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: Chronic relapsing EAE ; Serum-induced demyelination ; Central demyelination ; Peripheral demyelination
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Sera from guinea pigs with acute or chronic relapsing experimental allergic encephalomyelitis (EAE) were injected into the lumbosacral subarachnoid space of normal recipient rats. Seventeen of 37 sera induced demyelination in the CNS, and 27 of 37 sera caused demyelinated peripheral nerve fibers in the roots. The highest incidence of demyelinating activity of EAE sera was noted in those from donor animals sampled during the early chronic stage of the disease [40–100 days post sensitization (dps)]. Only few sera from animals sampled during the acute and subacute stage (10–40 dps) were able to induce demyelination. Sera from animals sampled between 100 and 200 dps showed a lower incidence of demyelinating activity as compared to those from the early chronic phase of the disease. There was no clear-cut correlation between the serum-demyelinating activity and the severity of the demyelinating disease in the donor animals. The patterns of demyelination in the central as well as peripheral nervous system of recipient animals were characterized by vesicular disruption of myelin or myelin stripping. Myelin degradation was performed mainly by macrophages. In the CNS some astrocytes also contained debris. Astrocytes increased in size, and mitosis of astrocytes was observed. Oligodendrocytes appeared to be unaffected. No demyelination was found when the sera from animals sensitized with CFA alone or with guinea pig liver tissue were injeted into the subarachnoid space of normal recipient rats. Two possible mechanisms of demyelination are diseussed: Antibody-mediated complement-dependent and antibody-dependent cell-mediated demyelination.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 2
    ISSN: 1432-0533
    Keywords: Chronic relapsing experimental allergic encephalomyelitis ; Blood-brain barrier ; Tracer study ; Cerebrospinal fluid proteins
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Blood-brain barrier (BBB) permeability in chronic relapsing experimental allergic encephalomyelitis was studied morphologically in tracer studies with horseradish peroxidase (HRP) as well as by quantitative determination of HRP, albumin, and IgG in serum and cerebrospinal fluid (CSF), BBB damage was found to be localized in demyelinating plaques and in blood vessels with vasculitis. Actively demyelinating lesions showed massive increase in BBB permeability, whereas in inactive or remyelinated lesions BBB damage was either minimal or absent. Determination of serum proteins in the CSF of animals with severe disease and a high incidence of actively demyelinating lesions showed evidence of BBB damge (reduction of Q-albumin) and an IgG-index in the normal range. In animals with only inactive lesions the Q-albumin was normal, the IgG index, however, was elevated. This finding indicates intrathecal IgG synthesis. A correlation between morphologically visualized tracer leakage in the central nervous system (CNS) with serum protein concentrations in the CSF revealed that elevated CSF albumin is a reliable indicator for BBB damage in lesions, located near the inner or outer surface of the brain and spinal cord. However, singular focal lesions with BBB damage located in the depth of the CNS parenchyma may not be accompanied by CSF protein alterations. The invariable presence of BBB damage in active inflammatory demyelinating lesions and its absence in inactive plaques or in the unaffected nervous tissue may be important in therapy, not only in experimental allergic encephalomyelitis but also in multiple sclerosis (MS).
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 3
    ISSN: 1432-0533
    Keywords: Ganglioside-antibodies ; Cholera toxin ; Cytotoxicity ; Demyelination
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Ganglioside-antisera, the ganglioside GM1-ligands, cholera toxin (CT), and CT subunit B, respectively, were injected into the lumbosacral subarachnoid space of normal rats. The cytotoxic effects of the injected compounds on the peripheral and central nervous system were investigated by light and electron microscopy; the severity of CNS lesions was evaluated by quantitation of macrophages containing debris. In contrast to control sera and GM2-antiserum, antisera against a mixture of the major brain gangliosides GM1, GD1a, GD1b, and GT1b (MaBG) or against GM1 induced demyelination in spinal roots and spinal cord, as well as alterations of astroglia. CT induced the same cytotoxic effects as MaBG- and GM1-antisera, whereas CT subunit B was without effect. The ineffectiveness of GM2-antiserum is obviously due to the very low concentration of the specific binding target, GM2, on cell surfaces; that of CT subunit B to the lack of the cytotoxic operator, subunit A. Our results indicate that a similar pattern of neuropathological lesions may be effected by different cytotoxic mechanisms through attachment of the cytotoxic agent onto the cell surface via a common target molecule, and further substantiate the role of GM1-antibodies in the pathogenesis of demyelination.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 32 (1975), S. 299-312 
    ISSN: 1432-0533
    Keywords: Mouse ; Peripheral nerve ; Perimeurium ; Nerve dissection ; Nerve regeneration ; Autoradiography
