A cytochemical procedure for polysaccharides was carried out on a brain biopsy specimen, the thin-section study of which had shown excess glycogen granules and the corpora amylacea variety of polyglucosan bodies. Both granules and amyloid bodies were stained positively in contrast to the remaining structures of the brain tissue which remained unstained. This demonstrates that beta-granules as well as filamentous and amorphous components of amyloid bodies are just different aspects of the polysaccharide molecule. Up to now the same kind of cytochemical evidence has been supplied for Lafora bodies of human material and Lafora-like bodies of rat material. The present study on corpora amylacea of human material shows that amyloid, Lafora, and Lafora-like bodies all behave the same way when stained for polysaccharides.
Unlike lymphocytes, blood monocytes possess in their cytoplasm peroxidase-positive (azurophil) granules (ppg) which largely correspond to the homonymous organelles of neutrophil granulocytes. We tested whether ppg, demonstrated cytochemically at the submicroscopic level, could serve as markers of monocyte-derived reactive mononuclear cells in encephalitic lesions. Samples of cerebrocortical tissue from adult albino mice with experimental yellow fever virus encephalitis were incubated in a medium containing diaminobenzidine and H2O2 for localization of peroxidatic activity. Mononuclear cells exhibiting ppg were found (1) in the lumen of brain venules, (2) in different stages of migration through the walls of such vessels, (3) in perivascular areas, (4) in the glioneuropil, either loosely scattered or forming small clusters, (5) in a satellite position to neurons, and (6) in leptomeningitic inflitrates. Several mononuclear elements harboring ppg had assumed an elongated, rod cell-like outline. Amongst the peroxidase-negative mononuclears were fully developed brain macrophages and elements showing morphologic features characteristic of activated lymphocytes. Most mononuclear cells without ppg resembled the peroxidase-reactive ones. The results of this study provide direct evidence in favor of a monocytic origin of, at least, numerous reactive mononuclear elements in encephalitic lesions. The approach followed in the present study is not suitable for quantitative investigations of the histogenesis of mononuclear cells responding to brain injuries, since emigrated blood monocytes rapidly lose their ppg, particularly, when they display enhanced phagocytic activity.
Crystalline arrays of so-called 'virus-like particles' were found in post-mortem samples of skeletal muscle obtained from an 11-month-old female infant. In a large number of skeletal muscle fibres crystalline inclusions were abundant, variously configurated and positively stained with a cytochemical method for polysaccharides. A battery of enzymatic tests, including some with diastase and alpha-amylase, was, however, entirely noncontributory. A muscle biopsy studied 5 months before death had disclosed no crystalline inclusions of any kind. The literature concerning similar cases of 'virus-like particles', crystalline glycogen aggregates or protein-glycogen complexes in muscle is reviewed. Possible reasons underlying the aggregation of protein-glycogen complexes into crystalline arrays are discussed.
In experimental yellow fever virus encephalomyelitis of adult albino mice, the occurrence of intranuclear inclusions within nerve cells, in particular, within spinal and bulbar motoneurons, is a constant finding. The light microscopic features of these so-called neuronal Torres bodies correspond entirely to the criteria laid down by Cowdry for the type A intranuclear inclusions. At the ultrastructural level, these karyoplasmic formations consist of haphazardly distributed patches of an essentially amorphous material of various density. Unlike the Cowdry type A intranuclear inclusions characteristic of several herpesvirus and paramyxovirus infections, neuronal Torr-s bodies do not contain any viral structures. The frequency with which neuronal Torres bodies, certain nucleolar alterations and severe tigrolytic changes occur together, possibly indicates that this sort of type A intranuclear inclusion developes as a consequence of a virus induced disturbance of the cell nucleic acid and/or protein anabolism.
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