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Biomedical subjects

R E Olson

Publications and source records attributed to R E Olson.

At least 91 records · Page 5Linked to original sources

Perceived control of nutrition behavior: a study of the locus of control theory among healthy subjects.

This study was conducted to gain insight into individuals' perceptions of their willingness and ability to change their nutrition behavior. As eating habits are primarily socially learned, the locus of control theory, a social learning theory, was applied to the understanding of nutrition behavior. Responses from 105 young male and female subjects to a questionnaire devised to examine individuals' beliefs about the internal and external factors which control, or determine, dietary habits and health were analyzed. Individual values and assessment of personal health and diet were measured, and demographic data were collected. Two major findings were obtained. First, the locus of control theory was too narrow a construct to explain the subjects' responses and beliefs. The data suggested six categories which differentiated between individuals' expectations about factors controlling outcomes of behavior and those controlling actual personal behaviors. Second, there were significant differences in responses to locus of control statements on the basis of certain demographic variables, especially religious affiliation. Religious/traditional Jewish subjects tended to be more internally oriented than nonreligious/nontraditional Jewish subjects, independent of other demographic variables. Subjects with greater willingness and perceived ability to change their nutrition behavior appeared to take responsibility for choosing what is "right" or "better" and had firmly established personal guidelines for what is, or is not, acceptable.

Adolescent↗

The regulation of ubiquinone-6 biosynthesis by Saccharomyces cerevisiae.

Increasing concentrations of glucose (1-5%) in the growth medium depressed ubiquinone-6 biosynthesis in continuously cultured wild type Saccharomyces cerevisiae. In addition, an early intermediate in the pathway of ubiquinone-6 biosynthesis, i.e. 3,4-dihydroxy-5-hexaprenylbenzoate (3,4-DHHB), was found to accumulate. The increase in 3,4-DHHB levels varied inversely with the diminished levels of ubiquinone-6, suggesting that O-methylation of 3,4-DHHB is a regulated step in catabolite repression. Experiments using protoplasts demonstrated that the effect of catabolite repression on this pathway was reversible by 1.2 mM cAMP but not by other nucleotides and cyclic nucleotides. This response to cAMP was unaltered by the protein synthesis inhibitor cycloheximide, indicating that the regulatory control for this reaction must occur at the enzymatic level. Additional experiments demonstrated the presence of a heat-labile component of the cytoplasm, which was essential for this effect of cAMP. This observation suggests that this cytosolic effector may be translocated to the inner membrane of the mitochondria, the intracellular site for ubiquinone-6 biosynthesis.

Cyclic AMP↗

Effects of dietary cholesterol and fatty acids on plasma lipoproteins.

The effects of dietary cholesterol and fatty acids on low density and high density lipoproteins (LDL and HDL) were studied in 20 young men. After 2-3 wk of evaluations on ad lib. diets, basal diets, which consisted of 15% protein, 45% carbohydrates, 40% fat, and 300 mg/day of cholesterol, were given for 4-5 wk (Basal). The ratio of dietary polyunsaturated to saturated fatty acids (P/S) for different groups of subjects were 0.25, 0.4, 0.8, or 2.5. 750 and 1,500 mg/d of cholesterol were added to the basal diets as 3 and 6 eggs, respectively. Total cholesterol and LDL cholesterol were lower in all subjects on the basal diets than on the ad lib. diets. Addition of 750 mg cholesterol to the diet with P/S = 0.25-0.4 raised LDL cholesterol by 16 +/- 14 mg/dl to 115% of basal diet values (n = 11, P less than 0.01); 1,500 mg increased LDL cholesterol by 25 +/- 19 mg/dl to 125% (n = 9, P less than 0.01). On the diet with P/S = 0.8, 750 mg produced insignificant increases in LDL cholesterol, but 1,500 mg produced increases of 17 +/- 22 mg/dl to 115% of basal (n = 6, P less than 0.02). On the P/S = 2.5 diet, neither 750 nor 1,500 mg produced significant changes. Thus, both the cholesterol contents and P/S ratios of diets were important in determining LDL levels. The lipid and apoprotein compositions, flotation rates, molecular weights, and binding by cellular receptors of LDL were virtually unchanged by the addition of cholesterol to the diets high in saturated fat. These diets, therefore, caused an increase in the number of LDL particles of virtually unchanged physical and biological properties. On the diet with low P/S ratio, HDL2 rose, whereas this effect was absent on diets with high P/S ratios. The response of LDL to dietary manipulations is consonant with epidemiologic data relating diets high in cholesterol and saturated fat to atherogenesis. The response of HDL2, however, is opposite to that of its putative role as a negative risk factor. Further work is needed to clarify this interesting paradox.

Adult↗

Psychological factors in the etiology, progression, and treatment of MPD syndrome.

