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Biomedical subjects

J C Sullivan

Publications and source records attributed to J C Sullivan.

9 recordsLinked to original sources
PubMed1986

Clients' satisfaction survey in a psychiatric inpatient population attached to a general hospital.

A clients' satisfaction survey was undertaken on the population of a psychiatric inpatient facility in a general hospital setting. The responses were analysed statistically and the results showed that the patients were highly satisfied with the services provided. The results are reviewed within the context of the literature available, and the methodological issues involved are discussed. It is felt that existing questionnaires need to be further refined to make them more sensitive to dissatisfaction felt by patients.

Adolescent↗
PubMed1976

The effects of N-hexyl-O-glucosyl sphingosine on normal cultured human fibroblasts: a chemical model for Gaucher's disease.

Normal human skin fibroblasts were grown in the presence of N-hexyl-O-glucosyl sphingosine (HGS), an inhibitor of aryl glucosidase and glucocerebrosidase. Tests of the cells with aryl glycosides showed that beta-glucosidase activity in the cells was drastically reduced while other enzyme activities (alpha-glucosidase, beta-galactosidase, and N-acetyl-beta-hexosaminidase) were normal or elevated. Exposure of cells to HGS for 28 days resulted in increased values for cell weight per plate, glucocerebroside concentration, and galactosyl-galactosylglucosyl ceramide concentration. The concentrations of total lipid, cholesterol, and protein were unchanged, as was the fatty acid distribution within the glycolipids. Chemically, the inhibitor-treated cells exhibited a model form of Gaucher's disease. Although many membranous cytoplasmic inclusions were induced by HGS, they were unlike the characteristic inclusions seen in individuals with the genetic disorder. Skin fibroblasts from a Gaucher patient showed no abnormalities in composition or appearance.

Cell Line↗
PubMed1968

Study of the Hurler syndrome using cell culture: definition of the biochemical phenotype and the effects of ascorbic acid on the mutant cell.

Fibroblasts from patients with Hurler syndrome retain a distinctive biochemical phenotype when grown in culture which is characterized by increased synthesis of both nonsulfated and sulfated glycosaminoglycans. Ascorbic acid reinforces the phenotypic expression of the biochemical abnormality, producing not only increased synthesis of sulfated glycosaminoglycans, but selective retention of sulfated glycosaminoglycans within the cell. Although the synthesis of nonsulfated glycosaminoglycans is also increased, these compounds, particularly hyaluronic acid are not retained by the cell but are secreted into the medium. Analyses of urine from patients with Hurler syndrome show increased absolute concentrations of nonsulfated glycosaminoglycans in addition to the expected increase in sulfated glycosaminoglycans. This indicates that the biochemical phenotype as defined in cell culture is not an artifact of the experimental model but reflects the biochemical defect in the patient. Redefinition of the biochemical defect to include nonsulfated as well as sulfated glycosaminoglycans contradicts explanations of this disease which are based on a single structural gene mutation.

Ascorbic Acid↗
PubMed1966

Vitamin C-induced increase of dermatan sulfate in cultured Hurler's fibroblasts.

In fibroblasts taken from patients witli Hurler's syndromne and grown in cultlure, dermatan sulfate constituted a larger percentage of the total sulfated glycosaminoglycans than it did in cultured fibroblasts from unaffected individuals. Moreover, the addition of ascorbic acid (vitamnin C) to the culture medium markedly increased the concentration of dermatan sulfate in the Hurler's fibroblasts but not in the normal fibroblasts. The biochemical phenotype of the Hurler's cells persisted during 28 weeks of serial culture.

Ascorbic Acid↗