Pneumococcal pericarditis: a rare complication of pneumonia.
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Biomedical subjects
Publications and source records attributed to R L Hood.
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The antioxidant activity of tocotrienols toward peroxyl radicals was compared with that of other natural lipid-soluble antioxidants in three different systems by measuring the temporal disappearance of antioxidants and the formation of lipid hydroperoxides. In homogeneous solution, the initial rates of consumption of the various antioxidants, assessed by competition experiments between pairs of antioxidants for radicals, decreased in the order: ubiquinol-10 approximately ubiquinol-9 > alpha-tocopherol approximately alpha-tocotrienol > beta-carotene approximately lycopene > gamma-tocopherol approximately gamma-tocotrienol. Following in vitro incubation of human plasma with alpha-tocotrienol, this form of vitamin E was present in all classes of lipoproteins isolated from the supplemented plasma. Dietary supplementation of rats and humans with a tocotrienol-rich preparation resulted in a dose-dependent appearance of alpha- and gamma-tocotrienols in plasma and all circulating lipoproteins, respectively. Exposure of such enriched rat plasma to aqueous peroxyl radicals resulted in simultaneous consumption of the alpha- and then gamma-isomers of vitamin E. The sequence of radical-induced consumption of antioxidants in freshly isolated, in vitro and in vivo tocotrienol-enriched low density lipoprotein (LDL) was again ubiquinol-10 > alpha-tocotrienol approximately alpha-tocopherol > carotenoids > gamma-tocopherol approximately gamma-tocotrienol. Under conditions where radicals were generated at constant rates, the rate of lipid hydroperoxide formation in LDL was not constant. It proceeded in at least three stages separated by the phase of ubiquinol-10 consumption and, subsequently, that of alpha-tocopherol/alpha-tocotrienol. Our results show that dietary tocotrienols become incorporated into circulating human lipoproteins where they react with peroxyl radicals as efficiently as the corresponding tocopherol isomers.
Male adult rats were fed on diets containing 80 g/kg galactomannans with different galactose (G): mannose (M) ratios/kg. The galactomannans were compared with purified cellulose (Solkaflok) and the animal were also fed on a basal diet free from fibre. All diets contained cholesterol (10 g/kg) and sodium cholate (2 g/kg). The three galactomannans were fenugreek gum (1G:1M), guar gum (1G:2M) and locust-bean gum (1G:4M). In comparison with the fibre-free and Solkaflok diets, all three galactomannans lowered the concentrations of cholesterol in both liver and blood plasma. The galactomannans also decreased the rate of hepatic synthesis of cholesterol. Dietary galactomannans increased caecal volatile fatty acids, particularly propionic, increased the weight of the caecum and its contents and increased the amount of water in the faeces. The increase in propionic acid production was significantly related to a decrease in caecal pH, but not to changes in plasma cholesterol or hepatic cholesterol synthesis. These effects were significantly influenced by chemical composition and structure of the galactomannan; they were most evident when the proportion of galactose in the galactomannan was highest (i.e. fenugreek gum). The three galactomannans also differed markedly in their effects on the viscosity of the digesta, but the galactomannan which gave the highest viscosity was least effective in lowering plasma cholesterol. A separate experiment with perfused loops of small intestine in vivo showed that the most effective galactomannan, fenugreek gum, had no direct effect on cholesterol absorption.
Blood lipid concentrations and hepatic cholesterol synthesis were compared in Japanese quail fed diets containing fats with different fatty acid profiles. The quail fed a diet containing tuna oil had the lowest blood cholesterol concentration; those fed beef drippings the highest, and those fed safflower oil or linseed oil had intermediate concentrations. Rates of hepatic cholesterol synthesis mirrored the results for serum cholesterol concentration. Serum triglyceride concentrations were lower in the quail fed the two diets containing n-3 fatty acids in comparison with the beef and safflower treatment groups.
A comparison of acetate, glucose, mevalonate, or water as radioactive substrates for the hepatic synthesis of cholesterol, fatty acids, and glyceride-glycerol was made in Japanese quail fed diets containing either beef fat or tuna oil. The quail fed a diet containing beef fat were fatter and had a significantly higher (P less than .01) concentration of serum cholesterol (5.6 mM per L) than that measured in the serum of quail given tuna oil (4.1 mM per L). Both in vitro cholesterol and fatty-acid synthesis were greater in the quail fed a diet of beef fat than in those fed a diet containing tuna oil. The results showed that mevalonate was the most-suitable radioactive substrate for measuring cholesterol synthesis, whereas glucose was the most-suitable radioactive substrate for measuring fatty-acid and glyceride-glycerol synthesis.
