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 availability of epsilon-lysine residues of apolipoprotein B in LDL for chemical or enzymic modification was investigated. Amino acid analyses of detergent-solubilized apolipoprotein B, following cyanoethylation with acrylonitrile, revealed that 10% of the lysine in apolipoprotein B were unreactive. The unreactive residues were associated with the most hydrophobic subfraction of apolipoprotein B. Since apolipoprotein B has a high molecular weight a study was undertaken to determine whether lysine residues were crosslinked to glutamic acid via epsilon-(gamma-glutamyl)lysine as demonstrated for fibrin. Apolipoprotein B was digested exhaustively with proteases. The content of epsilon-(gamma-glutamyl) lysine was determined by chromatography and isotope dilution. In contrast to earlier reports for serum LDL the data showed that less than 0.01 moles of lysine/mole of LDL apolipoprotein B were present as epsilon-(gamma-glutamyl)lysine in plasma LDL. It was determined also that the crosslinks were not found in apolipoprotein B during clotting since LDL was not a substrate for clotting factor XIII which forms the bond in fibrin. Furthermore, the lipoprotein contained no inherent transglutaminase activity. It is concluded that the lysine residues in LDL, which are unreactive to cyanoethylation, can not be detected in the digests as epsilon-(gamma-glutamyl)lysine.
Atherosclerosis 1986 Jul
PMID:The biochemistry of epsilon-amino groups of lysine residues from apolipoprotein B of human low density lipoprotein. 373 52

An immunoperoxidase procedure was used to localize the apolipoprotein B in the atherosclerotic lesions of vein grafts removed 5 years after an aortocoronary bypass operation and preserved by embedding in paraffin. Apolipoprotein B was mainly found at the cell-rich interface of the lesion proper and the underlying fibrous tissue. The findings of this study indicate that the immunoperoxidase procedure can be used to investigate the localization of immunoactive components in paraffin-embedded tissue sections.
Atherosclerosis 1980 Nov
PMID:Apolipoprotein B (Apo B) in vein graft atherosclerosis. An immunoperoxidase study. 616 18

Extracts of fresh senile human peripheral cornea with varying degrees of arcus were prepared by soaking minced tissue in buffered saline/EDTA. Apolipoprotein B was, at most, an occasional feature of these extracts; interactions involving glycosaminoglycans were not evident; and the lipid composition, particularly of the cholesterol ester fraction, was also not consistent with a recent origin from plasma components and particularly form low density lipoprotein. Assuming this origin, substantial secondary changes must follow insudation, involving protein loss and lipid reesterification, as is described for lipid deposits forming intracellularly at other sites. The manner of these changes in deposit forming extracellularly in the avascular peripheral cornea is not clear.
Atherosclerosis
PMID:Lipid-protein constituents of human corneal arcus. 728 55

Lipoprotein(a) [Lp(a)] represents an independent risk factor for atherosclerotic disease. In the present study, the extent to which Lp(a) accumulated in normal and various degrees of atheromatous lesions and the distribution pattern of Lp(a) in these lesions have been studied in thoracic aorta from the autopsy tissues by means of immunohistochemistry, immunoelectronic microscopy, enzyme-linked immunosorbent assay and computer-assisted image processing. Lp(a) was found to be localized preferentially in lesion areas and had its own distribution pattern in each kind of lesion. Lp(a) associated primarily with extracellular matrix and was detected in only a small number of foamy cells. Apolipoprotein B was also detected, whose staining pattern was always found to be congruent with that of Lp(a). This suggests that the immunoreactivity of apoB is related to the presence of Lp(a) at least in part, since Lp(a) possesses apoB in addition to apo(a). It was concluded that both low density lipoprotein and lipoprotein(a) play an important role in the pathogenesis of atherosclerosis.
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PMID:[Detection and quantification of lipoprotein (a) in atherosclerotic lesions of human aorta]. 778 Nov 16

