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Biomedical subjects

S Ando

Publications and source records attributed to S Ando.

At least 397 records · Page 22Linked to original sources

[Cerebral amyloid angiopathy in senile dementia--a comparison between senile dementia and Alzheimer disease].

The brain was examined neuropathologically in 16 elderly patients with severe dementia (8 cases of senile dementia, 5 of vascular dementia and 3 of combined senile-vascular dementia), focussing an attention on amyloid angiopathy and and other senile changes. The findings were compared with the results obtained in 10 cases of Alzheimer disease described previously. Amyloid angiopathy was noted in all cases of senile dementia and its distribution was similar to that of Alzheimer disease. The frequency of cerebral amyloid angiopathy in elderly patients with severe dementia was more closely related to disease than to age. One patient each with senile dementia and combined senile-vascular dementia showed markedly advanced amyloid angiopathy. The cases who showed other senile changes (e. g., senile plaque, Alzheimer neurofibrillary tangle, nerve cell deciduation) were frequently seen in patients with Alzheimer disease than in those with senile dementia. Further, there was a tendency that the brain weight was lighter in patients with Alzheimer disease than in those with senile dementia.

Age Factors↗

[A case of Pick's disease with long duration--an extraordinary cerebral change in the fore part of cerebrum].

An autopsied case of Pick's disease, having an extraordinary cerebral change in the anterior portion of Lobus frontalis and temporalis, was reported. Our case is a 71 year-old woman at death with a fourteen year history of chronic progressive dementia and mental deterioration, and it may be stressed that the existence lasted 8 years, over the latter half of clinical course, was depended on the tube feeding. The first symptoms suddenly appeared in 1964, 2 months after her husband's death of illness, when she was 57. She prepared the table for breakfast late at night, calculated wrongly in her domestic account book, and stole foods in the grocery. Two years later, her illness was diagnosed as presenile dementia by characteristic personality change and marked dilatation of anterior horn of lateral ventriculus. On admission to National Musashi Sanatorium, three years after the first symptoms' appearance, she presented restless walking, insomnia, memory loss, weakness of concentration, and high degree of disorientation. Particularly, it was noticeable that she behaved with bizzare contact. After 1970, tube feeding was introduced continuously, because of swallowing difficulty. Death occurred in July 1978 from a general weakness and a broncho-pneumonia, 14 years after the onset of the first symptoms. Autopsy revealed small and atrophied brain weighed 820 g. Cerebral cortical atrophy extended to frontal, temporal, insular, and parietal lobes, but right T-1 was relatively well preserved. On section, frontal and temporal ventriculus were remarkably enlarged and caudate nuclei were extremely atrophic.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

Deterioration of chum salmon muscle during spawning migration--VI. Changes in serum protease inhibitory activity during spawning migration of chum salmon (oncorhynchus keta).

A relation between muscle protease activity and serum protease inhibitory activity of chum salmon during spawning migration was studied with regard to their physiological states. The autolytic activity of chum salmon muscle significantly increased, while the trypsin inhibitory activity in serum significantly decreased during spawning migration. Serum trypsin inhibitor was inactivated following treatment with androgen. It was consequently proved that androgen was trigger to the inactivation of serum protease inhibitor, resulting in high levels of muscle protease activity during spawning migration.

Animals↗

Two positional isomers of sialylheptasaccharides isolated from the urine of a patient with sialidosis.

We describe the structures of two positional isomers of sialylheptasaccharide isolated from the urine of a patient with sialidosis with partial deficiency of beta-galactosidase. Based on structural studies including compositional sugar analysis, exoglycosidase digestion, chemical ionization mass spectrometry, proton nuclear magnetic resonance spectrometry, and methylation analysis, their structures were deduced to be as follows: AcNeu alpha 2----6Gal beta 1----4GlcNac beta 1----2Man alpha 1----3(Man alpha 1----6)Man beta 1----4GlcNac; AcNeu alpha 2----6Gal beta 1----4GlcNac beta 1----2Man alpha 1----6(Man alpha 1----3)Man beta 1----4GlcNac. Sialyloligosaccharide 1 has previously been found in the urine and liver of patients with mucolipidosis I and II and sialidosis, but sialyloligosaccharide 2 has not been found yet in human urine. These two sialyloligosaccharides could not be completely separated by any chromatographic procedures tested. The analytical techniques, including methylation study and NMR spectroscopy, could not clearly detect the differences between them. However, alpha-mannosidase treatment gave important information for the structural analyses of these sialyloligosaccharides.

Carbohydrate Metabolism, Inborn Errors↗

High-resolution proton NMR studies of gangliosides. III. Elucidation of the structure of ganglioside GM3 lactone.

