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Biomedical subjects

H M Wiśniewski

Publications and source records attributed to H M Wiśniewski.

At least 19 recordsLinked to original sources
PubMed1978

Peripheral nervous system pathology in relapsing experimental allergic encephalomyelitis.

A recurrent type of primary demyelination was found in the anterior roots and dorsal root ganglia of strain 13 guinea-pigs with relapsing experimental allergic encephalomyelitis. Single nerve fibre studies revealed a predominant nodal--paranodal distribution of the destruction of myelin in these nerves. Damage of the Schwann cell--axolemmal junction was found in the majority of the abnormal nodes of Ranvier. This was accompanied by the formation of supernumerary adaxonal Schwann cell processes which further altered the normal myelinating cell--axon relationship. It is concluded that variations in antigenic composition may play a role in the selective involvement of the anterior roots. The pathogenesis of the observed nodal changes is discussed.

Animals↗
PubMed1977

Chronic relapsing experimental allergic encephalomyelitis. Studies in vascular permeability changes.

The vascular permeability in the nervous system to Evans blue-albumin and horseradish peroxidase was studied in chronic relapsing EAE in strain 13 and Hartley guinea pigs. The disease was induced by single sensitization of immature animal and was characterized clinically by remissions and relapses. Recent and old demyelinating plaques in the spinal cord were present. These showed an increased permeability to the protein tracers. The blood-brain barrier in these plaques are therefore disturbed and also in this respect the condition is similar to the multiple sclerosis lesions.

Animals↗
PubMed1977

Studies on the encephalitogenic effects of purified preparations of human and bovine oligodendrocytes.

Bulk-isolated human and bovine oligodendroglia, practically free from myelin, have been used in attempts to elicit an autoimmune response which has been compared with acute experimental allergic encephalomyelitis (EAE). For these experiments, a total of 20 Hartley guinea pigs, 33 Lewis rats and 16 rabbits have been studied. Animals were inoculated with a range of doses of purified preparations of both human and bovine oligodendroglial cells in complete Freund's adjuvant (CFA) and compared with others challenged with whole white matter in CFA. The latter animals all developed clinical and histological signs of experimental allergic encephalomyelitis (EAE) 2-3 weeks post-inoculation. In general, oligodendroglial cells were encephalitogenically less potent than white matter. Guinea pigs were the most susceptible to inoculations of oligodendroglia. In several given human oligodendroglia 14 days earlier, a paraparesis indistinguishable from conventional EAE was seen. Animals receiving bovine cells showed no clinical signs. Histologically, the CNS of afflicted guinea pigs displayed severe inflammation but, in contrast to conventional EAE in the same species, demyelination was rare in the small group of animals tested. After sensitization with oligodendroglia, rats displayed no clinical disease. Histologically, some given human cells had positive evidence of disease while bovine cells in others gave a mild response. Rabbits showed no clinical and very little histological disease. Although more extensive studies are needed to confirm the findings, from the animals studied it appears that (1) variation in response to inocula containing oligodendroglia exists among the species tested, (2) that human oligodendroglia are more potent immunologically than bovine cells, (3) that CNS lesions produced by these cells in guinea pigs, lack a strong demyelinative component and (4) a specific antigen might exist in oligodendrocytes which is distinct from myelin basic protein. The possible reasons underlying our findings are discussed.

Animals↗
PubMed1977

Axonal degeneration in demyelinating disorders.

Changes in the L7 and S1 segments of the spinal cord and the corresponding dorsal root ganglia (DRG), spinal roots and sciatic nerves of guinea pigs immunized with whole rabbit sciatic nerve in complete Freund's adjuvant have been studied and compared with the changes found in guinea pigs immunized with purified P.N.S. myelin. In both groups of animals, pathological changes were found in the posterior roots, DRG and root entry zones. In the posterior roots, axonal degeneration and segmental demyelination evolved in parallel, affected different populations of myelinated axons and showed no indication of interdependence. The aetiology of axonal degeneration in this and other demyelinating disorders is discussed. It is concluded that axons can be damaged by being in the vicinity of areas where cell-mediated immune reactions are taking place, i.e. as a consequence of the so-called 'bystander' effect.

Animals↗
PubMed1977

Liposome toxicity in the mouse central nervous system.

This study has shown that while some liposomes are highly toxic to the central nervous system, others, of different composition, are tolerated well in the dosage used (0.02-0.05 ml = 4-12 mg of lipid/inoculum). Those composed of lecithin-cholesterol-dicetyl phosphate or lecithin-cholesterol-stearylamine produced generalised epileptic seizures and some deaths due to respiratory failure immediately after injection,and a subsequent widespread tissue necrosis. However liposomes composed of lecithin-cholesterol-phosphatidic acid, or dipalmitoyl lecithin only, produced minimal morphological changes and by the sixth day post-injection the pathology was limited to the mechanical trauma caused by the injection. It is concluded that liposomes of appropriate composition may be sufficiently benign to use as carriers of therapeutic agents into the CNS.

Amines↗
PubMed1976

Neurofibrillary tangles of paired helical filaments.

The abnormal aggregates of fibrillar material found in neurons in Alzheimer's disease, senile dementia, the Guam Parkinsonism-Dementia complex, Down's syndrome, and postencephalitic Parkinsonism were studied by means of tilt-stage electron microscopy and with X-ray images of scale models of a bifilar helix. The model fulfills the structural criteria established by electron microscopy. These studies showed that the "twisted tubule" which makes up the neurofibrillary tangle in many pathological situations is a bifilar helix made up of 130 A filaments.