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The regeneration of transected peripheral nerves of mice was studied using autoradiographical and electron microscopical techniques. In general, maximal proliferation occurred between the 5th and 7th day after dissection and stopped when the cells emigrating from the proximal and distal stumps of the nerve started to contact one another. Special attention was paid to the reaction of the connective tissue cells of the endo-, epi- and peri-neurium. The perineurial cells seemed to dedifferentiate between the 3rd and 5th day after the transection and then started to proliferate into the defect. Labelled perineurial cells were completely absent, when the minifascicles were fully developed in the neuroma. The epineurial fibroblasts started to proliferate during the 1st day. Even 6 weeks after transection the multiplication rate was about ten fold that of the controls. The results are discussed with special reference to clinical nerve repair.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 44 (1978), S. 91-102 
    ISSN: 1432-0533
    Keywords: Myclin degradation ; Wallerian degeneration ; Optic nerve ; Electron microscopy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The ultrastructural events in myelin degradation in the rat optic nerve following transection have been studied. Myelin debris was found in cells similar to multipotential glia cells (Vaughn and Peters, 1968) as well as in astrocytes and in few oligodendrocytes. The different types of inclusions found during myelin degradation were described in their quantitative relations. Similarities to inclusions described in adrenoleukodystrophy and multiple sclerosis are discussed. By comparison of the ultrastructural findings with histochemical and biochemical data available a hypothetical model of myelin degradation is presented. The process starts with the degradation of digestible proteins resulting in uniformly layered lipid inclusions. Lipid degradation leads to the formation of unstructured lipid droplets and crystals. During the late stages of Wallerian degeneration numerous polymorph inclusion types can be found, probably representing poorly digestible lipids or lipoproteins.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 6
    ISSN: 1432-0533
    Keywords: Guinea pigs ; Chronic relapsing experimental allergic encephalomyelitis (EAE) ; Myelin-associated glycoprotein (MAG) ; Myelin basic protein (MBP) ; Glial fibrillary acidic protein (GFAP)
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Chronic relapsing experimental allergic encephalomyelitis (EAE) lesions that resemble those seen in multiple sclerosis (MS) were produced in young Hartley and strain 13 guinea pigs (Lassmann and Wisniewski 1979). To study distributions of myelin-associated glycoprotein (MAG), myelin basic protein (MBP), and glial fibrillary acidic protein (GFAP) in these lesions, paraffin and semithin epon sections of CNS from eight of these guinea pigs were immunostained with antisera to these proteins according to the peroxidase-antiperoxidase (PAP) method. In lesions with active myelin sheath breakdown, changes in anti-MAG and anti-BP immunoreactivity corresponded closely. Abnormal and/or decreased anti-MAG staining did not extend beyond margins of lesions into surrounding areas containing myelin sheaths stained normally by anti-BP and by histological stains for myelin. GFAP-stained astrocyte processes were more numerous and much larger in more chronic lesions. Anti-MAG and anti-BP both stained regenerating myelin sheaths which were very numerous in both paraflin and epon sections. In the latter, anti-MAG also stained some myelin-forming oligodendroglia. The results are additional evidence suggesting that in chronic relapsing EAE, myelin sheaths are the primary target. Oligodendroglia appear to be relatively unaffected and remyelinate most of the demyelinated axons.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 7
    ISSN: 1432-0533
    Keywords: Relapsing EAE ; Multiple sclerosis ; Demyelinating diseases
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Experimental allergic encephalomyelitis was induced by sensitization with guinea pig spinal cord in complete Freund's adjuvant with increased content of myobacterium in Hartley guinea pigs between the first and 28th day after birth. The animals either died during acute EAE or showed chronic progressive, chronic relapsing or chronic EAE with delayed onset. In animals immunized between the 1 and 13 day after birth, predominatly ordinary and chronic progressive EAE was noted, whereas animals sensitized between the 14th and 23rd day frequently suffered from hyperacute or chronic relapsing EAE. Immunization on the 24th day led to very high mortality in acute EAE. The relation of the pathohistologic alterations to different types of human inflammatory demyelinative disease is discussed.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 8
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 56 (1982), S. 52-62 
    ISSN: 1432-0533
