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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
PubMed1999

Immunoultrastructural expression of intercellular adhesion molecule-1 in endothelial cell vesiculotubular structures and vesiculovacuolar organelles in blood-brain barrier development and injury.

Blood vessels from the vasculature of mouse brains during postnatal development and from human brain tumors (hemangiomas) removed at biopsy were examined immunocytochemically by transmission electron microscopy (TEM) or high-voltage transmission electron microscopy (HVEM) to determine the expression of intercellular adhesion molecule-1 (ICAM-1). In the mouse brains, ICAM-1 was shown to be initially expressed on the luminal and abluminal endothelial cell (EC) surfaces on day 3 after birth. ICAM-1 intensity increased on the luminal EC surfaces and labeled vesiculotubular profiles (VTS, defined in the present report) between days 5 and 7. After 2 weeks and at 6 months after birth, ICAM-1 labeling was weak or absent on the luminal EC surfaces. The hemangiomas presented a strong ICAM-1 reaction product on the luminal EC surfaces of small and large blood vessels associated with the VTS, with a weaker labeling of the abluminal or adventitial aspects of larger blood vessels. TEM of vesiculovacuolar structures (VVOs) within ECs from arteries and veins also demonstrated reaction product for ICAM-1 labeling. Three-dimensional stereo-pair images in the HVEM enhanced the visualization of gold particles that were attached to the inner-delimiting membrane surfaces of EC VTS, and VVOs, respectively. These observations raise the possibility that the neonatal leukocytes and tumor cells may utilize these endothelial structures as a route across the developing and injured blood-brain barrier (BBB).

Animals↗
PubMed1998

Reduced number and altered morphology of microglial cells in colony stimulating factor-1-deficient osteopetrotic op/op mice.

The numerical density of microglial cells is reduced by 47% in the corpus callosum, by 37% in the parietal cortex and by 34% in the frontal cortex of mice mutant at the op locus which are totally devoid of colony stimulating factor-1 (CSF-1), the major growth factor for macrophages. Moreover, microglia in the frontal cortex of the op/op mice are smaller and have shorter cytoplasmic processes compared to control mice. Study suggests that CSF-1 plays a role in vivo in the formation and maturation of microglia and has little or no effect on perivascular cells.

Animals↗
PubMed1997

Ultrastructural studies of PECAM-1/CD31 expression in the developing mouse blood-brain barrier with the application of a pre-embedding technique.

The aim of this study was to investigate the time of expression of the adhesion molecule platelet endothelial cell adhesion molecule-1 (PECAM-1/CD31) in the developing mouse blood-brain barrier (BBB). Ultrastructural studies employing a preembedding technique described herein demonstrate that PECAM-1 is initially expressed on the luminal and abluminal endothelial cell surfaces in the newborn animals. This adhesion molecule expression appears to increase in intensity at 7-10 days post partum and then decreases to a weak labelling of the luminal endothelial cell surfaces at two weeks after birth. Our results present immunocytochemical detection of active angiogenesis during early brain development in the mouse. Moreover, because of the important role that adhesion molecules play in immune responses in the central nervous system, upregulation of PECAM-1 prior to structural maturity of the BBB may suggest that the development of an "immune BBB" manifests prior to anatomical closure of the BBB in the mouse.

Animals↗
PubMed1996

Beta-protein immunoreactivity in the human brain after cardiac arrest.

Brain of twelve, 44-78 years old non-demented patients affected by total ischemia after cardiac arrest, were used in the study. All of them were resuscitated within a few minutes after cardiac arrest and they survived for 3 to 36 days afterward. In all cases, after cardiac arrest, beta PP overexpression was found by immunocytochemical methods in many cortical and subcortical neurons as well as in ependymal and choroid plexus cells. This overexpression of beta PP, was concomitant with formation of many A beta nonfibrillar (thioflavine-negative) plaques in the neuropil. Because of a break in the blood-brain barrier around many vessels, weakly A beta-immunoreactive material was also found. The data presented provided strong evidence that the total brain ischemia resulting from cardiac arrest is a risk factor for beta-amyloidosis.

Adult↗
PubMed1995

Apolipoproteins E3 and E4 induce, and transthyretin prevents accumulation of the Alzheimer's beta-amyloid peptide in cultured vascular smooth muscle cells.

Cultured brain vascular smooth muscle cells (SMCs) accumulate beta-peptide in intracytoplasmic granules [9,10,33]. We show here that apoE3 and E4 induces the intracytoplasmic beta-peptide accumulation in cultured human and canine SMCs. The induction is dose-dependent and the accumulated granules also contain apoE and some were thioflavine S-positive. The deposits induced with apoE3 were more abundant though less stable than with apoE4. Transthyretin at physiological concentrations blocked the effects of apoE3/E4. Thus, accumulation of beta-peptide appears to be regulated by beta-peptide carrier proteins.

Aged↗
PubMed1994

Early blood-brain barrier changes in the rat following transient complete cerebral ischemia induced by cardiac arrest.

This study examined regional patterns of increased vascular permeability following transient global cerebral ischemia. Rats underwent 3.5, 5 or 10 min of cardiac vessel bundle occlusion, i.e. cardiac arrest. The animals were killed at 2, 3, 5 and 15 min, or 1, 3, 6 and 24 h after global cerebral ischemia. Thirty minutes before the end of each blood recirculation period, the electron dense protein tracer--horseradish peroxidase (HRP) was intravenously injected and rats were perfusion-fixed for light and electron microscopic analysis. Control rats showed no HRP leakage. Post-ischemic rats demonstrated random blood-brain barrier (BBB) alterations. Permeability alterations were spotty and widespread in cortical, thalamic, basal ganglia, hippocampal, brain stem regions, cerebellum and white matter. Peroxidase extravasation frequently involved arterioles, veins and venules surrounded by perivascular spaces. Routes of increased HRP permeability included endothelial cell (EC) vesiculo-canalicular profiles and diffuse leakage through damaged ECs. Barrier damage determined by HRP permeability revealed a biphasic nature. The first stage appeared immediately after ischemia at the 2nd min and involved the 1st post-insult hour. There was no HRP leakage in rats sacrificed 3 h after insult. BBB opening appeared again 6 h after ischemia and remained open 24 h after cardiac arrest. The openings of BBB did not increase in frequency with longer periods of ischemia and recirculation. These results demonstrate that cardiac arrest produces a spotty BBB disturbances at vessel bifurcations and suggest that BBB changes associated with cardiac arrest may be multifactorial in time course and location.

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↗
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↗