Thirty six individuals with angiographic evidence of coronary atherosclerosis and thirty six individuals without coronary disease, matched for a variety of cardiovascular risk factors including age, sex, smoking, hypertension, diabetes and family history, were evaluated for their serum concentrations of vitamin E, total cholesterol, triacylglycerols, high density lipoprotein-cholesterol, low density lipoprotein-cholesterol, apolipoprotein A-I, and apolipoprotein B. Apolipoprotein B, low density lipoprotein-cholesterol and total cholesterol concentrations were unequivocally higher in patients with coronary artery disease. Triacylglycerols were marginally higher in patients with disease. The antioxidant vitamin E (alpha-tocopherol) was significantly higher in patients with atherosclerosis when compared with controls (35.1 +/- 17.0 mumol/l vs. 29.0 +/- 13.2 mumol/l, p = 0.017). However, alpha-tocopherol concentrations were strongly associated with lipid concentrations and normalization to the total cholesterol concentrations produced ratios which were not significantly different in the two groups. Logistic regression analysis revealed that the association of lipid risk factors with coronary stenosis was determined primarily by the difference in total cholesterol values. This study demonstrated that in this group of patients referred for angiography and matched for other risk factors, higher alpha-tocopherol concentrations were associated with patients with coronary disease and were not useful for assessing risk of coronary artery disease.
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PMID:Vitamin E compared with other potential risk factor concentrations in patients with and without coronary artery disease: a case-matched study. 781 29

In diabetic plasma, glycated albumin and glycated LDL coexist with augmented levels of peroxides, conditions frequently associated with the development of accelerated atherosclerosis. The direct interaction between irreversibly glycated albumin, LDL and oxidation have not been explored yet. We tried to elucidate whether irreversibly glycated albumin (AGE-Alb) induces changes in the chemistry and morphology of LDL particle, and if AGE-Alb has the ability to scavenge free radicals, as reported for native albumin. LDL isolated from normal (nLDL) or diabetic human subjects (dLDL) was incubated in vitro with AGE-Alb in conditions of autoxidation (37 degrees C, 24-48 h in the absence of oxidation inhibitors) or of Cu2+ induced-oxidation. The results showed that, especially in the latter condition, AGE-Alb induced marked physico-chemical modifications of both nLDL and dLDL without significant changes in the level of peroxides. Incubation with AGE-Alb decreased the cholesteryl esters/unesterified cholesterol ratio of nLDL by 30% and of dLDL by approximately 50%. Concomitantly, in oxidative conditions a marked increase (approximately 3-fold) in the lysophosphatidylcholine/phosphatidylcholine ratio of dLDL was detected. Apolipoprotein B integrity as well as the morphology of the lipoprotein particles were drastically affected. To a lesser extent, these modifications occurred also in the presence of inhibitors of oxidation at 37 degrees C, but not at 4 degrees C. The above described effects were constantly more pronounced in the case of dLDL. These results indicated that in the absence of other plasma or vascular tissue components (e.g., endothelial cells, extracellular matrix) AGE-Alb by itself induces alterations in the chemistry and morphology of LDL, especially of glycated LDL, modifications that may account for the occurrence of accelerated atherogenesis in diabetes.
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PMID:Irreversibly glycated albumin alters the physico-chemical characteristics of low density lipoproteins of normal and diabetic subjects. 782 32

Apolipoprotein B-containing lipoproteins play a central role in the pathogenesis of atherosclerosis. The processes that determine the atherogenicity of these lipoproteins, however, remain unclear. A new development that involves the interactions of lipoproteins, enzymes, apolipoproteins, and cell-surface heparan sulphate may explain, at least in part, the enhanced atherogenicity of these lipoproteins. In addition, the development of specific transgenic apolipoproteins, and apolipoprotein-deficient mice models that develop atherosclerosis, provide new tools for studies on the role of native apolipoprotein-B containing lipoproteins in atheroma formation.
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PMID:The role of native apolipoprotein B-containing lipoproteins in atherosclerosis: cellular mechanisms. 785 9

