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J Simon

Publications and source records attributed to J Simon.

At least 667 records · Page 37Linked to original sources

[Use of leukocytes labelled with 99m Technetium sulfide colloids for the detection of experimental aseptic inflammatory foci].

The authors propose a technique of labelling of leukocytes based on the phagocytic power of these cells with regard to sulphide particles in the colloidal state labelled with 90mmTc. These labelled leukocytes maintain their normal function and can be detected in the inflammatory foci created in experimental animals in the form of an abscess. Satisfactory results were thus obtained by scintiscanning after auto and allo-transfusion of labelled leukocytes. The role of hyperemia in the results obtained is eliminated by comparative study using non-diffusible vascular tracers. The type of vector, tracer and marker, the innocuity of the method suggest that it may be used in human clinical medicine for the early diagnosis of certain inflammatory foci.

Abscess↗

[Sensitization against the antigens of the brain after experimental vaccinia infection. I. Evidence for cell-mediated immune response to brain-antigens (author's transl)].

Vaccinia virus infection was performed by scarification of the shaved skin (5 times 5 cm2) on the back of Pirbright guinea pigs. The macrophage migration inhibition test was performed with peritonealexudate cells 7, 11, 14 and 21 days after infection. Macrophage migration inhibition occurred after exposure of the cells to whole brain tissue antigen on the 7th, 11th, 14th day after infection (s. table 1). Lymphocyte transformation responses were examined by 14C-2-Thymidin uptake using blood cultures and basic encephalitogenic protein and whole brain tissue extract as antigens. A positive transformation response could be demonstrated from one to 8 weeks after infection (s. table 2). The specificity of the transformation response to brain antigen was established using control cultures stimulated with PHA or PPD. In no case stimulation occured with PPD. Stimulation with PHA was not altered. On the other hand the spontaneous lymphocyte transformation was enhanced at one week after infection and lymphocyte cultures exposed to heat inactivated vaccinia virus showed transformation from the 3th week after infection until the end of the observation period (i.e. 8 weeks) (s. table 2). The reason why cell mediated hypersensitivity to brain antigen is induced following vaccinia infection remains unknown. The most probable among several possible mechanisms seem a) the induction of virus-specific antigens on the surface of infected cells or b) the release of brain specific antigen through virus infection.

Administration, Topical↗

[Sensitization against the antigens of the brain after experimental vaccinia infection. II. Humoral anti-brain antibodies and morphological changes in the CNS (author's transl)].

29 guinea pigs, strain Pirbright, were infected with vaccinia virus, strain Elstree, by the dermal route. The observation period was 14 days. Thereafter, the animals were killed and their central nervous systems (CNS) histologically and immunohistologically, the blood fluorescence-serologically examined. Histological examination revealed meningitis, ependymitis or disseminated meningoencephalitis with slight perivascular cuffing in 72% of the animals. The viral antigen was found in 3 animals (10%). It was present most often in the cytoplasma of the arachnoidal and/or ependymal cells, as well as in the cells of the vessel walls and less often in the glial and/or nerve cells. The infected cells showed no severe degenerative changes. The blood-brain-barrier displayed localized disturbances. The examination of the myelin sheaths revealed disseminated foci of disappearance of myelin fluorescence in the perivascular, paraventricular and subcortical regions. Antibodies directed against myelin sheaths, or nerve cells could be detected in the sera of 48% of the animals. The results give evidence that the vaccinia infection is capable to induce a potentially pathogenic autoimmune reaction directed against brain. Such an immunomechanism can be triggered without any signs of acute lytic infection of the CNS. The mechanism and significance of this reaction are discussed.

Animals↗