Food Use and Health Effects of Soybean and Sunflower Oils

This review provides a scientific assessment of current knowledge of health effects of soybean oil (SBO) and sunflower oil (SFO). SBO and SFO both contain high levels of polyunsaturated fatty acids (PUFA) (60.8 and 69%, respectively), with a PUFA:saturated fat ratio of 4.0 for SBO and 6.4 for SFO. SFO contains 69% C18:2n-6 and less than 0.1% C18:3n-3, while SBO contains 54% C18:2n-6 and 7.2% C18:3n-3. Thus, SFO and SBO each provide adequate amounts of C18:2n-6, but of the two, SBO provides C18:3n-3 with a C18:2n-6:C18:3n-3 ratio of 7.1. Epidemiological evidence has suggested an inverse relationship between the consumption of diets high in vegetable fat and blood pressure, although clinical findings have been inconclusive. Recent dietary guidelines suggest the desirability of decreasing consumption of total and saturated fat and cholesterol, an objective that can be achieved by substituting such oils as SFO and SBO for animal fats. Such changes have consistently resulted in decreased total and low-density-lipoprotein cholesterol, which is thought to be favorable with respect to decreasing risk of cardiovascular disease. Also, decreases in high-density-lipoprotein cholesterol have raised some concern. Use of vegetable oils such as SFO and SBO increases C18:2n-6, decreases C20:4n-6, and slightly elevated C20:5n-3 and C22:6n-3 in platelets, changes that slightly inhibit platelet generation of thromboxane and ex vivo aggregation. Whether chronic use of these oils will effectively block thrombosis at sites of vascular injury, inhibit pathologic platelet vascular interactions associated with atherosclerosis, or reduce the incidence of acute vascular occlusion in the coronary or cerebral circulation is uncertain. Linoleic acid is needed for normal immune response, and essential fatty acid (EFA) deficiency impairs B and T cell-mediated responses. SBO and SFO can provide adequate linoleic acid for maintenance of the immune response. Excess linoleic acid has supported tumor growth in animals, an effect not verified by data from diverse human studies of risk, incidence, or progression of cancers of the breast and colon. Areas yet to be investigated include the differential effects of n-6- and n-3-containing oil on tumor development in humans and whether shorter-chain n-3 PUFA of plant origin such as found in SBO will modulate these actions of linoleic acid, as has been shown for the longer-chain n-3 PUFA of marine oil

Molecular characterization of WFS1 in patients with Wolfram syndrome

Wolfram (diabetes insipidus, diabetes mellitus, optic atrophy, and deafness) syndrome is a rare autosomal-recessive neurodegenerative disorder that is characterized by juvenile-onset diabetes mellitus, optic atrophy, diabetes insipidus, and sensorineural hearing impairment. A gene responsible for Wolfram syndrome (WTS1) has been identified on the short arm of chromosome 4 and subsequently mutations in WFS1 have been described. We have screened 12 patients with Wolfram syndrome from nine Dutch families for mutations in the WFS1-coding region by single-strand conformation polymorphism analysis and direct sequencing. Furthermore, we analyzed the mitochondrial genome for gross abnormalities and the A3243G point mutation in the leucyl-tRNA gene, because Wolfram syndrome shows phenotypic similarities with mitochondrial disease. Seven mutations in WTS1 were identified in six of nine families: two missense mutations, one frameshift mutation, one splice donor site mutation, and three deletions. in addition, a splice variant near the 5'UTR of WFS1 was identified, present in patient as well as control RNA samples in various percentages, alternating the translation initiation consensus sequence. Whether this WTS1 splice variant displays impaired translation efficiency remains to be deter mined. No MtDNA lesions were identified in any of the Wolfram patients. Our results demonstrate the usefulness of molecular analysis of WFS1 in the refinement of clinical diagnostic criteria for Wolfram syndrome that helps to dissect the clinically overlapping syndromes sharing diabetes mellitus and optic atrophy

