Hard times for hard margarines.
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Biomedical subjects
Publications and source records attributed to M Ball.
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The characterization of site-specific glycosylation is traditionally dependent on the availability of suitable proteolytic cleavage sites between each glycosylated residue, so that peptides containing individual glycosylation sites are recovered. In the case of heavily glycosylated domains such as the O-glycosylated mucins, which have no available protease sites, this approach is not possible. Here we introduce a new method to gain site-specific compositional data on the oligosaccharides attached to a single amino acid. Using a model glycopeptide from a mutant human albumin Casebrook, glycosylated PTH-Asn was recovered after sequential solid-phase Edman degradation, subjected to acid hydrolysis and the sugars were identified by high performance anion exchange chromatography with pulsed amperometric detection. The PTH-Asn(Sac) derivative was further characterized by ionspray mass spectrometry. Comparison between an endoproteinase Glu-C glycopeptide and a tryptic glycopeptide showed that the oligosaccharide attached to Asn494 was stable after at least 10 cycles of Edman degradation.
It has been suggested that the metabolic consequences of a given diet may depend in part on the frequency with which meals are eaten. To investigate the effects of meal frequency on plasma lipid metabolism, 16 free-living hypercholesterolaemic men and women consumed their usual diet as 3 or 9 meals/day in random order for 4 weeks. Dietary macronutrient intake and body weight remained similar on the 2 regimens. Fasting plasma lipids were measured after 2, 3 and 4 weeks on each regimen and there were no significant differences in the fasting concentrations of plasma total, LDL, and HDL cholesterol, triglycerides, apolipoprotein A-I and B and the ratio of total: LDL and LDL:HDL cholesterol (HDL-C) on the two diets. The mean (+/- S.D.) fasting total cholesterol was 6.73 +/- 0.74 and 6.81 +/- 0.88 mmol/l on 3 and 9 meals/day, respectively and LDL-C was 4.77 +/- 0.66 and 4.87 +/- 0.78 mmol/l, respectively. There was also no significant variation in the response of plasma triglycerides or serum insulin to a high fat meal following a 3 week adaptation to regimens of 3 and 9 meals/day. Finally the 24 h urinary output of C-peptide was similar on each diet. The consumption of isoenergetic diets as 3 and 9 meals/day did not influence fasting plasma lipid levels, C-peptide excretion or the plasma triglyceride response to a high fat meal of a group of free living hypercholesterolaemic subjects.
The effects of a low-fat, low-cholesterol diet (LFD) or a higher-fat, higher-cholesterol diet (HFD) on plasma concentrations of lipids, lipoproteins, lathosterol (an index of cholesterol synthesis rate), and plant sterols were determined in 19 patients with familial hypercholesterolemia (FH) treated with simvastatin. The study followed a randomized crossover design including two 8-week diet periods. The LFD significantly decreased plasma lathosterol (-22%), cholesterol (-6%), low-density lipoprotein (LDL) cholesterol (-6%), and high-density lipoprotein (HDL) cholesterol (-7%) levels compared with the HFD. Decreases in plasma lathosterol and LDL cholesterol concentrations in patients during the LFD were significantly correlated (r = .522, n = 19, P < .05). These results suggest that a LFD may enhance the decrease in cholesterol synthesis induced by simvastatin treatment, and in this way might contribute to the decrease in plasma cholesterol levels when the fat content of the diet is reduced in simvastatin-treated FH patients.
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Food, especially meat, milk, and fish, is the immediate source of almost all polychlorinated dibenzo-p-dioxins (PCDDs), dibenzofurans (PCDFs), and dioxinlike compounds in the general population. To estimate intake of these highly toxic compounds, we performed congener-specific dioxin analyses for the first time on U.S. food for 18 dairy meat, and fish samples from a supermarket in upstate New York. 2,3,7,8 Tetrachlorodibenzo-p-dioxin (TCDD, "dioxin") toxic equivalents (TEqs) on a wet weight basis for the dairy products ranged for 0.04 to 0.7 ppt, meat TEqs ranged from 0.03 to 1.5 ppt, and fish TEqs ranged from 0.02 to 0.13 ppt. Previous human breast milk and infant formula analyses were used with the current preliminary food data to estimate a range of dioxin intake for Americans. Average daily food intake of TEqs for an adult weighing 65 kg was estimated to be between 0.3 and 3.0 pg/kg body weight, for a total of 18-192 pg TEq, using 1986 American consumption rates. Due to the relatively high level of PCDDs and PCDFs commonly found in human breast milk from American women and from women in other industrial countries, a nursing infant may consume an average of 35-53 pg TEq/kg body weight/day in its first year of life. This may be compared with the current U.S. EPA virtually safe dose of 0.006 pg TCDD/kg body weight per day over a 70-year lifetime based on an upper limit cancer risk of 10(-6), or the 10 pg/kg/day used by some European government agencies.
During the past decade a considerable amount of data has been generated concerning polychlorinated dibenzodioxin (PCDD) and polychlorinated dibenzofuran (PCDF) levels in humans from many geographical locations. To organize these data in a useful fashion for environmental purposes and for consideration of human toxicity, selected portions of our data are presented in a somewhat atypical fashion, by percentage contribution of individual congeners to total PCDD/Fs in human tissue, and to the total dioxin equivalents (TEq). This is done to better characterize congener contributions from environmental contamination in various geographical regions at this time and health-related levels. To present the findings in a global perspective, data from widely different locations are presented including the United States, Germany, Vietnam, the former Soviet Union, Thailand, Cambodia, China, South Africa, and Guam.
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A two site electrochemical enzyme immunoassay for thyrotropin (TSH) has been developed. This assay is based on the use of an immobilized capture antibody and a biotinylated second antibody. Detection is achieved via avidin labelled with alkaline phosphatase. The substrate 1-naphthyl phosphate was used and the product 1-naphthol was detected at disposable screen-printed carbon 8-electrode combs using specially designed instrumentation.
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