Ganglioside GM3 lactone (1) was prepared in 95% yield from the parent ganglioside by incubation at 25 degrees C for 4 days in glacial acetic acid. Inspection of the 500 MHz proton NMR spectra of 1 and its precursor in dimethylsulfoxide-d6-deuterium oxide at 30 degrees C revealed a large deshielding (+1.42 ppm) of the H-2 resonance of the galactosyl residue. This suggests that 1 must be the lactone formed by esterification of the sialic acid carboxyl group with the C-2 hydroxyl of the galactosyl residue. Consideration of all the NMR data leads to a specific structure proposal in which 1 has a highly rigid structure. Interesting features of the structure include a hydrophobic inner surface and a semicircular outer edge of seven-oxygen atoms, which may have physiological importance.

Chemical Phenomena↗

Studies of peptide antibiotics. XLVI. Syntheses of gramicidin S analogs containing D-alpha,beta-diaminopropionic acid or alpha,beta-dehydroalanine.

A gramicidin S (GS) analog ([D-Dpr4,4'] GS) containing D-alpha,beta-diaminopropionic acid (D-Dpr) in place of D-Phe at 4,4' positions was derived from [L-Orn(delta-formyl)2,2', D-Dpr(beta-Z)4,4']GS, which was synthesized by conventional method in solution. An analog [delta Ala4,4']GS was synthesized from [L-Orn(delta-Boc)2,2', D-Dpr4,4']GS through Hofmann degradation of the D-Dpr residues. Antimicrobial activities of these analogs were tested; [D-Dpr(beta-Z)4,4']GS and [delta Ala4,4']GS showed high antimicrobial activities against Gram-positive bacteria. [D-Dpr4,4']-GS showed an appreciable activity against Gram-negative bacteria such as Escherichia coli. Four semigramicidin S (semiGS) analogs such as [delta Ala4]semiGS were synthesized; these had no antimicrobial activity. Analogs containing delta Ala residues were hydrogenated, and the formation of L-Ala or D-Ala residues was determined. The delta Ala residues in [delta Ala4,4'] GS were reduced to DL-Ala, and delta Ala in [delta Ala4]semiGS mostly to L-Ala. The relationships of the antimicrobial activity, CD curves and asymmetric hydrogenation to the structure were discussed.

Alanine↗

Abnormalities in gangliosides and other lipids of monkey, rabbit and human brains with chronic organic mercury intoxication.

The distribution patterns of gangliosides and other major lipids in the monkey, rabbit and human brains with chronic organic mercury intoxication were examined. Various areas of the monkey brains were tested for alterations in the lipid composition in detail. Phosphatidylethanolamine and phosphatidylcholine slightly decreased, and sphingomyelin increased in all the areas tested of the intoxicated brains. The total ganglioside concentration was elevated in the frontal and basal ganglia gray matter tissues. In the percentage distribution of gangliosides, GD1b, GT1b and GQ1b (B pathway, [19, 20]) increased, while GM2, GM1 and GD1a (A pathway, [19, 20]) decreased. Similar ganglioside pattern changes were observed also in a human brain and in a rabbit brain with chronic organic mercury intoxication. The altered distribution patterns of gangliosides may be attributable to the proliferation of reactive astrocytes due to organic mercury.

Animals↗

[Cerebellar degeneration in chronic alcoholism: with special reference to an autopsied case showing the restricted form of cerebellar cortical degeneration (Victor)].

The brains of 8 patients with chronic alcoholism were neuropathologically examined. The findings obtained in the cerebellum of case 1 (male, aged 52) were in agreement with the restricted form of cerebellar cortical degeneration which was described by Victor et al (1958). The clinicopathological report on the cerebellar degeneration of this type was very rare in Japan. The cerebellar changes were more pronounced in the anterior vermis than in the posterior vermis and hemisphere. Furthermore, some old lesions of Wernicke's encephalopathy were found in this brain. 7 other cases showed very mild cerebellar degeneration. Partial loss of Purkinje cells was found near the tops of cerebellar folia. But their distribution and intensity had no individual variation and there was no tendency that the anterior vermis was more affected. This fact suggests that the alcoholic cerebellar degeneration may have some other cause than the direct toxic effect of ethylalcohol or its metabolites. The etiology of this disease was discussed with reference to thiamine deficiency and mal-nutrition.

Adult↗

Compositional changes in brain lipids, especially cerebroside and gangliosides, of rats treated with methylmercury chloride.

Rats were orally given 4 mg of methylmercury chloride per kg per day up to 14 days, and killed at 4-day or arbitrary intervals. Parietal gray matter and cerebellum were taken for lipid analyses. The ganglioside content increased during the early stage before the manifestation of clinical symptoms. After the onset of clinical signs, the total lipid concentration was elevated, and especially the levels of phosphatidylethanolamine and cerebroside were increased. The ganglioside distribution patterns were also altered in the late stage, showing decreased proportion of GD1a and increased percentages of GD1b and GQ1b.

Animals↗