Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of LPSw (a lipopolysaccharide from wheat flour) on cholesterol catabolism was examined using WHHL (Watanabe heritable hyperlipidemic) rabbit, which is an experimental model of familial hyperlipidemia. The serum cholesterol level of the animal decreased by the addition of LPSw to drinking water. Following cessation of the addition of LPSw to the drinking water, the cholesterol level was decreased for 30 to 40d and then gradually elevated. The serum level of apolipoprotein B, which is a constituent of apolipoprotein of low density lipoprotein (LDL), also decreased in accord with serum cholesterol at a nearly coincident rate. Conversely, the level of apolipoprotein A-I, which is a constituent of apolipoprotein of high density lipoprotein (HDL), did not change, nor did HDL-cholesterol. Furthermore, the atherosclerosis risk factor, expressed as the ratio of apolipoprotein B to apolipoprotein A-I, was decreased by LPSw administration.
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PMID:Homeostasis as regulated by activated macrophage. VII. Suppression of serum cholesterol level by LPSw (a lipopolysaccharide from wheat flour) in WHHL (Watanabe heritable hyperlipidemic) rabbit. 139 46

In 1987, the lipid work-up forms now an integral part of a rational policy of prevention of often dramatic and unfortunately often fatal clinical accidents of atherosclerosis, especially coronary atherosclerosis coronary atherosclerosis where an extremely high mortality, around 60,000 par year, requires that all prevention efforts be mobilized, as everything seems to indicate that it will be quickly rewarding and will substantially reduce this main scourge of mortality and morbidity in this country. It is desirable that every french person, in a relatively near future, with the new simplified techniques of cholesterol and triglycerides controls, be aware of his/her cholesterol level when prevention is effective: i.e. at a relatively early age, if possible around the age of 30, before the warnings of common atherosclerosis in the fifth or sixth decade. If the lipid work-up is normal, limited in a known patient without any personal or familial risk factor, to a simple dosage of fasting blood cholesterol and triglycerides, and costing merely 45 French Francs, it is not necessary to repeat that test in these patients, except every 5 years approximately. The cost to the national community is extremely low. On the contrary, in all cases where the first dosage indicate abnormalities, or are found in a family with major cardio-vascular risk in several of its members, or in case of familial hyperlipidemia, this work-up must be improved, associated with the dosage of HDL cholesterol by the precipitation technique enabling to recover the computed dosage of LWDL cholesterol, and the dosage of apoprotein B, currently rather well standardized and if possible, in the near future, the dosage of apoprotein Al.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The lipid profile in 1987. Where to start and where to end?]. 343 84

Hyperlipidemia is common in diabetic patients. While our understanding of lipid and lipoprotein metabolism in diabetes is incomplete, a pathophysiologic approach to this problem is presented. It is based on the recognition that diabetes is metabolically heterogeneous. Thus the roles of insulin deficiency, insulin resistance, obesity, and genetic factors are discussed in relation to their effects on lipoprotein production and catabolism. The most important defect in insulin-deficient subjects appears to be a deficiency of lipoprotein lipase, which is responsible for the removal of the triglyceride-rich lipoproteins. In non-insulin-dependent subjects there is evidence for a removal defect as well as, in some patients, for overproduction of VLDL-triglyceride. Cholesterol levels may be elevated and it is important to distinguish between VLDL, LDL, and HDL as the causes for these increases. HDL-cholesterol levels may be increased in insulin-dependent subjects, whereas they may be decreased in obese non-insulin-dependent patients. Mild elevations of LDL-cholesterol may occur in inadequately controlled type I and II diabetic patients, while elevated VLDL may raise the serum cholesterol in addition to the triglyceride levels. The rationale for therapy is based on the complications of severe hypertriglyceridemia and the risk of occlusive atherosclerosis. Management is directed at improving glycemic control, altering dietary composition, and reducing calories in obese patients. Improved glycemic control is effective in reducing triglyceride and cholesterol levels in insulin-deficient subjects. The response of the non-insulin-dependent diabetic patient to improved control may be complicated by associated obesity or familial hyperlipidemia. The advantages and disadvantages of fat versus carbohydrate restriction in the diet are discussed. Finally, resistant hyperlipidemia may require drug therapy. Diabetic hyperlipidemia should be viewed as resulting from an interaction between the diabetic syndrome, the genetic background of the patient, and the environment.
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PMID:Lipid disorders in diabetes. 675 32

