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Biomedical subjects

G Dawson

Publications and source records attributed to G Dawson.

At least 253 records · Page 14Linked to original sources
PubMed1979

Factor M as a correlate of physical fitness: imagination or just more energy.

Determined whether 16PF scale scores could contribute significantly to the prediction of a measure of fitness. Sixty-three firemen from a large metropolitan area in the Southeast were Ss. Factor M contributed significantly to the prediction of one measure of fitness (i.e., treadmill time). The assumption cited in the literature that Factor M reflects "imagination" in individuals who score high on fitness measures was questioned. The article concluded that Cattell's earlier work relating high Factor M to high energy and endurance suggests a more logical interpretation of Factor M vis à vis measures of fitness.

Adult↗
PubMed1979

Opiates and enkephalins inhibit synthesis of gangliosides and membrane glycoproteins in mouse neuroblastoma cell line N4TG1.

When mouse neuroblastoma clonal cell line N4TG1 cells were cultured in the presence of opiates or enkephalins, in the range 10(-6)-10(-10) M for 24 hr, a dose-dependent inhibition of the incorporation of [3H]glucosamine and [14C]-galactose into sialoglycosphingolipids and glycoproteins was observed. The gangliosides most affected comigrated in thinlayer chromatographic systems with GM2 (GalNAc[AcNeu]-Gal-Glc-ceramide), GM1 (Gal-GalNAc[AcNeu]Gal-Glc-ceramide), and GDla (AcNeu-Gal-GalNAc[AcNeu]Gal-Glc-ceramide). The effects were stereospecific and naloxone-reversible. Polyacrylamide gel electrophoresis revealed that the synthesis of a large number of membrane glycoproteins was also stereospecifically inhibited. Synthesis of other proteins and glycoproteins, proteoglycans, DNA, and membrane phospholipids and the rate of cell division were not altered in any specific or stereospecific manner. Moreover, clonal cell lines (neuroblastomas and oligodendroglioma) and human skin fibroblasts, which do not possess opiate receptors, did not respond to opiates or enkephalins in a stereospecific manner.

Animals↗
PubMed1978

Evidence for the noninvolvement of sulfogalactosylceramide (cerebroside sulfate) in the enkephalin (opiate) receptor.

Mouse neuroblastoma clonal cell line N4TG1 has 20,000 enkephaline (opiate) receptor binding sites/cell, but contains undetectable levels of sulfogalactosylceramide as judged by quantitative and isotope-labeling studies. Mouse glioma cell lines G26-20 and G26-24 contain substantial quantities of sulfogalactosylceramide, but do not bind enkephalins. Preincubation of cells with sulfogalactosylceramide or other anionic glycosphingolipids did not enhance or induce opiate receptors. Thus, sulfogalactosylceramide is not an integral part of the opiate receptor of N4TG1 cells.

Cell Line↗
PubMed1977

The effect of glycosaminoglycans on the in vitro activity of human skin fibroblast glycosphingolipid beta-galactosidases and neuraminidases.

The apparent low level of synthetic substrate beta-D-galactosidase activity in liver from patients with the Hurler-Hunter syndrome is caused by the inhibitory effect of accumulated glycosaminoglycans. We have demonstrated complete inhibition of GM1 ganglioside beta-galactosidase activity in vitro by both heparan sulfate and dermatan sulfate, but the effect on lactosylceramide and galactosylceramide hydrolysis was less marked. In contrast, lysosomal neuraminidase activity in vitro was enhanced by the addition of glycosaminoglycans. These observations are discussed in relationship to the observed storage pattern of glycosphingolipids in liver from patients with mucopolysaccharidoses.

Cells, Cultured↗
PubMed1977

Synthesis of myelin glycosphingolipids (galactosylceramide and galactosyl(3-O-sulfate)ceramide (sulfatide)) by cloned cell lines derived from mouse neurotumors.

