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Biomedical subjects

S Oyanagi

Publications and source records attributed to S Oyanagi.

At least 55 records · Page 3Linked to original sources
PubMed1976

Presenile dementia with Alzheimer-, Pick- and Lewy-body changes.

An autopsy case of unclassifiable presenil dementia is reported. The outstanding pathological findings were as follows; 1. presence of senile plaques, neurofibrillary changes, Pick bodies, Hirano bodies, granulovacuolar degeneration of neurons, etc. 2. numerous Lewy bodies in the brain stem and diencephalon, 3. peculiar swollen neurons with intracytoplasmic, eosinophilic and argentophilic inclusions ("Lewy-like-bodies") in the cerebral cortices. Detailed study of the last mentioned inclusions indicates that they are almost identical to Lewy bodies, though there are some minor differences, in histochemical and electronmicroscopic findings. Nosologically, this case may represent either a combination of Alzheimer's disease, Pick's disease and idiopathic Parkinsonism with "Lewy-like-bodies" in the cerebral cortices, or a single disease. As far as we know, no similar case been reported.

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PubMed1971

Comparison of subacute sclerosing panencephalitis and measles viruses: an electron microscope study.

The ultrastructure of CV-1 cells infected with subacute sclerosing panencephalitis (SSPE) viruses was compared with that of CV-1 cells infected with the wild or Edmonston strain of measles virus. Both SSPE viruses and the measles viruses produced two types of nucleocapsid structures: smooth filaments, 15 to 17 nm in diameter, and granular filaments, 22 to 25 nm. The smooth and granular filaments produced by SSPE and measles virus did not differ in appearance. In CV-1 cells infected with SSPE viruses, smooth filaments formed large intranuclear inclusions and granular filaments occupied a large area of the cytoplasm, but always spared the area under the cell membrane. Particles budding from the surface of these cells contained no nucleocapsids. In CV-1 cells infected with measles virus, only small aggregates of smooth filaments were seen in the nuclei. Granular filaments in the cytoplasm predominantly occupied the area under the cell membrane, and were aligned beneath the cell membrane in a parallel fashion and assembled into budding particles. These differences between SSPE and measles virus may be regarded as quantitative, but they do distinguish SSPE viruses from measles virus. Moreover, the formation of large nuclear inclusions filled with smooth filaments appears to be a characteristic process of SSPE, but not of measles, since this type of inclusion is invariably seen in SSPE brain tissues, brain cultures derived from them, and CV-1 cells infected with SSPE viruses.

Antigens↗
PubMed1970

Electron microscopic observations in subacute sclerosing panencephalitis brain cell cultures: their correlation with cytochemical and immunocytological findings.

Three cell cultures established from brain tissue obtained by biopsy of patients with subacute sclerosing panencephalitis (SSPE) were studied with the electron microscope in an attempt to correlate ultrastructural changes with those found by cytochemistry and immunocytology. These cells contained a large number of nucleocapsids resembling those of a paramyxovirus concentrated in the nuclear inclusions, but also seen free in the nucleus and occasionally in the cytoplasmic inclusions. Nuclear bodies associated with the nucleocapsids and granular filaments occupied a vast area of the cytoplasm. The nuclear inclusions containing nucleocapsids corresponded to the eosinophilic and fluorescent nuclear inclusions. The areas occupied by granular filaments corresponded to the diffuse cytoplasmic fluorescence. The ultrastructural changes were similar to those seen in the original brain biopsies. In addition papova-like virions were noted in brain cell cultures derived from a biopsy but not in the brain tissue itself. Their relationship to SSPE remains undetermined.

Brain↗
PubMedDate not supplied

A fetal type of Minamata disease. An autopsy case report with special reference to the nervous system.

Our knowledge concerning the pathology of fetal cases of human Minamata disease (methylmercury poisoning) is relatively limited. We report here a case with description of the distribution of mercury in the systemic organs, and the ultrastructural changes of the nervous system after a survival of 29 yr. The patient was a female born in 1957, with a body wt of 3000 g, who died in 1987. She carried a diagnosis of cerebral palsy, and had a convulsion at age 3 yr. Mercury levels in her mother's hair were 101 micrograms/g at the time of examination in 1959. At autopsy, the body measured 43 cm and weighed 23 kg. The brain weighed 920 g and showed marked cerebral atrophy, mild neuronal loss in the calcarine, postcentral and precentral cortices, cerebellar atrophy, and segmental demyelination of peripheral nerves. Mercury granules were present in the brain, kidney, and liver. Ultrastructural examination of the calcarine, post- and precentral cortices, and cerebellar cortices, showed severe atrophy of nerve cells, with a decrease in rough ER and an increase in nuclear chromatin and preservation of mitochondria. Autophagosomes were increased in number. In addition, high electron density, globular and dense bodies, measuring 0.3-1.8 microns in diameter, were found, surrounded by limited membrane, within both cerebral and cerebellar neurons. In the cellebellum, synapses were well-preserved.

Adult↗
PubMedDate not supplied

Pseudo-intracellular collagen tangles in human spinal ganglia.

A new structure was found in the spinal ganglia of 6 out of 215 human autopsy cases with various disorders. It was composed of ballooned cells fully packed with fibrillar structures showing the same staining properties as collagen. Ultrastructurally the fibrillar structures were bundles of collagen fibres with a striation of about 70nm periodicity, and they were enclosed by the cell membrane invaginated in a very complex manner into the cytoplasm. This structure, which we named 'pseudo-intracellular collagen tangle', was considered to result from a disturbance in the releasing process of collagen fibre from fibroblasts. The aetiology of the structure is unknown, but it might represent one of regressive or senile changes in human spinal ganglia.

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