Molecular biology has given a strong impact on cardiovascular medicine, not only clinical but also laboratory medicine. cDNA cloning and analysis of gene structures encoding functional proteins or peptides in the cardiovascular system provided insight into molecular mechanisms underlying heart diseases or atherosclerosis. Nucleotide or amino acid sequences for these molecules are useful information for manufacturing bioactive peptides or developing immunoassays. These cDNA clones or genes are useful molecular tools diagnosing patients with high risks for cardiovascular diseases. Recent advances in this field have been made in identification of point mutations of many genes important for cardiovascular functions, including LDL receptors in familial hyperlipidemia, cardiac myosin heavy chain genes in familial hypertrophic cardiomyopathy, mitochondrial DNA in mitochondria cardiomyopathy, or dystrophin genes in secondary cardiomyopathy. Molecular probes are further used in detection of microorganisms causing myocarditis. These progresses that have been made in laboratories of basic researchers will be introduced into clinical medicine and expand the field the laboratory medicine is involved.
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PMID:[Molecular biology in cardiovascular medicine]. 773 12

Each hyperlipidemia patient requires individual management. Treatment choices are thus made for each patient on the basis of evaluation of their overall cardiovascular risk. This evaluation involves four types of characteristics: those which cannot be changed (age, gender), classical lipid and non-lipid risk factors, and finally cardiovascular status with two types of evaluation (clinical status and sub-clinical, atherosclerosis). Three examples are presented here, enabling more precise assessment of lipid risk: syndrome X which shows to what extent risk factors are often associated, combined familial hyperlipidemia which emphasises the importance of family history, and lipoprotein (a). The latter is a risk factor relatively inaccessible to treatment but which enables better evaluation of the risk of the patient and choice of a stricter treatment goal when it is very high.
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PMID:[New lipid factors of cardiovascular risk]. 782 48

Risk factors such as hypercholesterolemia, hypertension and smoking are already operative in children and during adolescence; it has been demonstrated that they favour the development of early atherosclerosis lesions in young adults. This fact poses the question of diagnosis and treatment of risk factors. There is still controversy whether hypercholesterolemia should be searched for by universal or by selective screening, or by no screening at all. Several professional organizations favour a selective screening strategy, i.e. determination of serum cholesterol if one parent has premature coronary heart disease (before age 55 yr) or if the family has familial hyperlipidemia, in particular familial hypercholesterolemia. This strategy is advocated here: cholesterol should be measured early, i.e. between age 6 and 8 yr. A total serum cholesterol of > 5.2 mmol/l is elevated (approx. 75th percentile) and should be further evaluated and possibly treated. The presence of familial hypercholesterolemia should be looked for in particular: such individuals can now be diagnosed with molecular genetic tools, and they are particularly prone to develop premature coronary heart disease. Treatment of hypercholesterolemia is mainly of a dietary nature, or possible with a bile acid binding resin (cholestyramine). Other drugs have not been sufficiently evaluated for efficacy and safety; they may be indicated in special cases such as patients with a very high risk. Young people with familial hypercholesterolemia should be particularly counselled to avoid other risk factors such as smoking.
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PMID:[Hypercholesterolemia in children and young adults: should screening be done?]. 787 3

