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  • 1
    Electronic Resource
    Electronic Resource
    Nervous tissue injury induced by immune complexes (1982)
    Springer
    Acta neuropathologica 56 (1982), S. 279-284 
    Details
    ISSN: 1432-0533
    Keywords: Ferritin ; Galactocerebroside ; Immune complexes ; Proliferative changes in choroid plexus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Studies on acute and chronic serum sickness in mice were carried out to clarify the effects of immune complexes on the brain. These complexes were prepared with either anti-ferritin or anti-galactocerebroside rabbit antibodies and were injected i.m. into C57/BL mice. They were shown to be deposited in the choroid plexus, subependymal regions and meninges, and were accompanied by proliferative and destructive changes. The probable allergic mechanisms involved in the pathogenesis of these lesions are discussed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00691259
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  • 2
    Electronic Resource
    Electronic Resource
    Re-examination of ex-boxers' brains using immunohistochemistry with antibodies to amyloid β-protein and tau protein (1991)
    Springer
    Acta neuropathologica 82 (1991), S. 280-285 
    Details
    ISSN: 1432-0533
    Keywords: Dementia pugilistica ; Alzheimer's disease ; Amyloid angiopathy ; β-protein ; Tau protein
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A histopathological study was carried out on the brains of eight ex-boxers (ages 56 to 83) using conventional histological staining methods and immunocytochemistry with antibodies to amyloid β-protein and the PHF-related tau protein. All cases showed a large number of tau-immunoreactive neurofibrillary tangles and also β-protein immunoreactive senile plaques in the cortex. In the areas with many neurofibrillary tangles, neuropil threads with tau-immunoreactivity were also observed, and some of the senile plaque lesions were surrounded by abnormal neurites with tau-immunoreactivity. Moreover, three cases revealed β-protein-type cerebrovascular amyloid deposits on both leptomeningeal and cortical blood vessels. The present observations indicate that the cerebral pathology of dementia pugilistica is very similar to that of Alzheimer's disease and suggest that these two disorders share some common etiological and pathogenic mechanisms.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00308813
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  • 3
    Electronic Resource
    Electronic Resource
    Spinal cord vascular and leptomeningeal amyloid β-protein deposition in a case with cerebral amyloid angiopathy (1992)
    Springer
    Acta neuropathologica 84 (1992), S. 207-210 
    Details
    ISSN: 1432-0533
    Keywords: Cerebral amyloid angiopathy ; Amyloid β-protein ; Alzheimer's disease ; Spinal leptomeningeal vessels
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Cerebral amyloid angiopathy (CAA) is characterized by the deposition of amyloid fibrils on leptomeningeal and cortical blood vessels, and the incidence of this disorder increases with age. However, this form of vascular amyloid deposition rarely involves tissues outside of the brain. A 71-year-old woman first developed some deterioration in memory, and soon afterwards suffered from recurrent episodes of subcortical hemorrhage. Histopathological examination of this case revealed typical pathology of Alzheimer's disease with an extensive appearance of β-protein type CAA, and additionally, the spinal leptomeningeal vessels and the pia-arachnoid membranes were also affected by amyloid β-protein deposits. The spinal cord involvement associated with CAA and Alzheimer's disease is unusual, and the present case provides additional important information on the pathogenesis of disorders with β-protein deposition including Alzheimer's disease.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00311397
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  • 4
    Electronic Resource
    Electronic Resource
    Peripheral nervous tissue injury induced by galactocerebroside and galactocerebroside immune complexes (1985)
    Springer
    Acta neuropathologica 66 (1985), S. 274-282 
    Details
    ISSN: 1432-0533
    Keywords: Galactocerebroside ; Immune complexes ; Vasculomyelinopathy ; Experimental allergic neuritis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary It was demonstrated that New Zealand Albino rabbits sensitized to galactocerebroside had high levels of anti-galactocerebroside antibody and of immune complexes. The rabbits with high titers of immune complexes developed demyelination in the peripheral nerves. Lesion were produced in the peripheral nerves of mice by the i.m. injection of galactocerebroside immune complexes. The lesions were characterized by axonal degeneration, infiltrating macrophages containing myelin debris, and an inflammatory infiltrate of polymorphonuclear and mononuclear cells. Rabbit immunoglobulin and mouse C3 were observed around the endoneural blood vessels. These results suggest that galactocerebroside immune complexes may play a role in the pathogenesis of mouse peripheral nerve lesions, due to the production of vasculomyelinopathy.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00690959
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  • 5
    Electronic Resource
    Electronic Resource
    Transthyretin-type cerebral amyloid angiopathy in type I familial amyloid polyneuropathy (1991)
    Springer
    Acta neuropathologica 81 (1991), S. 524-528 
    Details
    ISSN: 1432-0533
    Keywords: Cerebral amyloid angiopathy ; Familial amyloid polyneuropathy ; Amyloid ; Transthyretin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary To clarify the pathogenesis of cerebrovascular amyloid deposits, histological and immunocytochemical studies were performed on the central nervous system (CNS) in ten casès with type I familial amyloid polyneuropathy (FAP). They commonly suffered from peripheral somatic and autonomic nerve disorders without any CNS dysfunctions. However, all cases showed CNS amyloid deposits, mainly on the leptomeningeal vessels and pia-arachnoid membranes, with arteries and arterioles in the subarachnoidal space being the predominant site of cerebral amyloid accumulation. Using immunocytochemical staining methods with antibodies to amyloid β-protein, human cystatin C and transthyretin (prealbumin), all of these amyloid deposits were specifically immunolabeled by the anti-human transthyretin antibody. However, there were no transthyretin-related amyloid deposits in the brain parenchyma. It is concluded that CNS transthyretin-immunoreactive amyloid deposition with cerebral amyloid angiopathy (CAA) is a common pathological finding in this disease. Moreover, the patients with type I FAP are known to have an amyloid protein precursor (a variant of transthyretin) in serum. This transthyretin type of CAA, therefore, seems to be an example of cerebrovascular amyloid deposits derived from a serum precursor.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00310133
