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Biomedical subjects

S D Clarke

Publications and source records attributed to S D Clarke.

104 records · Page 6Linked to original sources
PubMed1977

One hundred kidney transplants in the Belfast city hospital.

100 kidney transplants have been carried out on 91 patients (7 had 2 transplants and 2 had 3 transplants). 4 transplants were from living related donors and 96 from cadavers. 76 patients survive, all but one with functioning kidneys. The cumulative survival of patients was 82% at 2 years and 80-7% at 5 years. 8 patients died with functioning grafts, and 2 of the other deaths took place more than 3 months after removal of a rejected kidney and resumption of haemodialysis. There were no deaths from sepsis in the first 60 days after transplantation. The cumulative survival of all grafts was 82-1% at 2 and 5 years. The cumulative survival of first grafts was 82-5% at 2 and 5 years.

Adolescent↗
PubMed1976

Specific inhibition of hepatic fatty acid synthesis exerted by dietary linoleate and linolenate in essential fatty acid adequate rats.

Dietary linoleate and linolenate were investigated for their ability to specifically inhibit liver and adipose tissue lipogenesis in meal-fed (access to food 900-1,200 hr), essential fatty acid (EFA) adequate rats. Supplementing a high carbohydrate diet containing 2.5% safflower oil with 3% palmitate 16:0, oleate 18:1, or linoleate 18:2 did not affect in vivo liver or adipose tissue fatty acid synthesis. However, 18:2 addition to the basal diet did result in a significant (P less than 0.05) decline of liver fatty acid synthetase (FAS) and glucose-6-phosphate dehydrogenase (G6PD) activities. When the safflower oil content of the basal diet was reduced to 1%, the addition of 3% 18:2 or linolenate 18:3 significantly (P less than 0.05) depressed hepatic FAS, G6PD, and in vivo fatty acid synthesis by 50%. Addition of 18:1 caused no depression in hepatic FAS activity but did result in a significant (P less than 0.05) decline in liver G6PD activity and fatty acid synthesis which was intermediate between basal and basal +18:2- or +18:3-fed animals. Adipose tissue rates of lipogenesis were completely unaffected by dietary fatty acid supplementation. Similarly, the addition of 3 or 5% 18:3 to a basal diet for only one meal resulted in no change in lipogenesis relative to that in animals fed the basal diet. The data indicate that, like rats fed EFA-deficient diets, dietary 18:2 and 18:3 exert a specific capacity to depress rat liver FAS and G6PD activities and rate of fatty acid synthesis.

Adipose Tissue↗
PubMed1976

Studies of the effect of dietary cholesterol on hepatic protein synthesis, reduced glutathione levels and serine dehydratase activity in the rat.

A basal diet or a basal diet plus 1% of cholesterol and 0.33% cholic acid was fed to rats for varying lengths of time and (1) the activities of liver phosphoenolpyruvate-carboxykinase (PEP-CK), tyrosine transaminase (TT), and serine dehydratase (SD); (2) the rate of total hepatic protein synthesis and (3) the concentration of hepatic reduced glutathione (GSH) were quantitated. The specific activity of PEP-CK was significantly depressed by cholesterol plus cholic acid feeding, while the specific activity of TT was unchanged. No significant effect of dietary cholesterol plus cholic acid was found on the total liver activities. In contrast, SD specific activity was increased 3-fold. The rate of (U-14C)-L-leucine incorporation into total TCA precipitable protein following ingestion of cholesterol plus acid was significantly reduced when the data were expressed as dpm (U-14C)-L-leucine/mg protein. After correcting this expression for specific radioactivity of the liver tissue free leucine pool, no significant effect of dietary cholesterol plus cholic acid on hepatic protein synthesis existed. In fact, the amount of 14C-leucine incorporated into protein on a total liver basis was 50% greater for the cholesterol group. On a per gram of liver basis, the concentration of GSH in the liver of rats fed a cholesterol plus cholic acid diet was significantly decreased. Considering the liver enlargement in rats fed cholesterol plus cholic acid, total organ GSH was found to be significantly greater than for rats fed a basal diet.

Animals↗
PubMedDate not supplied

Coordinate induction of peroxisomal acyl-CoA oxidase and UCP-3 by dietary fish oil: a mechanism for decreased body fat deposition.

Rats fed dietary fats rich in 20- and 22-carbon polyenoic fatty acids deposit less fat and expend more energy at rest than rats fed other types of fats. We hypothesized that this decrease in energetic efficiency was the product of: (a) enhanced peroxisomal fatty acid oxidation and/or (b) the up-regulation of genes encoding proteins that were involved with enhanced heat production, i.e. mitochondrial uncoupling proteins (UCP-2, UCP-3) and peroxisomal fatty acid oxidation proteins. Two groups of male Fisher 344 rats 3-4 week old (n=5 per group) were pair fed for 6 weeks a diet containing 40% of its energy fat derived from either fish oil or corn oil. Epididymal fat pads from rats fed the fish oil diet weighed 25% (P < 0.05) less than those found in rats fed corn oil. The decrease in fat deposition associated with fish oil ingestion was accompanied by a significant increase in the abundance of skeletal muscle UCP-3 mRNA. The level of UCP-2 mRNA skeletal muscle was unaffected by the type of dietary oil, but the abundance of UCP-2 mRNA in the liver and heart were significantly lower (P < 0.05) in rats fed fish oil than in rats fed corn oil. In addition to inducing UCP-3 expression, dietary fish oil induced peroxisomal acyl-CoA oxidase gene expression 2-3 fold in liver, skeletal muscle and heart. These data support the hypothesis that dietary fish oil reduces fat deposition by increasing the expression of mitochondrial uncoupling proteins and increasing fatty acid oxidation by the less efficient peroxisomal pathway.

Acyl-CoA Oxidase↗
PubMedDate not supplied

Nutritional control of lipid synthesis.

Dietary modification for the manipulation of lipid biosynthetic pathways has currently become a major direction for improving health status. Certainly changing dietary constituents can alter lipogenic processes and blood lipid parameters. However, the extremes of such modifications are often impractical, and the impact of major changes are not without consequence. For example, high carbohydrate diets are hyperlipemic and increased fish oil intake prolongs blood clotting time. Thus, no dietary fat modifications can be undertaken without considering the organism as a whole and the complexity of interactions within the individual. Such definition requires appreciation of human individuality and greater understanding of the regulation of lipogenic pathways.

Acetyl-CoA Carboxylase↗