Familial hyperlipidemia has received little attention as a possible cause of stroke in young patients. Some recent studies have demonstrated that lipoprotein (a) is a key factor for atherogenesis in familial hypercholesterolemia. Hypogonadism may also contribute to the elevation of serum lipids, but their influence as a risk factor for stroke is still less understood. A 34-year-old patient with heterozygous familial hypercholesterolemia presented with a left pure motor hemiparesis secondary to a right striatocapsular infarction. Arteriography showed atherosclerotic lesions in both internal carotid arteries. High levels of cholesterol, cLDL, apo B, and lipoprotein (a) were found. Clinical signs of hypogonadism were present and the karyotype led to the diagnosis of Klinefelter's syndrome (47,XXY). The early clinical course was excellent, and the levels of serum lipids were normalized with diet, lipid-lowering drugs and androgens. The importance of hyperlipidemia as a risk factor for stroke in the young, specially when it occurs in the context of familial hypercholesterolemia with elevated lipoprotein (a) levels, as well as the possible contribution of hypogonadism to the development of accelerated atherosclerosis in young patients, are discussed upon.
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PMID:[Striatocapsular infarct in a young patient with heterozygous familial hypercholesterolemia and Klinefelter's syndrome]. 828 24

Since the application by Thompson et al. in 1975 of plasma exchange for the treatment of 2 patients with familial hyperlipidemia, plasma purification techniques for selective low-density lipoprotein (LDL) removal (i.e., LDL apheresis) have been developed and adopted for the management of this disease. Thermofiltration is one of the LDL apheresis systems that utilizes membrane techniques developed by Nose and Malchesky's group in 1985. This article reviews its rationale, in vitro studies, animal studies, and clinical investigation. Thermofiltration effectively and selectively removes LDL cholesterol while retaining in the plasma physiologically important macromolecules such as albumin and high-density lipoprotein (HDL) cholesterol. Based on the global view of the treatment of atherosclerosis by LDL apheresis, membrane techniques are as effective, safe, and simpler to apply than other methods. Additionally, these methods are effective for the removal of lipoprotein (a) and fibrinogen; thus, they can address the needs in these application areas.
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PMID:Low-density lipoprotein removal methods by membranes and future perspectives. 913 23

Increased secretion and levels of ApoB-containing lipoproteins (BLp) commonly occur in familial hyperlipidemia, obesity and diabetes. The plasma phospholipid-transfer protein (PLTP) is known to mediate transfer of phospholipids between BLp and HDL during their intravascular metabolism. To address a possible role of PLTP in dyslipidemia and atherogenesis, we bred mice deficient in the gene encoding PLTP (PLTP-deficient mice) using different hyperlipidemic mouse strains. In ApoB-transgenic and ApoE-deficient backgrounds, PLTP deficiency resulted in reduced production and levels of BLp and markedly decreased atherosclerosis. BLp secretion was diminished in hepatocytes from ApoB-transgenic PLTP-deficient mice, a defect that was corrected when PLTP was reintroduced in adenovirus. The studies reveal a major, unexpected role of PLTP in regulating the secretion of BLp and identify PLTP as a therapeutic target.
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PMID:Apolipoprotein B secretion and atherosclerosis are decreased in mice with phospholipid-transfer protein deficiency. 1143 51

Coronary artery disease and diabetes mellitus are among the primary mortality and morbidity causes in Mexico. Genetic factors play a fundamental role in the development of these entities. In the past few years due to the recognition and study of families with monogenic forms of diabetes and dislipidemias associated with development of atherosclerosis, several genes and loci have been associated with these conditions through genetic linkage studies. These studies have provided evidence of the genetic heterogeneity that exists and the type of genes involved in different ethnic groups. The study of Mexican families with early-onset diabetes and combined familial hyperlipidemia showed the participation of different genetic loci associated with these conditions in the Mexican population. These findings show the value of gene mapping strategies in the identification of the genetic component in these entities in our population.
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PMID:[Identifying different susceptibility loci associated with early onset diabetes and cardiovascular disease in Mexican families]. 1589 59


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