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  • 6
    Electronic Resource
    Electronic Resource
    Autoimmune encephalomyelitis in rhesus monkeys induced by immunization with cerebral endothelial cell membrane (1988)
    Springer
    Acta neuropathologica 77 (1988), S. 39-46 
    Details
    ISSN: 1432-0533
    Keywords: Multiple sclerosis ; Cerebral endothelial cell membrane ; Rhesus monkeys ; Autoimmune encephalomyelitis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary It is postulated that multiple sclerosis might be an autoimmune demyelinating disease of the central nervous system (CNS). The mechanisms involved are unknown but, since the blood-brain barrier (BBB) is damaged, injury to endothelial cells is likely to have occurred. Our previous studies have led us to investigate the autoimmune effect of injuring the blood-brain barrier by immunizing rhesus monkeys with an endothelial cell membrane from the same kind of animals. The immunized animals developed a chronic or a relapsing neurological illness. Histological and ultrastructural examinations of the brain in the acute stage showed infiltrates of mononuclear cells around the blood vessels of the white matter of cerebrum, cerebellum, pons and midbrain, while in the chronic phase, large areas of demyelination and remyelination, especially in the white matter regions, were present. The animals immunized with extraneural antigen, an endothelial cell membrane obtained from human umbilical cord, developed no neurological illness. This results indicate that the brain endothelial cell membrane has an inflammatory encephalitogenic activity which could produce widespread demyelination in animals. The animal model described here may prove to be useful in the pathogenetic investigation of human autoimmune demyelinating diseases.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00688241
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  • 7
    Electronic Resource
    Electronic Resource
    A new model for multiple sclerosis: Chronic experimental allergic encephalomyelitis induced by immunization with cerebral endothelial cell membrane (1987)
    Springer
    Acta neuropathologica 73 (1987), S. 259-266 
    Details
    ISSN: 1432-0533
    Keywords: Multiple sclerosis ; Cerebral endothelial cells ; Experimental allergie encephalomyelitis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Multiple sclerosis is considered to be an autoimmune demyelinating disease of the central nervous system. Damage to the blood-brain barrier, of which endothelial cells are the main constitutent, occurs in multiple sclerosis, probably due to immunological mechanisms. We report here the results of immune-mediated damage to these cells, produced by immunizing guinea pigs with an endothelial cell membrane fraction. The fraction was obtained from cerebral endothelial cells grown in vitro and was free from myelin basic protein. The immunized animals developed a chronic neurological illness with evidence of delayed hypersensitivity to the cell membrane fraction but not to myelin antigens. Histological examination of the brain in the acute stage showed mononuclear cell infiltrates aroud blood vessels, while in the chronic phase large areas of demyelination, especially in the periventricular region, were present. This bore a striking similarity to the brain in multiple sclerosis. This may prove to be a useful new animal model for the investigation of the human demyelinating disease.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00686620
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  • 8
    Electronic Resource
    Electronic Resource
    Changes in reciprocal ia inhibition during voluntary contraction in man (1984)
    Springer
    Experimental brain research 53 (1984), S. 400-408 
    Details
    ISSN: 1432-1106
    Keywords: H-reflex ; Ia inhibition ; Tonic voluntary contraction ; Ankle muscles ; Man
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Reciprocal Ia inhibition from ankle flexors to extensors was studied during voluntary tonic isometric dorsiflexion and plantar flexion in five normal subjects. The Ia inhibition was examined as the short-latency suppression of the soleus H-reflexes by stimulation of the low-threshold afferents in the common peroneal nerve (Mizuno et al. 1971). At rest, weak Ia inhibition was demonstrated in four subjects out of five, the maximal amount being 14.1 ± 5.0% suppression of the control H-reflex. The absolute amount of inhibition, which was calculated by subtracting the mean size of the conditioned H-reflex from that of the control H-reflex and expressed as a percentage of the maximal M-response, increased during ankle dorsiflexion, and decreased or disappeared during plantar flexion in parallel with the amount of contraction. The neural mechanisms for facilitation of the Ia inhibitory pathway during dorsiflexion were considered to support the hypothesis of “α-γ-linkage in reciprocal inhibition”, i.e. combined facilitatory effects on the Ia inhibitory interneurone from the supraspinal centers directly and indirectly via the γ motoneurone — Ia afferent route. The mechanism for inhibition of the pathway during plantar flexion was considered to be inhibition of the Ia interneurone of the flexor side by Ia interneurone of antagonist extensors. A quantitative aspect of activity in the reciprocal Ia inhibitory pathway on the performance of voluntary movement is revealed in this study.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00238170
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  • 9
    Electronic Resource
    Electronic Resource
    A Hippocampal Protein Associated with Paraneoplastic Neurologic Syndrome and Small Cell Lung Carcinoma
    Amsterdam : Elsevier
    Biochemical and Biophysical Research Communications 199 (1994), S. 1200-1208 
    Details
    ISSN: 0006-291X
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1006/bbrc.1994.1358
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  • 10
    Electronic Resource
    Electronic Resource
    Methionyl-tRNA synthetase of Escherichia coli A zinc metalloprotein
    Amsterdam : Elsevier
    BBA - Protein Structure 576 (1979), S. 128-133 
    Details
    ISSN: 0005-2795
    Keywords: (Escherichia coli) ; Metalloprotein ; Zn^2^+ ; methionyl-tRNA synthetase
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1016/0005-2795(79)90491-4
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