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Biomedical subjects

H Lassmann

Publications and source records attributed to H Lassmann.

At least 253 records · Page 14Linked to original sources
PubMed1981

Inflammatory demyelinating polyradiculitis in a patient with multiple sclerosis.

A case of multiple sclerosis (MS) occurred in which there were recent demyelinated plaques in the CNS, and inflammatory demyelination and remyelination in the peripheral (Schwann cell) portions of the spinal roots. The lesions in the peripheral nervous system (PNS) were characterized by inflammation, primary segmental demyelination, myelin stripping, the occurrence of lipid debris-containing macrophages in the endoneurium, and remyelination. To our knowledge, this is the first description of simultaneous acute inflammatory demyelination in the CNS and PNS in MS.

Acute Disease↗
PubMed1981

Fractionation of spinal cord tissue affects its activity to induce chronic relapsing experimental encephalomyelitis.

Chronic relapsing experimental allergic encephalomyelitis (EAE), an animal disease closely resembling multiple sclerosis, was induced in young guinea pigs by sensitization with guinea pig spinal cord tissue together with complete Freund's adjuvant and a high amount of mycobacterium tuberculosis. Sensitization of animals with myelin basic protein leads to an acute form of EAE, but not to a chronic demyelinating disease. The present study was designed to trace the factors of spinal cord tissue responsible for chronic disease and demyelination by using fractionated spinal cord tissue for sensitization. The following preparations were tested for encephalitogenic activity: a) total guinea pig spinal cord homogenized in chloroform/methanol (C/M), b) C/M residue (protein fraction), c) C/M extract (lipid fraction) and d) bovine brain gangliosides. C/M treated spinal cord preparations were less encephalitogenic as compared to untreated spinal cord. The protein fraction showed very little encephalitogenic activity, the histological changes were limited to perivascular inflammation without demyelination. A crude lipid fraction induced some chronic inflammation. Neither the purified lipid fraction nor gangliosides produced any EAE symptoms. The conclusion can be made that protein is necessary for the induction of chronic relapsing EAE, whereas lipid or a protein-lipid complex seems to be responsible for the demyelinating component of this disease.

Animals↗
PubMed1981

Isolated leptomeninges of the spinal cord: an ideal tool to study inflammatory reaction in EAE.

Isolated and stretched leptomeninges have several advantages for the study of basic mechanisms in inflammation of the CNS. They offer a three dimensional view of the vascular tree which has basically the functional characteristics of cerebral vessels (the tight barrier, excluding macromolecules to enter the CNS compartment). The limited, small thickness of the specimen facilitates the performance of histochemical and immunohistochemical methods.

Animals↗
PubMed1981

In vivo effect of sera from animals with chronic relapsing experimental allergic encephalomyelitis on central and peripheral myelin.

Sera from guinea pigs with acute or chronic relapsing experimental allergic encephalomyelitis (EAE) were injected into 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 be 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 injected into the subarachnoid space of normal recipient rats. Two possible mechanisms of demyelination are discussed: Antibody-mediated complement-dependent and antibody-dependent cell-mediated demyelination.

Animals↗
PubMed1981

Ultracytochemical studies of the blood-meningeal barrier (BMB) in rat spinal cord.

Alkaline phosphatase(AP),5'-nucleotidase(5'N) and nucleoside diphosphatase (NDPase) activities were studied by cytochemical methods applied to light and electron microscopy in the microvasculature of spinal cord leptomeningeal strips of normal and protamine sulfate (PS) treated rats. The increased permeability to intravenously injected horseradish peroxidase was observed in some segments of microvessels of PS treated rats. Enhanced formation of plasmalemmal pits and deep invaginations, formation of numerous pinocytic vesicles and the appearance of channel-like structures in the cytoplasm of endothelial cells were the most striking ultrastructural evidence of increased permeability of the affected microvessels. All of these structures also showed activity of AP, and to lesser extent, of NDPase; 5'N activity was mainly associated with the delimiting membranes of pinocytic vesicles. Our data present evidence that a shift of enzymatic activity from luminal to abluminal surface of affected endothelial cells results from membrane flow accompanying increased transport activity via formation of pinocytic vesicles and channel-like structures.

Alkaline Phosphatase↗
PubMed1981

Histogenesis of demyelinating lesions in the spinal cord of guinea pigs with chronic relapsing experimental allergic encephalomyelitis.