Molecular characterization of WFS1 in patients with Wolfram syndrome

Item does not contain fulltextWolfram (diabetes insipidus, diabetes mellitus, optic atrophy, and deafness) syndrome is a rare autosomal-recessive neurodegenerative disorder that is characterized by juvenile-onset diabetes mellitus, optic atrophy, diabetes insipidus, and sensorineural hearing impairment. A gene responsible for Wolfram syndrome (WFS1) has been identified on the short arm of chromosome 4 and subsequently mutations in WFS1 have been described. We have screened 12 patients with Wolfram syndrome from nine Dutch families for mutations in the WFS1-coding region by single-strand conformation polymorphism analysis and direct sequencing. Furthermore, we analyzed the mitochondrial genome for gross abnormalities and the A3243G point mutation in the leucyl-tRNA gene, because Wolfram syndrome shows phenotypic similarities with mitochondrial disease. Seven mutations in WFS1 were identified in six of nine families: two missense mutations, one frameshift mutation, one splice donor site mutation, and three deletions. In addition, a splice variant near the 5'UTR of WFS1 was identified, present in patient as well as control RNA samples in various percentages, alternating the translation initiation consensus sequence. Whether this WFS1 splice variant displays impaired translation efficiency remains to be determined. No MtDNA lesions were identified in any of the Wolfram patients. Our results demonstrate the usefulness of molecular analysis of WFS1 in the refinement of clinical diagnostic criteria for Wolfram syndrome that helps to dissect the clinically overlapping syndromes sharing diabetes mellitus and optic atrophy

A COMPARISON OF INTERNAL MAMMARY ARTERY AND SAPHENOUS-VEIN GRAFTS AFTER CORONARY-ARTERY BYPASS-SURGERY - NO DIFFERENCE IN 1-YEAR OCCLUSION RATES AND CLINICAL OUTCOME

Background Superior patency rates for internal mammary artery (IMA) grafts compared with vein coronary bypass grafts have been demonstrated by retrospective studies. This difference may have been affected by selection bias of patients and coronary arteries for IMA grafting. Methods and Results To estimate the difference between IMA and vein grafts, we analyzed graft patency data of 912 patients who entered a randomized clinical drug trial. In this trial, 494 patients received both IMA and vein grafts (group 1) and 418 only vein grafts (group 2). Occlusion rates of IMA grafts and IMA plus vein grafts in group 1 were compared with those of vein grafts in group 2. Multivariate analysis was used to compare occlusion rates of IMA and vein grafts while other variables related to graft patency were controlled for. In addition, 1-year clinical outcome was assessed by the incidence of myocardial infarction, thrombosis, major bleeding, and death. Occlusion rates of distal anastomoses in group 1 versus group 2 were 5.4% (IMA grafts) versus 12.7% (vein grafts) (P Conclusions The observed difference in 1-year occlusion rates between IMA and vein grafts can be explained by a maldistribution of graft characteristics by selection of coronary arteries for IMA grafting rather than being ascribed to graft material. One-year clinical outcome is not improved by IMA grafting

A COMPARISON OF INTERNAL MAMMARY ARTERY AND SAPHENOUS-VEIN GRAFTS AFTER CORONARY-ARTERY BYPASS-SURGERY - NO DIFFERENCE IN 1-YEAR OCCLUSION RATES AND CLINICAL OUTCOME

Background Superior patency rates for internal mammary artery (IMA) grafts compared with vein coronary bypass grafts have been demonstrated by retrospective studies. This difference may have been affected by selection bias of patients and coronary arteries for IMA grafting. Methods and Results To estimate the difference between IMA and vein grafts, we analyzed graft patency data of 912 patients who entered a randomized clinical drug trial. In this trial, 494 patients received both IMA and vein grafts (group 1) and 418 only vein grafts (group 2). Occlusion rates of IMA grafts and IMA plus vein grafts in group 1 were compared with those of vein grafts in group 2. Multivariate analysis was used to compare occlusion rates of IMA and vein grafts while other variables related to graft patency were controlled for. In addition, 1-year clinical outcome was assessed by the incidence of myocardial infarction, thrombosis, major bleeding, and death. Occlusion rates of distal anastomoses in group 1 versus group 2 were 5.4% (IMA grafts) versus 12.7% (vein grafts) (P Conclusions The observed difference in 1-year occlusion rates between IMA and vein grafts can be explained by a maldistribution of graft characteristics by selection of coronary arteries for IMA grafting rather than being ascribed to graft material. One-year clinical outcome is not improved by IMA grafting