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Biomedical subjects

R Kuramoto

Publications and source records attributed to R Kuramoto.

14 recordsLinked to original sources
PubMed1991

Ultrastructure of neurofibrillary tangles in Alzheimer's disease by means of tilt-stage electron microscopy.

Neurofibrillary tangles (NFT) in the brains of patients with Alzheimer's disease were examined by means of tilt-stage electron microscopy. Observing a longitudinal direction, constricted parts of the NFT did not move in an axial direction. In a transverse section, a fibril of the NFT consisted of globular subunits having a hollow structure in the center and did not appear as paired filaments. From these findings, it was considered that a fibril of NFT consists of twisted protofilaments made up of globular subunits and does not consist of paired helical filaments.

Aged↗
PubMed1989

Ultrastructure of neurofibrillary tangles in Alzheimer's disease.

The ultrastructure of neurofibrillary tangles (NFT) was examined by electron microscopy. The fibrils of NFT seemed to consists of about eight protofilaments consisting of globular subunits; these protofilaments were helically wound in a longitudinal direction. The fibrils of NFT had hollow structures at their centers surrounded by the eight globular subunits. The subunits were tightly connected in the narrow parts of the fibril, but more loosely connected in the wider parts. From these findings, it seemed that the fibrils of NFT consist of a twisted tubule having periodical constrictions and is made up of eight helically wound protofilaments, forming globular subunits.

Alzheimer Disease↗
PubMed1989

Ultrastructural study of senile plaques and microvessels in the brain with Alzheimer's disease and Down's syndrome.

This study examined the relation between amyloid fibrils and senile plaques in brains of patients with Alzheimer's disease. All the senile plaques contained some amyloid fibrils, which seemed to be produced in the basement membranes of capillary endothelial cells and projecting into surrounding parenchyma. Even when amyloid fibrils could not be seen in senile plaques using light microscopy, at least one degenerate capillary containing amyloid fibrils was found when serial sections were examined by electron microscopy. Amyloid fibrils consisted of hollow rods and were composed of filaments arranged as a tightly coiled helix, each turn comprising five globular subunits. Many capillaries and microvessels showed degenerative changes. Many terminal arterioles had smooth muscle cells with an irregular shape and arrangement, often showing a series of focal constrictions. The findings suggest that the capillary degeneration with the formation of amyloid fibrils may be a primary change in the genesis of senile plaques. Furthermore, degenerative changes in the microvessels may also be an important factor in the loss of neurons in the brain of subjects with Alzheimer's disease.

Alzheimer Disease↗
PubMed1989

Histopathological study on a case of idiocy--morphological mechanism of idiocy appearance.

A male, aged 42, had idiocy without any somatic or neurological signs. In laboratory examination, no abnormal finding could be observed. Brain weight was 1,330 g. and no abnormal finding was observed macroscopically. Histopathologically, gross changes were not observed, however, many nerve cells contained a lot of lipofuscin granules in the cytoplasms for the patient's age. Some astrocytes in the cerebral cortex contained homogenous amorphous inclusion bodies in their cytoplasms. From these findings, it was speculated that the change of astrocyte may play an important role in causing mental deficiency.

Adult↗
PubMed1988

Ultrastructure of perivascular amyloid fibrils in Alzheimer's disease.

Perivascular amyloid fibrils in the brains of patients with Alzheimer's disease have been examined by electron microscopy. The amyloid fibrils showed a hollow rod structure and consisted of globular substances. Each turn appeared to be composed of five globular subunits. These findings coincide with the ultrastructure of amyloid fibrils obtained from replicas made by a rapid freezing method.

Aged↗
PubMed1988

Morphological changes of microvessels in the brain with Alzheimer's disease.

The pathological changes of microvessels in the cerebral cortex in Alzheimer's disease were examined at the ultrastructural level. With transmission electron microscopy (TEM), the endothelial cells of many capillaries and their pericytes exhibited atrophy and swelling with a narrowed lumen. The capillary basal laminas were thickened and tortuous. After isolation of the microvessels by ultrasonic treatment and collagenase digestion, the vascular wall structure was viewed by scanning electron microscopy (SEM). Most of the terminal arterioles had smooth muscle cells with an irregular shape and arrangement and often showed a series of focal constrictions. In some areas, the capillaries were arrayed in a bundle and terminated with tapered ends. Associated with the microvessels were fine filaments which may represent amyloid fibrils. The findings indicate that diffuse atrophy and the deletion of nerve cells in the cerebral cortex might be caused, at least partly, by a circulatory disturbance through the pathomorphologically changed microvessels.

Alzheimer Disease↗
PubMed1988

Histopathological changes induced by disturbance of microcirculation in the rat brain.