A primary monolayer culture system from cockerel hepatocytes was established. The cultures synthesize and secrete proteins that comigrate with authentic serum proteins on polyacrylamide gels and are found in the same relative abundance. Addition of estradiol increased the synthesis of apoprotein B, found in very low density lipoprotein, under all culture conditions. Vitellogenin synthesis could not be induced directly by estradiol. However, when serum was obtained from cockerels injected with estradiol 4 days before blood collection and included in the culture medium, the cultures secreted a protein identified immunologically as vitellogenin by affinity chromatography. Furthermore, addition of growth hormone or prolactin to cultured cockerel hepatocyte monolayers resulted in the synthesis and secretion of a polypeptide that comigrates with authentic vitellogenin on polyacrylamide gels.
To study the pathway of lactate utilization as a carbon source for fatty acid synthesis, the effect of (-)-hydroxycitrate, agaric acid, sodium oxamate, 2-n-butyl malonate and alpha-cyano-4-hydroxycinnamate on the rate of in vitro conversion of lactate, acetate and glucose to fatty acids was measured in bovine and rat adipose tissues. Sodium oxamate and hydroxycitrate caused less fatty acid to be synthesized from lactate in bovine adipose tissue. Hydroxycitrate depressed fatty acid synthesis from glucose in rat adipose tissue. alpha-Cyano-4-hydroxycinnamate was an effective inhibitor of lipogenesis from all substrates and may act as a specific inhibitor in adipose tissue. Although the inhibitors were absorbed poorly into adipocytes, the results indicate that conversion of lactate to fatty acids probably occurs by way of the citrate cleavage pathway.
An enzymatic method for the determination of the amount of free fatty acids released from triglyceride by lipoprotein lipase is described. The quantity of free fatty acids present in media before and after incubation is measured spectrophotometrically by the oxidation of NADH in the final reaction of a series of coupled enzymatic reactions. This assay for lipoprotein lipase is unlike previously described assays in that radioactive substrates or titration procedures are not used in the free fatty acid determination. In addition, another method for assay of lipoprotein lipase activity that involves the separation of free fatty acids from triglycerides by adsorption chromatography with Florisil as a stationary phase is described.
Production of CO2 and fatty acids from acetate, glucose and lactate was determined in slices of liver and adipose tissue from prairie voles fed either a high-starch or a high-cellulose diet. Acetate and lactate were oxidized to CO2 and converted to fatty acids at greater rates than was glucose in both liver and adipose tissue. Fatty acid synthesis occurred at greater rates in adipose tissue than in liver. Fatty acid synthesis per adipocyte increased with increased adipocyte diameter. Fiber content of diets had only minimal effect on metabolic activities of liver and adipose tissue.
Activities of lipogenic enzymes and plasma very low density lipoprotein (VLDL) concentrations were measured in lines of chickens with large differences in food conversion efficiency (FCE) and body fat. Hepatic activities of malate dehydrogenase [EC 1.1.1.40 (MD)] and ATP citrate lyase [EC 4.1.3.8 (CL)] were correlated with the proportion of both abdominal and total body fat (r = 0.50) but were poorly correlated with gain: food ratio. Activities of MD and CL in plasma were low and variable and were not correlated with any other characteristics. Plasma VLDL concentration was significantly correlated with the proportion of abdominal and total body fat (r = 0.59), and gain: food ratio (r = 0.36).
Epididymal adipose tissue from non-fa/fa (lean) and fa/fa (obese) 14.5-week-old Zucker rats was used to study the influence of insulin and genotype on uptake of glucose and palmitate into adipocytes of different sizes. After incubation with radioactive substrate, adipocytes were inactivated and fixed by addition of osmium tetroxide; fixed adipocytes were isolated and separated by screening on the basis of size. Rates of substrate uptake into triacylglycerols were measured in adipocytes of each of ten size categories. Uptake rates of both glucose and palmitate increased as adipocyte size increased. Insulin had no effect on glucose uptake per adipocyte for fa/fa rats but had a highly significant (P less than 0.01) stimulatory effect on that for non-fa/fa rats. This stimulation became significantly greater with increasing adipocyte size. When insulin was included in the incubation media, glucose uptake rates were similar between similar sizes of adipocytes from non-fa/fa and fa/fa rats. Absence of insulin from the incubation media, however, resulted in lower rates of glucose uptake by adipocytes from non-fa/fa rats. Glucose uptake was maximal in adipocytes from fa/fa rats, even in the absence of insulin. Net uptake of palmitate into triacylglycerols was not influenced by insulin; a significant interaction was observed, however, between adipocyte size and genotype. Large adipocytes from fa/fa rats had greater rates of palmitate uptake than did adipocytes of similar size from non-fa/fa rats. The reverse was true for adipocytes less than 125 micron in diameter. The results of this study show that response to insulin of adipocytes of difference sizes varies with adipocyte size and with genotype.