Clonal cell lines derived from both spontaneous and chemically induced rat and mouse brain tumors were screened for their ability to incorporate H232SO4 into galactosyl(3-O-sulfate)ceramide (sulfatide). High levels of 35SO4 incorporation into sulfatide were found only in two of the mouse cell lines studied (G26-20 and -24). Tumors produced by subcutaneous injection of these cell lines into C57BL/6 mice were also unique in that they contained high levels of both sulfatide and galactosylceramide. The synthesis of large amounts of sulfatide and galactosylceramide by a clonal cell line of neurological origin suggests that the original tumor was of oligodendrocyte or Schwann cell origin. In common with a large number of mouse and rat astrocyte cell strains and their derived tumors, these glial cells lacked the ability to synthesize gangliosides such as monosialotetraglycosylceramide and disialotetraglycosylceramide (as judged by analytical and [3H]GlcNH2 incorporation studies). This appears to be a unique characteristic of neuroblastoma-derived cell strains such as N18, NB2a, and NB41A.

Animals↗
PubMed1977

Genetic linkage studies of the human glycosphingolipid beta-galactosidases.

The genetic linkage relationships of the human glycosphingolipid beta-galactosidases were determined using human--mouse somatic cell hybrids. A new method was devised for the estimation of human galactosylceramide, lactosylceramide, and GMI-ganglioside beta-galactosidase activities in the presence of their mouse counterparts, which takes advantage of the reproducible specific activity of lysosomal hydrolases under a given set of culture conditions and is based on differences in both pH optima and sensitivity to chloride ion. Human and mouse chromosomes were identified by their characteristic banding patterns obtained after quinacrine staining, and the optimum glycolipid beta-galactosidase activity was determined for three different substrates. A ratio was defined for each activity which was the specific activity at the human pH optimum divided by the specific activity at the mouse pH optimum. Linear regression analysis was used to test for concordant segregation between pH ratios for each enzyme and the frequency of occurrence of different human chromosomes in the man--mouse somatic hybrid clones. The results obtained from two independent series of hybrid clones indicated that human beta-galactosidase activities consistently segregated with human chromosome 12 in these somatic cell hybrids.

Animals↗
PubMed1976

Structure of the accumulating oligosaccharide in fucosidosis.

Two water-soluble complex carbohydrate storage products were isolated from tissues and urine of patients with an inherited deficiency of lysosomal alpha-L-fucosidase (fucosidosis). The major component was an oligosaccharide of approximate molecular weight 1700, indicating that it was a dekasaccharide. From a combination of sequential digestion with purified exo-glycosidases, periodate oxidation and permethylation in conjunction with gas-liquid chromatography mass spectrometric analysis, the structure was found to be: Fuc(alpha 1 leads to 2)Gal-(beta 1 leads to 4) GlcNAc (beta1 leads to 2)Man [Fuc(alpha1 leads to 2) Gal (beta1 leads to 4) GlcNAc(beta1 leads to 2) Man] (alpha 1 leads to 3/6) Man (beta1 leads to 4) GlcNAc, although there was some evidence for heterogeneity at the mannose branchpoint. This material is structurally related to the stored oligosaccharides in patients with inherited deficiencies of beta-galactosidase (G M1-gangliosidosis) and N-acetyl-beta-hexosaminidase (G M2-gangliosidosis). A dissaccharide with the probable structure Fuc(alpha1 leads to 6)GlcNAc was found in lesser amounts in tissues; both are believed to be derived from the impaired catabolism of large numbers of different glycoproteins.

Acetylglucosamine↗
PubMed1976

Progressive spastic paraparesis and adrenal insufficiency.

A 10-year-old boy with progressive paraparesis, personality change, and seizures had laboratory evidence of adrenal insufficiency. Pathologic study showed cerebral edema, but no loss of myelin. Notable pathologic changes were limited to the spinal cord, where the corticospinal and spinocerebellar tracts were demyelinated. Lipid analysis of the brain was normal apart from the finding that galactocerebroside contained a higher proportion than normal of alpha-hydroxy fatty acids. We suggest that this case represents a distinct disease, differing importantly from adrenoleukodystrophy. The underlying defect appears to be in the early enzymatic pathway before cholesterol synthesis, although it is also possible that the defect is at the cell membrane.

Adrenal Insufficiency↗