Microcirculatory disturbance was induced in 8 rats after injecting microsphere latex (5 micron in diameter) from the right carotid artery. Ultrastructural observations revealed that initial changes occurred in the vascular feet of astroglial cells and the subsequent swelling of postsynapses. Succeedingly presynapses and nerve cells also became atrophic but this was considered to be caused by astrocytic degeneration. From these findings, it is speculated that the neuronal atrophy was secondary to the changes in the neuropil around the capillary caused by disturbance of the nutritional supply from the blood induced by microcirculatory disturbance. The above described findings seemed to have some similarity to those of nonspecific degeneration of the cortex observed in the brain, such as Alzheimer's disease.

Animals↗
PubMed1982

The relationship between senile plaques and cerebral blood vessels in Alzheimer's disease and senile dementia. Morphological mechanism of senile plaque production.

Several kinds of senile plaque found in 6 brains (4 from patients with Alzheimer's disease and 2 from patients with senile dementia) were examined in serial sections by light electron microscopy. The results obtained were as follows. All the senile plaques contained at least some amyloid fibrils, and these seemed to be produced at the basement membranes of capillary endothelial cells and projected into the surrounding parenchyma. Even when the senile plaques themselves appeared to lack amyloid fibrils by light microscopy, at least one degenerable capillary containing amyloid fibrils was demonstrable when serial sections were examined ultrastructurally. The findings described above suggest that the amyloid fibrils which form the cores of the several kinds of senile plaque, seem to be produced at the basement membrane of the endothelial cell. It is speculated that the capillary degeneration with the formation of amyloid fibrils may be primary change in the genesis of senile plaques.

Aged↗
PubMed1981

Morphological observations of peripheral nerves by the scanning electron microscope.

In order to observe a normal peripheral nerve and a changed peripheral nerve by means of a scanning electron microscope, the present study was carried out. In the changed nerve fibers, they were enveloped by many processes of hypertrophied Schwann cells, and the processes of the Schwann cells seemed to make a pseudosyntitium-like structure with each other. From this finding, it was speculated that these Schwann cells seemed to follow the reverse process in the development of normal peripheral nerve fibers.

Animals↗
PubMed1981

[The phenol turbidity test for measurement of pulmonary surfactants in amniotic fluid--rapid test for fetal lung maturity (author's transl)].

A simple and sensitive procedure for the quantitative estimation of pulmonary surfactants in the amniotic fluid is described. The method is based on the formation of turbidity from the amniotic fluid surfactants with phenol. Amniotic fluid drawn through an intrauterine catheter was centrifuged at 2000 rpm for 5 min. One ml of 5% aqueous phenol solution was added to 1.0 ml of the diluted supernatant. Control solution was prepared by addition of 1.0 ml of distilled water to the supernatant, instead of phenol solution. The turbidity was measured spectrophotometrically against control at 340 nm 5 to 10 min after agitation on a Vortex mixer for 5 sec. The turbidity obtained from amniotic fluid with phenol was proportional to the increase in total phospholipids in the fluid measured enzymatically. Moreover, only lecithin in the phospholipids was related to the turbidity formation. Sphyngomyelin, lysolecithin, phosphatidylethanolamin did not produce any turbidity with phenol. The spectrophotometric reading of 87 cases (31-41 weeks) was ranged at 0.18-3.52. Four cases with lower value (0.40) showed neonatal respiratory problem. The phenol turbidity test is more useful for the detection of fetal lung maturity comparing with the generally used shake test.

Amniotic Fluid↗
PubMed1979

Electron-microscopical study on senile plaques in Alzheimer's disease.

The cerebral cortex taken post mortem from a case of Alzheimer's disease was examined especially with regard to the relation between blood vessels and senile plaques. Many senile plaques had central cores, composed of such matter as degenerated blood vessels and basement membranes with abundant amyloid fibrils. The components of senile plaques seemed to be degenerated neuronal and glial tissue compressed by developed basement membranes and amyloid fibrils. From this we would like to emphasize that senile plaques seem to be caused by amyloid fibrils and degenerated capillaries.

Alzheimer Disease↗
PubMedDate not supplied

An autopsy case of idiopathic superficial hemosiderosis of the central nervous system: a microscopic and immunohistochemical study.

The brain of a patient with idiopathic superficial hemosiderosis of the central nervous system was examined by light and electron microscopy. A histopathological study revealed massive, symmetrically situated necrosis in the temporal and insular lobes, which has not been described in previous reports. In addition, immunohistochemistry revealed ovoid bodies in the astroglia. Electron microscopy showed that these bodies were composed of fine granules, 50-60 A in diameter, and electron-dense amorphous material. Based on detailed histopathological and ultrastructural findings, the mechanism of ovoid body formation is discussed.

Aged↗