The evidence is abundant and clear: psychological factors do have an important role in the etiology, progression, and treatment of MPD syndrome. These findings have implications for therapists who wish to understand the disorder and to manage patients appropriately. In regard to etiology, they should appreciate the impact of psychological traits and states on the development of symptoms of MPD syndrome, but they should not waste time and energy in measuring or analyzing specific psychological factors in individual patients. In regard to perpetuation of the disorder, they should understand that some patients will not respond to conventional treatment despite the best efforts of any competent therapist. Finally, in regard to treatment, they should recognize the importance of nonspecific factors such as placebo effects, doctor-patient interactions, and spontaneous recoveries in the treatment response. This awareness will enhance their effectiveness as therapists and will help them to avoid using excessive or radical treatment methods.

Anxiety↗

Cholinergic stimulation of immunoglobulin A secretion in rat intestine.

This study was undertaken to assess a possible role for cholinergic agents in the regulation of intestinal immunoglobulin A secretion. Intestinal loops, constructed in anesthetized rats, were perfused with phosphate buffered normal saline. Immunoglobulin A concentrations were measured by radioimmunoassay. When compared with the effect of normal saline in the same rats, intravenous injection of pilocarpine, 10 mg/kg, increased immunoglobulin A concentrations in perfusates from ileal loops (p less than 0.001). Qualitatively similar results were obtained with muscarine and bethanechol, from jejunal and colonic loops, and from unanesthetized rats. Immunoglobulin A concentrations increased four- to eightfold during maximal cholinergic stimulation. Atropine, 250 micrograms intravenously, completely blocked the effect of pilocarpine on immunoglobulin A secretion (p less than 0.005), and also inhibited basal intestinal immunoglobulin A secretion for 40 min after injection. As determined on 10%-40% sucrose density gradients, much of the immunoglobulin A secreted after cholinergic stimulation sedimented in the 11S range. These data indicate that intestinal secretion of immunoglobulin A is stimulated by the muscarinic effect of cholinergic agonists, and suggest that basal secretion of immunoglobulin A may be influenced by the parasympathetic nervous system.

Anesthesia, General↗

Identification of 3-methoxy-4-hydroxy-5-hexaprenylbenzoic acid as a new intermediate in ubiquinone biosynthesis by Saccharomyces cerevisiae.

A ubiquinone-deficient mutant strain of Saccharomyces cerevisiae, 26H, was found to accumulate a previously unidentified intermediate in ubiquinone biosynthesis when grown in the presence of p-hydroxy[7-14C]- or -[u-14C]benzoic acid. This intermediate was isolated from the lipid extracts of a 100-L culture of 26H and purified by various chromatographic procedures to yield 20 mg of product. Analysis by means of NMR, IR, UV, and mass spectrometry revealed the structure of this new intermediate to be 3-methoxy-4-hydroxy-5-hexaprenylbenzoic acid (3-MHHB). In vitro experiments with isolated yeast and rat mitochondria showed that 3-MHHB could be converted to ubiquinone-6. These findings indicate that 3-O-methylation precedes decarboxylation of the prenylated protocatechuic acid intermediate in the biosynthesis of ubiquinone in eukaryotes.

Animals↗

Identification of 3,4-dihydroxy-5-hexaprenylbenzoic acid as an intermediate in the biosynthesis of ubiquinone-6 by Saccharomyces cerevisiae.

The mutant strain of Saccharomyces cerevisiae E3-24 is unable to synthesize ubiquinone-6. When this mutant is grown in the presence of p-hydroxy[U-14C]benzoate or p-hydroxy[carboxy-14C]benzoate, a radioactive compound accumulates. This new metabolite has been isolated and identified as 3,4-dihydroxy-5-hexaprenylbenzoate (3,4-DHHB). Aerobically grown prototrophic strains of S. cerevisiae were found to contain only low levels of this compound. When strain X963-18C, blocked at homoserine O-transacetylase (in methionine biosynthesis), was deprived of methionine, ubiquinone biosynthesis ceased, and 3,4-DHHB was observed to accumulate. This suggested that S-adenosylmethionine (SAM) could be the methyl donor for 3,4-DHHB. Restoration of methionine to the cultures released this block and resulted in the conversion of 3,4-DHHB to ubiquinone-6, demonstrating a precursor--product relationship. The identification of 3,4-DHHB as an intermediate in ubiquinone biosynthesis in yeast establishes an alternate pathway for ubiquinone biosynthesis in eukaryotes.

Carbon Radioisotopes↗

Effects of low temperature on the development of the microsporidan Glugea stephani in English sole (Parophrys vetulus).

Glugea stephani requires temperatures above 15 C for development in juvenile pleuronectid flatfishes in Yaquina Bay, Oregon. The effect of low temperature (10 C) on the development of recently established parasites was tested experimentally in juvenile English sole (Parophrys vetulus). Low temperature arrested parasite development, but did not kill the protozoan which resumed development on return to 19-20 C after as long as 42 days at 10 C. No parasites detectable with the light microscope were found in fish examined after 70 days at 10 C. Although most juvenile English sole move permanently from the estuary to cooler ocean waters in fall and do not contribute to the continuation of the parasite life cycle, the cycle may be maintained by low numbers of English sole that overwinter in the estuary.

Animals↗