    Keywords: Measles virus ; Subacute sclerosing panencephalitis (SSPE) ; Immunocytochemistry ; Immunoelectron microscopy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In a retrospective study of 42 cases with a histopathologic diagnosis of subacute sclerosing panencephalitis (SSPE) or similar panencephalitic processes, measles virus antigen was traced by means of indirect immunofluorescence (IF) and peroxidase-antiperoxidase (PAP) techniques on protease-pretreated histological sections from formol-fixed, paraffin-embedded brain biopsy or autopsy tissue, stored for up to 32 years. Measles virus antigen was detected in 28 brains which were thus definitely diagnosed as SSPE or in one case as subacute measles encephalitis under immunosuppression. These cases were divided into three groups: group A, nine brains with excessive antigen amounts; group B, seven cases with a patchy distribution of a moderate number of antigen-containing cells; and group C, twelve cases with very few scattered reacting cells. Patients with excessive antigen amounts usually died at an earlier age and after a shorter course than cases with very few antigen-containing cells. An adult onset (beyond 20 years) was seen in five patients. The brain of a 5-day-old baby born to an SSPE mother did not contain any measles virus antigen. Complement fixing measles serum antibody titers were negative or low in four patients with measles virus antigen in the brain. Most of the cases found to be negative for measles virus antigen in the brain did not show clinical and/or histopathologic features of typical SSPE, including cases with a “pseudosystemic” lesion pattern. Measles virus antigen was found almost selectively in cytoplasm, nuclei, and processes of pyramidal cells in the cerebral cortex, of large brain stem neurons, and oligodendrocytes. Protease pretreatment of the sections was important for best visualization of prominent dendritic involvement which was also confirmed by immunoelectron microscopy in one case. Apical dendrites of pyramidal cells were filled by viral antigen up to the upper cortical layers. Mononuclear cells in leptomeningeal and perivascular infiltrates and astrocytes rarely contained measles virus antigen. In contrast, IgG deposition was found mainly in astrocytes and mononuclear cells. Measles antigen production in most or all oligodendrocytes of a given area was not necessarily combined with demyelination in this area, especially in cases of short clinical duration.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 9
    ISSN: 1432-0533
    Keywords: Alzheimer's disease ; Progressive supranuclear palsy ; Immunocytochemistry ; Immune electron microscopy ; Tau proteins
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The antigenic profile of neurofibrillary tangles (NFT) in Alzheimer's disease (AD), senile dementia of Alzheimer type (SDAT), progressive supranuclear palsy (PSP) and in non-demented aged humans was investigated by light and electron microscopic immunocytochemistry using antisera and monoclonal antibodies to tubulin, microtubule-associated proteins (MAP1, MAP2 and tau), neurofilament proteins and determinants unique to Alzheimer paired helical filaments (PHF). Antibodies to tau proteins labeled NFT in all cases investigated (AD, SDAT, PSP and non-demented aged humans). However, one monoclonal antibody to PHF recognized numerous tangles in AD/SDAT, but only a small minority of the PSP tangles. Antibodies to tubulin, MAP1, MAP2 and neurofilament proteins did not selectively stain NFT. Whereas pretreatment of sections with phosphatase was required for the detection of tangles with Tau-1 monoclonal antibody, digestion of sections with either phosphatase or pronase had no significant effect on the staining pattern obtained with the other antibodies. Our studies show that, as previously described for AD/SDAT, phosphorylated tau polypeptides are also a major antigenic determinant of tangles in PSP, indicating that tangle formation may follow a common pathogenetic pathway in neurofibrillary degenerations. There is, however, at least one epitope in AD/SDAT tangles which seems to be absent on, or at least inaccessible in, the 15-nm straight fibrils of PSP.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 10
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 78 (1989), S. 497-503 
    ISSN: 1432-0533
    Keywords: Acquired immune deficiency syndrome (AIDS) ; Human immunodeficiency virus (HIV) ; Immunocytochemistry ; Vacuolar myelopathy ; Demyelination
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Vacuolar myelopathy (VM) is a frequent neurological complication of the acquired immune deficiency syndrome (AIDS). A suspected connection between VM and human immunodeficiency virus (HIV) has been based only on HIV isolation from affected spinal cord tissue. We report here an AIDS patient dying after 14 months of progressive dementia, including 3 months of spinal signs and symptoms. At autopsy, the brain revealed moderate diffuse damage of the white matter compatible with HIV-induced progressive diffuse leukoencephalopathy. The spinal cord showed VM mainly in the lateral and the posterior columns. Mono- and multinucleated macrophages were localized within intramyelinic and periaxonal vacuoles. Light and electron microscopic immunocytochemistry revealed the presence of HIV antigens restricted to mono- and multinucleated macrophages within the spongy lesions. Productive HIV infection is documented for the first time within VM lesions of this case. Therefore, VM should be included among HIV-induced lesions of the central nervous system. The intimate relation of infected macrophages to vacuolar myelinopathy could suggest secretion of a myelinotoxic factor by macrophages productively infected by HIV. Immune electron microscopy appears as promising tool to detect HIV in tissue even when the density of virus may be low.
    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...