We have examined the frequency of the EcoRI and XbaI RFLPs of the apoB gene in 95 white Type 2 diabetic patients aged between 45 and 80 years in order to ascertain whether variation in this gene may be influencing the development of Type 2 diabetes and associated atherosclerosis through obesity.
These results suggest that GP66 is rabbit vitronectin and that it is vitronectin which selectively accumulates in thoracic aorta with the development of atherosclerosis.
These data identify IL-4 and interferon gamma as physiological regulators of lipoxygenase expression and suggest an important link between 15-lipoxygenase function and the immune/inflammatory response in atherosclerosis as well as other diseases.
These data identify IL-4 and interferon gamma as physiological regulators of lipoxygenase expression and suggest an important link between 15-lipoxygenase function and the immune/inflammatory response in atherosclerosis as well as other diseases.
Thus, the genetic polymorphism of apolipoprotein E may contribute to the individual risk of accelerated atherosclerosis in patients under maintenance hemodialysis.
The molecular genetic defect of a female patient with apolipoprotein A-I (apoA-I) deficiency and premature atherosclerosis was examined.Her parents were first cousins.
Variation at the haptoglobin locus could have a direct effect on the degradation of elastin in atherosclerotic aorta, whereas variation at the cholesterol ester transfer protein locus could affect lipid metabolism and promote atherosclerosis.(ABSTRACT TRUNCATED AT 250 WORDS)
Variation at the haptoglobin locus could have a direct effect on the degradation of elastin in atherosclerotic aorta, whereas variation at the cholesterol ester transfer protein locus could affect lipid metabolism and promote atherosclerosis.(ABSTRACT TRUNCATED AT 250 WORDS)
In conclusion, (1) the presence of NIDDM in the proband appears to be associated in siblings with more profound lipid and lipoprotein changes (especially low HDL cholesterol and high total triglycerides) than a history of CHD in the proband, (2) a history of CHD in the proband is associated in children with apolipoprotein changes favouring atherosclerosis (low apolipoprotein A1, high apolipoprotein B, low apolipoprotein A1/B ratio).
The authors concluded that the most important methods of prevention of atherosclerosis in youth should be: identification of high-risk individuals (overweight, hypertension, hyperlipidemia, family history of CHD and PAD, ischemic postexercise ST segment depression), health education and motivation for change, modification nutritional habits in cases of hyperlipidemia and overweight (prevention of early atherosclerotic lesions in childhood), early diagnosis and control of hypertension, practice of low salt intake, avoidance of smoking, sufficient physical activity (prevention of atherosclerotic disease mainly in adulthood).
The authors concluded that the most important methods of prevention of atherosclerosis in youth should be: identification of high-risk individuals (overweight, hypertension, hyperlipidemia, family history of CHD and PAD, ischemic postexercise ST segment depression), health education and motivation for change, modification nutritional habits in cases of hyperlipidemia and overweight (prevention of early atherosclerotic lesions in childhood), early diagnosis and control of hypertension, practice of low salt intake, avoidance of smoking, sufficient physical activity (prevention of atherosclerotic disease mainly in adulthood).
The authors concluded that the most important methods of prevention of atherosclerosis in youth should be: identification of high-risk individuals (overweight, hypertension, hyperlipidemia, family history of CHD and PAD, ischemic postexercise ST segment depression), health education and motivation for change, modification nutritional habits in cases of hyperlipidemia and overweight (prevention of early atherosclerotic lesions in childhood), early diagnosis and control of hypertension, practice of low salt intake, avoidance of smoking, sufficient physical activity (prevention of atherosclerotic disease mainly in adulthood).
Restriction-fragment-length polymorphisms flanking the insulin and apolipoprotein A-I and C-III genes, although not associated with gestational diabetes mellitus, may be associated with hyperlipidemia and subsequent atherosclerosis.
Several recent reports have examined whether there is a correlation between the presence of some minor alleles of the highly polymorphic apolipoprotein B gene and atherosclerosis and premature heart disease.
Since human arterial SMC in culture express receptors for and are mitogenically responsive to platelet-derived growth factor, transcription of the sis gene by cells within lesions, whether these cells are SMC themselves, macrophages, endothelial cells, or another cell type, suggests that an autocrine and/or paracrine proliferative mechanism is important in the pathogenesis of atherosclerosis.
Defects in the low density lipoprotein receptor gene affect lipoprotein (a) levels: multiplicative interaction of two gene loci associated with premature atherosclerosis.
Defects in the low density lipoprotein receptor gene affect lipoprotein (a) levels: multiplicative interaction of two gene loci associated with premature atherosclerosis.
Arteriosclerosis seems to be increased in heterozygotes as well (cystathionine beta-synthase gene dosage 50%) but rare in Down syndrome (cystathionine beta-synthase gene dosage 150%).
Arteriosclerosis seems to be increased in heterozygotes as well (cystathionine beta-synthase gene dosage 50%) but rare in Down syndrome (cystathionine beta-synthase gene dosage 150%).
In summary, by showing that Lp(a) concentrations and apo(a) apparent size are highly correlated with the ratio of Kringle IV/Kringle V encoding domains in the apo(a) gene, we provide a DNA marker for this atherosclerosis risk factor as well as an important insight into the genetic mechanism regulating Lp(a) levels.
In summary, by showing that Lp(a) concentrations and apo(a) apparent size are highly correlated with the ratio of Kringle IV/Kringle V encoding domains in the apo(a) gene, we provide a DNA marker for this atherosclerosis risk factor as well as an important insight into the genetic mechanism regulating Lp(a) levels.