Spinal cord lesions in Hartley guinea pigs with chronic relapsing experimental allergic encephalomyelitis (EAE) were studied by light, transmission and scanning electron microscopy at different stages of the formation of demyelinated plaques. In addition the inflammatory response in the meninges was studied in isolated pia mater preparations separated from the spinal cord surface. In initial chronic lesions in the spinal cord, inflammation was restricted to penetrating parenchymal veins of the spinal cord and meninges. With the formation of large demyelinated plaques in the spinal cord, massive fibrosis of the meninges with infiltration by inflammatory cells was noted in an area covering the surface of the lesion. In plaques which reach the spinal cord surface, inflammatory cells could be seen passing between the pia and the spinal cord substance. In chronic remyelinated lesions, adhesions between meningeal fibroblasts and the astroglial limiting membrane were seen. In addition a topographical correlation between the distribution of spinal cord veins and venules and demyelinated plaques was found. These observations indicate that spinal cord lesions in chronic relapsing EAE are initiated by perivenous inflammation in the parenchyma and the meninges. Plaque formation, especially in spinal cord surface lesions, is additionally enhanced by the entrapment of inflammatory cells in the fibrosed meninges. The exchange of macrophages through the glia-limiting membrane may be responsible for the more rapid debris removal in the spinal cord in comparison with brain lesions in chronic relapsing EAE.

Animals↗
PubMed1981

Relapsing experimental allergic encephalomyelitis induced with isolated myelin and with myelin basic protein plus myelin lipids.

To test the ability of different spinal cord fractions to reproduce the clinicopathological features of relapsing experimental allergic encephalomyelitis (R-EAE), groups of young guinea pigs were inoculated with: (1) spinal cord myelin; (2) delipidated myelin; (3) reconstituted myelin and (4) MBP plus myelin lipids. The four sets of antigens induced acute EAE in most of the animals tested. During an observation period of 18 months, only one clinical relapse was observed in animals sensitized with myelin and with MBP plus myelin lipids. Extensive CNS demyelination was found in relapsing animals injected with myelin. No demyelinated lesions were observed in non-relapsing animals. By contrast, half of the surviving guinea pigs injected with MBP plus myelin lipids had demyelinated lesions, irrespective of whether they relapsed or not. The inability of the spinal cord myelin fractions to fully reproduce the R-EAE model suggest that other non-myelin antigens may be involved in the pathogenesis of multiple relapses.

Animals↗
PubMed1981

Neurological disease in a child with carnosinase deficiency.

Carnosinase deficiency presented as a progressive neurological problem with sensory polyneuropathy in a 12-year-old male. Carnosinuria was present, even on a meat-free diet, although carnosinemia was not observed. An increased amount of unmetabolized carnosine was found in the urine after a carnosine load. Serum and tissue (liver and nerve) from the patient showed deficient carnosinase activity (Fleisher et al. 1978, 1980). Morphometric and fine structural studies on the nerve and skin biopsies are presented, as is a review of the literature on carnosinase deficiency in mentally retarded patients.

Carnosine↗
PubMed1981

Myelin proteins, glycoproteins, and myelin-related enzymes in experimental demyelination of the rabbit optic nerve: sequence of events.

Wallerian degeneration of the rabbit optic nerve was investigated by the technique of retinal ablation which precludes edema, hemorrhage, or macrophage infiltration. After 8 days of degeneration, marked degradation of axons and some myelin abnormalities appeared in the optic nerve, optic chiasma, and optic tract. Myelin lesions were maximal 32 days after retinal destruction. The amount of material stained with a myelin dye decreased drastically between 32 and 90 days after the operation. Biochemical parameters gave the following sequence of events. The concentration of the major periodic acid--Schiff staining glycoproteins was decreased after 2 days, and 6 days later the presence of cholesterol esters was detected in the optic tissue. After 16 days of Wallerian degeneration, the specific activity of 2',3'-cyclic nucleotide 3'-phosphodiesterase not associated with myelin decreased, indicating a possible de-differentiation of oligodendrocytes. Degradation of myelin basic protein became significant at 32 days and the amount of myelin isolated decreased later. The loss of myelin basic protein coincided with a reduction of myelin periodicity as measured in purified fractions by electron microscopy. These results show that secondary myelin destruction in the absence of edema, hemorrhage, or macrophages is a very slow process, and in this situation myelin undergoes a selective and sequential loss of its constituents.

