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Biomedical subjects

K Eto

Publications and source records attributed to K Eto.

At least 217 records · Page 12Linked to original sources

Dirofilaria in the abdominal cavity of a man in Japan.

A case of human dirofilariasis of the abdominal cavity is reported from Japan. The patient, a 74-year-old man, died of liver cancer; postmortem examination revealed a granulomatous mass on the mesentery. In histologic sections there were cross-sections of a mature female nematode identified as a Dirofilaria. The cuticle had a smooth surface and consisted of four distinct layers. The inner cuticular layer had internal lateral longitudinal ridges, and the musculature of the body wall was of the high polymyarian type. On the basis of morphology of the worm, it is suggested that this may represent the first human case of Dirofilaria immitis occurring in the abdominal cavity.

Abdomen↗

Ultrastructural changes of human sural nerves in the neuropathy induced by intrauterine methylmercury poisoning (so-called fetal Minamata disease).

Biopsy of the sural nerve was performed on three patients with severe Minamata disease of more than 10 years duration. There were so many unmyelinated and poorly myelinated nerve fibers that myelinated fibers scattered irregularly in small numbers or in groups of peculiar features in the intraneural bundle. Abnormaly thin or poorly formed myelin sheaths were noticed. Incomplete myelination and abnormal myelination varied in size and shape appeared as fetal anomaly. Regenerated axons extremely small in size remained singly or in groups following regenerative sprouting. Sometimes, extremely small axons with normal myelination were noticeable, while the axons were lost, leaving myelin sheaths. Axons occasionally contained increased neurofilaments. Schwann cells were not so increased as in adult Minamata disease. Degenerative changes of nerve fibers still proceeded, presumably because the patients lived in the mercury-contaminated district. Myelin degenerations and glycogen deposits in the axoplasm were identified.

Adolescent↗

A pathological study of prolonged cases of Minamata disease. With particular reference to 83 autopsy cses.

This study consists of 83 autopsy cases including 64 prolonged cases of Minamata disease. Lesions were severe in the prolonged cases with an acute onset, while they tended to be mild in those with chronic onset. Cerebral cortex showed loss of nerve cells in many of the former, with the cortex often being in a loosening or spongy state, while the thinning-out or decrease of neurons not exceeding 30% of all cells was frequent in the latter. Glial reaction was also intense in the former, but relatively weak in the latter; gradual loss of degenerative neurons without glial reaction was not rare. A given selectivity was found in the localization of lesions of the cerebral cortex, but it was not so conspicuous in those with a chronic onset as in those with an acute onset. Secondary changes corresponding to the lesions of the cortex appeared in the medulla. Cerebellar lesions in the chronic onset cases, as compared with those in the acute onset ones, were milder. The selectively localized area was diminished; the nodulus, uvula and lingula of the vermis and the medial surface of the semilunar lobules were the most likely to be damaged. Of the spinal peripheral nerves, damages to the spinal sensory nerve were found, which were more predominant than those to the motor nerve system, and in which was noted prominent regeneration and repair. The deposited mercury found in organs tended to remain in the nervous system and the kidneys during the prolonged course of this disease, and the prolonged accumulation of mercury in the nervous system appeared to have an influence on the pathogenesis of chronic Minamata disease.

Adolescent↗

Effect of pyridoxal administration on the contents of pyridoxal phosphate and gamma-aminobutyric acid in mouse brain.

Many mice treated with a high single dose of PL died in convulsions. The convulsions were very similar to those induced with some anti B6 in several ways: (1) a long latent period occurs betfore convulsions; (2) PLP levels in brain decrease; (3) GABA levels in brain, especially in synaptosomal fraction, decrease. The possibility that a deranged GABA metabolism in nerve ending may be a major cause of the convulsions is discussed.

Animals↗

Pathological changes of human sural nerves in Minamato disease (methylmercury poisoning). Light and electron microscopic studies.

Biopsy of the sural nerve was performed on six patients with relatively mild Minamata disease of 10-year or longer duration. All of the six patients presented characteristic pathologic changes. Light microscopy disclosed the formation of irregularly shaped myelin sheaths and fine axons, an increase in them, which is suggestive of incomplete regeneration, cicatrization following the loss of nerve fibers, increase in Schwann's nuclei, and formation of Büngner's bands. Electron microscopy revealed incomplete myelinated fibers and ultrafine unmyelinated fibers associated with incomplete regeneration, formation of regeneration units, and collagen increase. The laminar encapsulation with the processes of Schwann's cells were often observed in ultrafine fibers. In view of the fact that small quantities of mercury-contaminated fishes are still being caught in the Minamata district, myelin degeneration, glycogen deposits and appearance of dense bodies in axons, and vesiculation and fragmentation of endoplasmic reticulum were observed as degenerative changes due to the effects of mercury accumulation.

Adult↗

Clinical and histologic observations of opalescent dentin associated with enamel defects.

The rare variant of opalescent dentin associated with enamel defect was found in a 1 1/2-year-old boy. The pulp chambers and root canals of the affected deciduous teeth were very large, with no sign of obliteration. The enamel layer of those teeth was markedly reduced in thickness, and the enamel prisms were not recognized even by scanning electron microscopy. The mantle dentin was abnormal, as were other portions of dentin.

Amelogenesis Imperfecta↗