Alzheimer Disease↗
PubMed1976

Penetration of protein tracers into the epiretinal portion of the optic nerve in the rabbit nerve.

Horseradish peroxidase and fluorescein-labelled globulin were injected into the vitreous of adult and 11- to 13-day-old New Zealand albino rabbits. Both tracers diffused rapidly into the myelinated nerve fibre layer (the "medullary rays"), which extends over a long distance within the retina in these animals. The tracers penetrated also for some distance into the optic nerve beyond the lamina cribosa, where they were incorporated into a large number of cells in the nerve. This finding of a rapid diffusion of macromolecules into the medullary rays after intravitreal injection makes this experimental model suitable for the study of factors interfering with myelin or myelination.

Animals↗
PubMed1976

Retroperitoneal ganglioneuroblastoma: a kaleidoscope of neuronal degeneration. A light and electron microscopic study.

The light and electron microscopic features of an unique retroperitoneal ganglioneuroblastoma in a four-year-old female are described. The unprecedented concurrence of Hirano, zebra, membranous cytoplasmic (MCB), and Pick bodies in the same population of neoplastic, sympathetic ganglion cells provides further evidence for their non-specificity. Although the pathogenesis of the membranous cytoplasmic bodies in this tumor is unclear, they ostensibly arise within endoplasmic cisterns, similar to the proposed origin of membranous cytoplasmic bodies in Tay-Sachs disease. Both the apparent continuum between argyrophilic bodies and central chromatolysis, and the incorporation of various cytoplasmic constituents within neurofilamentous proliferations reflect some of the dynamic factors involved in the formation of Pick bodies.

Cell Count↗
PubMed1975

Infectious etiology of neuritic (senile) plaques in mice.

Brains of inbred female VM mice infected with scrapie agent were studied with the use of the Bodian silver impregnation method and by electron microscopy. In brains affected with scrapie, after an incubation period of between 587 and 655 days, numerous primitive, classical, and amyloid plaques were found. No plaques of any type were seen in the control mice.

Amyloid↗
PubMed1975

Neurotoxicity of hexachlorophene: new pathological and biochemical observations.

Twenty female rats with nursing litters were fed a diet containing 500 p.p.m. of hexachlorophene (HCP). The blood concentrations of hexachlorophene in mother rats were 4.7-6.0 mug/ml and in infant rats 2.0-2.5 mug/ml. Fifty percent of mother rats and 75% of infant rats died. Most of the surviving animals were asymptomatic apart from imparied visual function. Ten adult and 20 infant rats were killed by perfusion. Light- and electron-microscopic studies showed vacuolation of myelin in the central and peripheral nervous system and axonal degeneration which was especially severe in the optic nerves. After withdrawal of HCP hydrocephalus ex vacuo was present in the chronically intoxicated infant rats and the optic nerves showed marked atrophy and gliosis. Studies with liver mitochondria prepared from lactating hexachlorophene-fed rats showed a 50-75% inhibition of respiration with succinate as substrate.

Animals↗
PubMed1975

On the relationship of brain vasculature to production of neurological deficit and morphological changes following acute unilateral common carotid artery ligation in gerbils.

The known susceptibility of the Mongolian gerbil to cerebral infarction following unilateral carotid artery ligation has been attributed in the past to the demonstrated absences of an anastomotic supply between the anterior and posterior cerebral circulations. In a study of 34 adult gerbils exposed to such a procedure, 11, or 33%, developed severe neurological sequelae and succumbed to the procedure in less than 30 hr, whereas 23 animals survived with only minor or transient neurological signs. All animals displayed the expected lack of an anastomosis between the anterior and posterior circulations, but in addition the animals which survived the procedure were found to have a prominent early cross-connection between the anterior cerebral arteries, whereas the animals which succumbed had no such connection. Neuropathological changes in susceptible animals were apparent as early as 3 and one-half hr after ligation and consisted of edema, initially perivascular and then intraneuronal, slowed by acute necrosis. A variety of other vascular anomalies was encountered. We conclude that the peculiar susceptibility of Mongolian gerbils to cerebral infarction following acute unilateral common carotid artery ligation is not related primarily to lack o adequate collaterals between the anterior and the anterior cerebral arteries, but to the degree of adequate adequacy of communication between the anterior cerebral arteries. The critical difference may be more one of degree, i.e. the point at which the medial branches of the anterior cerebral artery fust to become anazygos vessel, rather than an actual difference in the pattern of distribution of the anterior cerebral arteries. The presence of other variation in vascular supply in a relatively small series suggests that results of similar studies of infarction and response to treatment be interpreted with caution.

Animals↗
PubMed1975

Experimental allergic optic neuritis (EAON) in the rabbit. A new model to study primary demyelinating diseases.

In New Zealand albino rabbits the axons of the nerve fibre layer are myelinated over a long distance within the retina. Primary demyelination of these fibres was induced by sensitization of the animals to bovine cerebral white matter or myelin basic protein in complete Freund's adjuvant and challenge thereafter by intravitreous injection of basic protein (BP) or purified tuberculin (PPD). Production of segmental demyelination as a result of sensitization to brain-specific antigen (BP) and indifferent (PPD) antigen, shows that morphologically the same type of lesions can be induced by any antigen which will elicit cell-mediated immune reaction.

Animals↗