Biomedical subjects

Y Kawase

Publications and source records attributed to Y Kawase.

At least 145 records · Page 8Linked to original sources

PubMed1986

Congenital stationary night blindness with negative electroretinogram. A new classification.

An analysis of 64 patients with congenital stationary night blindness showed that all had essentially normal fundi. Electroretinography (ERG) showed a normal a wave with extremely reduced b wave (negative type) when recorded with a single bright white stimulus in the dark. We classified these patients into two groups based on the evaluation of rod ERG and/or psychophysical dark adaptation measured with an 11 degree test target at 15 degrees in the upper part of the retina. One group (35 patients) lacked rod function (complete type). Nine patients could not be classified. No pedigree showed a complete and incomplete type in one family. Differences between the two groups in refractive error, photopic function, and oscillatory potentials in the ERG suggest a different pathogenesis. Our analysis may provide a new classification of congenital stationary night blindness with a negative ERG.

Adolescent↗

PubMed1986

Joseph's disease: clinical and pathological studies in a Japanese family.

Joseph's disease is a hereditary ataxia found among descendants of Portuguese from the Azores Islands. We describe the clinical and pathological features of 4 members of a Japanese family who were diagnosed as having Joseph's disease. The illness began with cerebellar ataxia between the ages of 18 and 45 years. Nystagmus, dysarthria, and pyramidal signs were early manifestations. External ophthalmoplegia, dystonia and/or athetotic movements, and muscular atrophy appeared in the late stages. Neuropathological findings in one patient revealed degeneration of the dentatorubral and pallidoluysian systems, substantia nigra, pontocerebellar system, Clarke's column and spinocerebellar tracts, and anterior horn cells, as well as the cranial nuclei in the brainstem. Neurons in the inferior olivary nuclei, Purkinje's and granule cells, the cerebral cortex, thalamus, and striatum were spared. Involvement of the dentatorubral and pallidoluysian systems seems to be a characteristic feature of this disease in Japan.

Adolescent↗

PubMed1986

Pathological study on mucosal changes in small intestine of rat by oral administration of ricin. I. Microscopical observation.

A histological study on small intestine of Wistar rats after oral administration of ricin, a proteinous toxin from castor bean seeds, was carried out. In Experiment I, the jejunum was examined at 1, 2, 5, 10, 15, 20, 24, and 40 hours after oral administration of ricin 30 mg/kg. In Experiment II, ricin was administered at dose of 1, 3, 5, 10, 15, 30, and 60 mg/kg, and after 5 hours the jejunum, mid-portion, and ileum were examined. For comparison, ricin 0.5 mg/kg was administered intraperitoneally and castor bean hemagglutinin (CBH) 30 mg/kg orally. In both experiments, the changes of mucosa were essentially similar dependent on time-lapse and dose respectively, which were atrophy of villus, elongation of crypt, degeneration of epithelium, decrease of goblet cell, fusion of intervillous epithelia, infiltration of neutrophils and eosinophils, and dissociation between epithelium and lamina propria. These changes were most manifest in the jejunum that was contacted with ricin first in a high concentration. In contrast, intraperitoneal administration of ricin caused only dissociation between epithelium and lamina propria and oral administration of CBH caused only milder atrophic changes. The evidences suggest that the mucosal changes by oral administration were caused by direct contact with ricin.

Administration, Oral↗

PubMed1986

Degradation of insulin by insulin-degrading enzyme and biological characteristics of its fragments.

We have previously reported on the purification, characterization, and biological significance of insulin-degrading enzyme (IDE) from pig and rat skeletal muscle. In the present study, we have investigated the detection and the HPLC separation of degradation products of native insulin from the reaction of monocomponent porcine insulin with affinity-purified pig IDE. Insulin was degraded by IDE in a time- and dose-dependent manner. Eight peaks (peaks I through VIII) appeared after 1 h of incubation, and peak V was identified as insulin. Among seven peaks representing degradation products, peak VI appeared most rapidly at 30 sec of incubation, increased until 10 min, and then decreased after 15 min of incubation; and six degradation products other than peak VI were not detected within 15 min of incubation, suggesting that peak VI was an initial degradation product of insulin produced by IDE and converted into relatively low molecular weight products as incubation time increased. The generation of peak VI may be due to cleavage at a peptide bond between the interchain disulfide bonds of the A or B chain. Subsequently, the split insulin derivative (peak VI) was evidently further degraded to relatively low molecular weight intermediates, such as peaks III and IV, peaks II and VIII, or peaks I and VII, because these pairs of peaks appeared and were degraded concomitantly. The peptide products designated as peaks IV, VI, VII, and VIII had both immunoprecipitability by antiinsulin antibodies and binding capacity to IM-9 lymphocytes, whereas the less hydrophobic intermediates (peaks I, II, and III) did not have these activities. Since some of these peptides have insulin-like properties, amino acid analysis of these products may enable us to identify not only the splitting position of insulin by IDE but also the site of the hormone for receptor binding.

Animals↗

PubMed1986