2',3'-Cyclic-Nucleotide Phosphodiesterases↗
PubMed1981

Immunologic studies of chronic relapsing EAE in guinea pigs: similarities to multiple sclerosis.

IgG/albumin ratios and presence of oligoclonal bands were studied in neutral pH brain extracts and sera of guinea pigs with chronic relapsing experimental allergic encephalomyelitis (R-EAE). The ratios were found to be significantly increased in central nervous system extracts of animals sacrificed during the first relapse and late stages of the disease relative to those of controls and of animals with acute EAE. These results are consistent with an intracerebral synthesis of IgG found in patients with multiple sclerosis (MS). When the immunofixation (after isoelectric-focusing) patterns of brain extracts and CSF from R-EAE animals were compared with those of controls, R-EAE animals showed distinct oligoclonal IgG bands in the pH region of 7.0 to 9.3, in contrast to diffuse patterns seen in controls. The finding of oligoclonal IgG in brain extracts of these animals further supports the usefulness of R-EAE as an experimental model for MS.

Albumins↗
PubMed1980

Chronic relapsing experimental allergic encephalomyelitis. Immunohistochemical studies.

The immunohistochemical staining of immunoglobulins (Ig), complement (C3), and fibrinogen in chronic relapsing experimental allergic encephalomyelitis lesions showed different staining patterns in the acute vs the chronic stage of the disease. In the acute stage, Ig, C3, and fibrinogen were present in the perivascular tissue of the brain and the spinal cord. In hyperacute-type lesions, the binding of Ig and C3 to the parenchyma was especially pronounced. The chronic stage of the disease was characterized by Ig-containing cells and Ig binding to white matter in actively demyelinating lesions. Linear or granular deposits of immunoglobulin and complement, reminiscent of those described in immune complex disease, were found in the choroid plexus.

Animals↗
PubMed1979

Chronic relapsing experimental allergic encephalomyelitis: effect of age at the time of sensitization on clinical course and pathology.

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.

Age Factors↗
PubMed1979

Chronic relapsing experimental allergic encephalomyelitis: morphological sequence of myelin degradation.

Myelin degradation in chronic relapsing experimental allergic encephalomyelitis was studied using light microscopic histochemistry and electron microscopy. In the earliest stages, a large number of myelin stripping macrophages were found. The Luxol fast blue positive degradation products were then gradually transformed into PAS positive material. No sudanophilic stage of myelin degradation was found in this model. In electron microscopy, the Luxol fast blue positive material was identified as uniformly layered lipid inclusions with a periodicity of 4.0--4.5 nm. During further digestion, this material was transformed into polymorph structured material, consisting of lamellar leaflets with a diameter of 7--10 nm, curved cylindrical profiles and granular osmiophilic material.

Animals↗
PubMed1979

Chronic relapsing experimental allergic encephalomyelitis: clinicopathological comparison with multiple sclerosis.

Clinical and neuropathological observations in chronic, relapsing experimental allergic encephalomyelitis (EAE) are reported and compared with data available for multiple sclerosis (MS). Clinical, relapsing EAE was found in 95 of 119 of the strain 13 and 22 of 57 of the Hartley guinea pigs immunized. Examination of the brains and spinal cords of the guinea pigs showed a high incidence of macroscopically visible, demyelinated plaques. The topographic distribution of lesions resembled a pattern similar to that described in MS. Microscopic features of the lesions consisted of perivenous inflammation, primary demyelination, oligodendrocyte loss, and reactive gliosis. It is concluded that, with the exception of minor differences, the clinical and pathological alterations in chronic, relapsing EAE closely resemble those found in MS.

Animals↗
PubMed1979

Tactile corpuscle-like structures in a case of plexiform neurofibromatosis.

Tactile corpuscle-like structures were identified in a plexiform neurofibroma, which was localized on the right cranial hemisphere os a 16-year-old boy and had necessitated repeated surgery. These structures were studied by light and electron microscopy. The origin of their component cells is, however, still controversial. We believe to have accumulated sufficient evidence for a Schwann cell origin of these cells.

Adolescent↗
PubMed1978

Ultrastructural sequence of myelin degradation. I. Wallerian degeneration in the rat optic nerve.

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 adn 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 typed can be found, probably representing poorly digestible lipids or lipoproteins.

Animals↗