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Biomedical subjects

M G Khizhniak

Publications and source records attributed to M G Khizhniak.

6 recordsLinked to original sources
PubMed1989

[Immunomorphologic features of experimental allergic encephalomyelitis induced by the administration of tryptophan peptide].

Three patterns of EAE with different morbidity and mortality rates were induced in the guinea pigs inoculated with various doses of tryptophane peptide (TP) and complete Freund's adjuvant. TP-sensitized animals manifested the delayed type hypersensitivity (DTH) reactions to TP and circulating anti-TP and -BPF antibodies were not found, polypeptide fraction of myelin basic protein (BPF while a A correlation was revealed between the DTH-reactions and EAE development. Intracutaneous TP and BPF injections at the early period before the EAE onset resulted in reduction of morbidity rate from 90 to 50 per cent. For the first time with the help of modified Marchi method demyelination has been shown to be highly marked in CNS tissue process in CNS can be caused by cell-mediated immune of animals given TP. It is supposed that the demyelinating reaction to encephalitogenic fragment of BP molecule. The data indicate a possibility of EAE inhibition by means of TP and BPF injections in saline solution.

Animals↗
PubMed1988

[A method of detecting demyelinated nerve tissue in experimental allergic encephalomyelitis].

A method of rapid pathomorphological diagnosis of demyelinization with a simultaneous detection of cell elements in the nervous tissue has been described. The method tested on the model of experimental allergic encephalomyelitis (EAE) is a modified method of Marchi with subsequent staining of histological sections with toluidine blue. Due to a shorter period of nervous tissue exposure to potassium bichromate and osmium acid solutions (from 6-8 weeks to 5 days) the cells preserve their ability to uptake the dye and the endurance of histological sections increases. Their thickness (2-3 microns) makes it possible to examine them in immersion magnification of the light microscope. Using the above method, we succeeded in revealing hematogenic and glial elements in demyelinating foci in the central nervous system of animals with EAE. The method described can be used for studying pathomorphology of multiple sclerosis and other demyelinating diseases in humans and their experimental models, as well as for the express diagnosis of demyelinization in pathoanatomical practice.

Animals↗
PubMed1987

[Immunomorphological characteristics of experimental allergic encephalomyelitis induced by an encephalitogenic polypeptide].

Encephalitogenic, immunogenic properties of the polypeptide fraction of myelin basic protein (FBP) and CNS lesions have been examined in animals with experimental allergic encephalomyelitis (EAE). FBP was isolated from bovine spinal cord using column chromatography. Administration of 1.0 or 0.1 microgram FBP mixed with complete Freund adjuvant caused neurological and histological EAE manifestations in 76% and 26% of guinea-pigs, respectively. Circulating anti-FBP antibodies were not found in sensitized animals, whereas the incidence and intensity of skin reaction of delayed type hypersensitivity to FBP correlated with the development of EAE and the onset of the disease. Perivascular cell infiltration and demyelination noted in the spinal cord and brain of guinea-pigs were similar to those observed after inoculation of the brain white matter or brain tissue homogenate.

Animals↗
PubMed1987

[Dynamics of pathomorphologic changes in experimental allergic encephalomyelitis].

The new method of simultaneous identification of myelin degradation products and cellular elements in the demyelinated nervous tissue allowed one to determine some previously unknown regularities in the interaction of demyelination and inflammation processes during experimentally induced allergic encephalomyelitis. The most significant feature in the pathomorphology of this disease is shown to be the change in osmiophilia and the amount of myelin degradation products in the demyelination foci, with every stage of periaxonal changes corresponding to a certain type of cellular reactions. A close relation is revealed between the demyelination and inflammation processes determining the structure of demyelination foci at different stages of the disease.

Animals↗
PubMed1985

[Neurologic manifestations and periaxonal demyelination in the central nervous system in different forms of experimental allergic encephalomyelitis].

Comparing the neurological manifestations of experimentally-induced allergic encephalomyelitis (EAE) with the topography of developing demyelinization in the central nervous system of guinea-pigs allowed the authors to identify three forms of the diseases, namely spinal, cerebral and mixed. The spinal form caused by myelin decay in the lumbosacral segments of the spinal cord was expressed in the form of pareses and paralyses affecting the hind paws and also pelvic disorders. In the cerebral form, demyelinization was localized in the brain and was most frequently attended by vestibular disturbances. The mixed form characterized by pathological changes in both the spinal cord and brain was identified largely on the histological basis. In some animals (several of which died), EAE ran its course without apparent neurological symptoms and was identified only histologically.

Animals↗