An autopsy case of minamata disease (methylmercury poisoning)--pathological viewpoints of peripheral nerves.

The outbreak of methylmercury poisoning in the geographic areas around Minamata Bay, Kumamoto, Japan in the 1950s has become known as Minamata disease. Based on earlier reports and extensive pathological studies on autopsied cases at the Kumamoto University School of Medicine, destructive lesions in the anterior portion of the calcarine cortex and depletion predominantly of granular cells in the cerebellar cortex came to be recognized as the hallmark and diagnostic yardstick of methylmercury poisoning in humans. As the number of autopsy cases of Minamata disease increased, it became apparent that the cerebral lesion was not restricted to the calcarine cortex but was relatively widespread.

Cellular Synthesis of Macromolecular Glycogen and Its Deposition .

The largest macromolecules of glycogen synthesized histochemically in tissue cells were spherical branching bodies composed of several large branches with many smaller branches, presumably containing a Meyer structure of α-1,4-1,6-glucosidic linkages. The synthesized macromolecules of glycogen were variable in size and structure, and were closely related to the activities of enzymes, Phosphorylase, branching glycosyltransferase, and glycogen synthetase. The glycogen molecules appeared to be individually free in the cytoplasmic matrices.