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Cerebral white matter lesions in Alzheimer's disease (AD) consist of subcortical degeneration and ischaemic–hypoxic changes. Glial changes are intimately associated with the white matter lesions, and regressive changes in astrocytes and loss of oligodendroglial cells have been reported. We quantitatively compared glial changes including apoptosis and enhanced lysosomal activity in the frontal and temporal white matter by using terminal dUTP nick end labelling (TUNEL) and immunohistochemistry for glial markers, lysosomes and apoptosis-regulating proteins in non-familial AD brains. The degree of myelin pallor and axonal loss varied considerably in both the frontal and temporal white matter but fibrillary gliosis in demyelinated lesions tended to be less prominent in the temporal white matter in AD cases. A morphometric study with planimetric methods for cross-sectional areas of frontal and temporal white matter revealed that the white matter of AD cases manifested atrophy with significant reduction in frontal (11.9%) and temporal (29.4%) white matter compared to normal controls. Double immunolabelling for glial fibrillary acidic protein (GFAP) and KP1 (CD68) revealed KP1-positive fragmented structures within the weakly GFAP-labelled astrocytes. These KP1-positive structures correspond to process fragmentation and cytoplasmic vacuoles, which in turn indicate enhanced lysosomal activity during regressive changes in astrocytes. The KP1-modified astrocytes were not found in Pick's disease and corticobasal degeneration. The density of apoptotic glial cells, largely oligodendroglial, was significantly higher in the temporal than in the frontal white matter, and most GFAP-positive astrocytes with regressive changes were apoptotic. GFAP-positive astrocyte density was statistically the same in the frontal and temporal white matter, but the density of KP1-modified astrocytes was higher in the temporal than in the frontal white matter. The rate of white matter... [ABSTRACT FROM AUTHOR]

Aldehyde-fixed, EDTA-demineralized frozen sections of the rat maxillary incisor were histochemically stained for carbonic anhydrase activity, by use of Hansson's method. Intense staining was observed in the odontoblasts, all types of epithelial cells of enamel organ in the maturation zone, cementoblasts, and the cells of the lingual dental sac. Less intense but consistent staining was observed in all types of epithelial cells of odontogenic origin directly facing the pulp and pulp cells adjacent to the odontoblast cell layer in the apical part of the pulp, and was considered due to the carbonic anhydrase-catalyzed reaction. Staining of these cells was completely inhibited by heat pre-treatment (120°C, 30 min), 10-6 mol/L acetazolamide in the incubation medium, incubation by continuous immersion under the liquid surface, and omission of the substrate, NaHCO3. The dentin also exhibited heavy staining which was inhibited by the heat pre-treatment. However, this dentinal staining resisted the inhibition by 10-3 mol/L acetazolamide and was not inhibited by incubation by continuous immersion or incubation without the substrate NaHCO3. The dentinal staining was thus judged to have been due to non-enzymatic cobalt precipitation. [ABSTRACT FROM AUTHOR]

The article focuses on a study, which examines the association of the metabolic syndrome with nonalcoholic fatty liver disease over time. 4401 healthy Japanese adults who were participating in a medical checkup program at a general hospital in Japan were studied. Of the 4401 patients in the study, 812 had nonalcoholic fatty liver disease at the start of the study. This disease was more common in persons with the metabolic syndrome than in persons who did not have the metabolic syndrome. Over the course of the study, 308 participants developed nonalcoholic fatty liver disease.