroglia incorporate edema fluid and phagocytose cellular debris, and eventually degenerate as a result of cerebral edema.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 3
    ISSN: 1432-0533
    Keywords: Key words Alzheimer’s disease ; Binswanger’s disease ; White matter ; Amyloid angiopathy ; Fibrohyalinosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The pathogenesis of white matter lesions observed in Alzheimer’s disease (AD) is not completely clear. We tested the hypothesis that white matter lesions are correlated with medullary artery sclerosis rather than with amyloid angiopathy. A total of 57 brains were examined, including 39 derived from patients with AD and 13 from patients with Binswanger’s disease (BD) along with 5 from non-neurological patients. Moderate or severe amyloid deposits in the meningocortical segment were observed in 32 out of 39 AD patients (82.1%), and in 2 out of 13 BD patients (15.4%). These deposits were not observed in the white matter segment, except for 2 patients with AD. The BD patients invariably had marked white matter lesions and fibrohyalinosis in the medullary arteries, with a mean sclerotic ratio of 48.1%. In contrast, the AD patients had mild or moderate white matter lesions and a sclerotic ratio of 37.9%, which was significantly greater than the controls. The scores for white matter lesions were correlated with the sclerotic ratio of the medullary arteries, but not with the ages of onset or the scores for amyloid angiopathy. Although amyloid angiopathy is an independent risk of white matter lesions, its role is limited in the pathogenesis of those associated with AD. Wall thickening of the medullary arteries, likely due to fibrohyalinosis, is closely correlated with the white matter lesions in AD, thus indicating a heterogeneity in its etiology.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 4
    ISSN: 1432-0533
    Keywords: Immunoelectron microscopy ; Tubulin ; Microtubule-associated protein ; Cerebral ischemia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Differential vulnerability of microtubule components to cerebral ischemia has been reported previously. We investigated the disintegration of microtubules using immunoelectron microscopy for α-tubulin and microtubule-associated protein 1A and 2 (MAP1A and 2). Mongolian gerbils were subjected to bilateral carotid occlusion for 10 to 30 min and reperfusion for up to 72h following ischemia for 10 min. After ischemia for 10 min, some dendrites in the stratum moleculare of the subiculum-CA1 region lost immunoreaction products for α-tubulin and MAPs. Loss of the reaction products spread to the medial CA1 region during progressive ischemia for 30 min. In some dendrites, electron-dense precipitates for MAPs were dispersed in the dendritic cytoplasm with little reaction product on microtubules and without alteration of the reaction for α-tubulin. After recirculation, loss of electron-dense precipitates for α-tubulin and MAPs, as well as disintegration of microtubules, propagated further to the medial CA1 region and to the proximal dendrites. The present study demonstrated prompt disintegration of microtubules with rapid disappearance of the reaction for MAPs which seemed to be caused by detachment of MAPs from the microtubule cores.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 5
    ISSN: 1432-0533
    Keywords: Key words Cyclooxygenase ; Microglia ; Cerebral ¶ischemia ; Binswanger’s disease
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Cyclooxygenase-2 (COX-2) is known to be up-regulated in ischemic rodent brains, but only little information is available for the human brain. Using immunohistochemistry for COX-2, we investigated brains from control subjects and from patients with cerebrovascular diseases. COX-2 was markedly up-regulated in the neurons and endothelial cells in acute cerebral infarction, but was detected sparsely at chronic stages in these cellular compartments. In contrast, COX-2 immunoreactivity in glial cells was localized to the perinuclear region even in control brains. This immunolabeling was more intense and occurred also in the glial cytoplasm in the brains with chronic cerebral ischemia such as Binswanger’s disease. Double-labeling immunohistochemistry confirmed that COX-2-immunoreactive glia were mostly microglia. These results indicate that prostanoid synthesis is up-regulated in microglia during chronic cerebral ischemia, and that these cells may be involved in tissue repair or inflammation-mediated cell responses.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 6
    ISSN: 1432-0533
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In the brains of nine cases with cerebrovascular disease, one with mixed dementia, one with amyloid angiopathy and two non-neurological controls, we found three cases with focal accumulation of apolipoprotein E (apo-E) in dystrophic axons and accompanying macrophages. Since amyloid precursor protein (APP) and chromogranin A (CgA) accumulate after axonal damages, and are sensitive markers of the white matter lesions, the regional distribution of apo-E was compared to that of APP and CgA. apo-E-immunoreactive axons were present in the periphery of an infarction with neighboring macrophages, but not in mild white matter lesions that contained APP- or CgA-immunoreactive fiber bundles. The results suggest a role of apo-E in recycling cholesterol and other membrane components via macrophages into remodeling neurites in the brain, but this phenomenon is restricted to the periphery of infarction and may be less prominent than in the peripheral nervous system.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 7
    ISSN: 1432-0533
    Keywords: Key words Primary progressive aphasia ; Immunohistochemistry ; Ubiquitin ; Spongy degeneration
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We report the histopathological and immunohistochemical findings in a patient with primary progressive aphasia and abnormally ubiquitinated neurites in the cerebral cortex. Neuropathological examination showed severe neuronal loss and astrocytosis with a spongy change in the frontal cortex and neostriatum. Immunohistochemistry for ubiquitin antibody showed many immunoreactive dystrophic neurites in the superficial layer of the affected cortices and putamen. Those neurites were neither argentophilic nor stained with other antibodies against neurofilament, tau, or microtubule-associated protein-2. There were no neuropathological changes characteristic of Alzheimer’s disease, Pick’s disease, or Creutzfeldt-Jakob disease. Immunoelectron microscopy using anti-ubiquitin antibody showed inclusions in the dendrites, consisting mainly of granular and filamentous material. These pathological features, unusual in primary progressive aphasia, indicate the neuropathological heterogeneity of this disease condition.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...