Serum lipids were determined in 97 patients (56 men, 41 women; ages 42 +/- 15 years) undergoing long-term anticonvulsive treatment (longer than 6 months). The total group showed increased total cholesterol, decreased high-density lipoprotein HDL cholesterol, an increased ratio of total to HDL cholesterol, and decreased apolipoprotein A1 and B values compared to population means. Considering males and females separately, all differences were significant (P < 0.01) in men, whereas in women only the differences in HDL cholesterol, ratio of total to HDL cholesterol, and apolipoproteins A1 and B reached the level of statistical significance. Considering the different anticonvulsant groups, cholesterol was significantly increased only in phenytoin-treated males; HDL cholesterol was significantly lowered and the ratio of total to HDL cholesterol significantly increased in all groups. Apolipoprotein A1 levels were significantly decreased in phenytoin-treated females and valproate-treated patients of both sexes. Apolipoprotein B levels were significantly decreased in all groups except carbamazepine-treated males. Especially in men treated with anticonvulsants these lipid levels may be considered a risk factor for atherosclerosis.
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PMID:Changes of serum lipid patterns during long-term anticonvulsive treatment. 837 54

It is well known that coronary heart disease (CHD) is multifactorial, with environmental and inherited risk factors both playing a role. Apolipoprotein B (apo B) is of major importance in lipoprotein metabolism and might play a central role in atherogenesis. The apo B gene is the obvious candidate gene to study the relations between lipid concentrations and CHD. Some rare mutations in the apo B gene affect plasma cholesterol levels, leading to either familial hypobetalipoproteinemia or familial defective apolipoprotein B100. Other frequent polymorphisms have little biological effect but, because of their high frequency, might contribute to the development of CHD in a given population. Many apo B gene polymorphisms are associated with variations in plasma lipid concentrations, including the response of plasma lipids to dietary intervention, and peripheral and coronary atherosclerosis. Age, body mass index and gender affect the degree and nature of the association between apo B genetic markers and normal lipid and lipoprotein levels. However, negative and contradictory results have also been reported. One likely explanation is differences between studies, including populations of different geographic origin, arbitrary definition of cases and controls and multiple criteria for CHD. Future work on the effect of the apo B locus on hyperlipidaemia and atherosclerosis must involve large numbers of patients belonging to carefully defined populations. Prospective studies using a combination of genetic markers in well-defined populations should lead to firm conclusions on the role of apo B in atherogenesis and coronary heart disease.
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PMID:[Genetic variation in the apolipoprotein B gene]. 862 6

Increased plasma lipoprotein (a) (Lp(a)) levels are associated with premature cardiovascular diseases and stroke. Since Lp(a) immune reactivity is found in urine we compared urinary apolipoprotein (a) (apo(a)) with plasma Lp(a) levels in 116 patients suffering from angiographically proven coronary artery diseases with that of 109 controls. Urinary apo(a) investigated by immuno blotting, revealed a distinct apo(a) fragmentation pattern with molecular weights between 50 and 160 kDa. Apolipoprotein B however was not secreted into urine. Lp(a) and apo(a) were measured by a fluorescence immuno assay. Within single individuals, urinary apo(a) levels correlated significantly with creatinine (Rho, 0.98; P < 0.0005). Medians and 25/75 percentiles of urinary apo(a) in coronary artery disease (CAD) patients were 5.70, 3.25 and 10.35 microg/dl and in controls 2.64, 1.43 and 3.50 microg/dl respectively. At cut-off levels of 30 mg/dl for plasma Lp(a) and 10 microg/dl of urinary apo(a) respectively, both paramenters showed comparable sensitivities (33.8% vs. 26.7%), yet the specificity (76.1% vs. 91.7%) and the positive predictive value (60.0% vs.76.4%) of urinary apo(a) were much higher. In receiver-operating characteristic plots, urinary apo(a) was much more sensitive at high specificities i.e. greater than 60% as compared to Lp(a). Urinary secretion of apo(a) fragments normalized to creatinine is stable in a given individual and significantly associated with coronary artery disease.
Atherosclerosis 1997 Feb 28
PMID:Urinary apo(a) discriminates coronary artery disease patients from controls. 906 24


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