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Cellular growth of the abdominal fat pads from Tegel TM70 white broiler chickens was characterized by both hyperplasia and hypertrophy of adipose cells until the chickens were approximately 14 weeks old, after which hypertrophy of existing adipose cells was solely responsible for increases in the mass of these fat deposits. The percent body fat was linearly and positively correlated with the weight of abdominal fat. However, at a constant percent body fat, male birds had a larger deposit of fat in the abdominal region than did females. Thus, a different relationship to predict body fat would be required for each sex. In mature birds the mass of an adipose tissue deposit is generally reflected in the size of adipose cells rather than the number of cells in an adipose organ.
In early postnatal development, growth of adipose tissue is due to both cellular hypertrophy and hyperplasia. Adipose cell (adipocyte) hypertrophy is the major mechanism in fattening of ruminants grown to market weight, although evidence is accumulating that preadipose cells can proliferate postnatally, even in mature animals. In interfasicular adipose tissue (marbling), however, small adipose cells are present and their number makes a positive contribution to the size of this fat depot in ruminants of market weight. Present information does not indicate whether these small cells are newly synthesized cells or are cells that differentiated early in postnatal development and fill with lipid at some later time. Limitations on detecting small adipose cells in cell-counting techniques are partly responsible for conflicting conclusions on the cellular basis for adiposity. Nutritional modification of adipose cell number has been reported in rodents. However, the extreme nutritional modifications required to alter cell number have little practical application in the growth of ruminants for meat production. Adipose cells of various sizes respond differently in the esterification and synthesis of fatty acids. The greater rates of lipid synthesis from acetate in large adipose cells may be related to increased uptake of substrate in cells with a large surface area.
The influence of feeding cows formaldehyde-treated polyunsaturated oilseed supplement on fatty acid composition and distribution of particle size of milk fat globules has been studied. Supplement increased linoleic acid in milk fat from 1.7 to 27.4%. Distributions of particle size measured by a Coulter counter showed that milk fat from cows receiving supplement had large milk fat globules than those in milk fat of the same cows when supplementation was discontinued. However. this difference in size could not be attributed to percent linoleic acid in the milk fat since correction of the data of supplemented cows for percent milk fat and size of milk fat globules resulted in particle distributions strikingly similar in shape.
A diet which is marginally deficient in the vitamin biotin may cause sudden unexpected death of young broiler chickens when they are exposed to stress. Chickens affected with this disorder have low levels of biotin in their livers. In conditions of biotin insufficiency, we postulate that a similar disorder, triggered by mild stress, may occur in the human infant. We have now used a radiochemical technique to measure the biotin content of 204 livers obtained from infants at autopsy. The levels of biotin in the livers of infants who had died of sudden infant death syndrom (SIDS; cot death) were significantly lower than those in livers of infants of similar age, who had died of explicable causes. These findings support an association of biotin with SIDS.
The effects of including protected lipid supplements in the sheep diet have been studied by measuring the incorporation of [1-14C]acetate into tissue fatty acids in vivo and in vitro. Supplementing the diet with protected lipid significantly (P > 0.05) depressed lipogenesis in adipose tissue both in vovo and in vitro. However, when protected lipids of different fatty acid composition were given to lambs, the protected safflower oil supplement containing high levels of linoleic acid was the only treatment to cause a significant (P > 0.05) depression in fatty acid synthesis in adipose tissue, the major site of lipogenesis in the sheep. Larger adipose cells in the lipid-supplemented sheep indicate that these sheep were fatter than those receiving the basal diet. Therefore, supplemented wethers deposited more fat than sheep receiving the basal diet and this fat was derived from the supplement rather than from de novo synthesis.