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 possibility of selective removal of VLDL, IDL and LDL by double filtration (DF) and dextran-sulfate cellulose (DSC) column plasmapheresis was investigated in hypercholesterolemia. Two and a half liters of plasma were treated. Sixty six percent of TC and 68% of LDL-C were removed by DF plasmapheresis. The removal rate of HDL-C was 50% which was significantly lower than that of LDL-C. The removal rate of apoprotein A-I and A-II was also significantly lower than that of apoprotein B. Sixty percent of LDL-C and 61% of apoprotein B were removed by DSC column plasmapheresis while the decrease of HDL-C, apoprotein A-I and A-II was minimal. Therefore, DSC column plasmapheresis could remove atherogenic lipoproteins more selectively than DF plasmapheresis.
Atherosclerosis 1986 Apr
PMID:Comparison of selectivity of LDL removal by double filtration and dextran-sulfate cellulose column plasmapheresis. 242 96

We describe a new low density lipoprotein (LDL) apheresis system using dextran sulfate cellulose column in an automated column regenerating unit (LDL continuous apheresis). Two columns containing 150 ml of dextran sulfate cellulose were used, and the whole extracorporeal circulation was about 400 ml in volume. After 600 ml of plasma was adsorbed into the first column, the second column was used as an adsorbent and meanwhile the first column was regenerated. Thus, the 2 columns were used alternately without losing the potency of the columns. As the apparatus was automatically controlled by a computerized unit, no extra manipulation is necessary compared with the conventional single-column method. By treating 4-5 liters of plasma, non-high density lipoprotein (HDL)-cholesterol levels decreased by 63-71%, and HDL-cholesterol levels remained unchanged. Thus, this new method of LDL apheresis can safely reduce LDL-cholesterol to any desired level and will be applicable for the treatment of child and adult family hypercholesterolemic patients with severe coronary heart disease.
Atherosclerosis 1987 Nov
PMID:A new low density lipoprotein apheresis system using two dextran sulfate cellulose columns in an automated column regenerating unit (LDL continuous apheresis). 244 36

The two more widely available techniques for the extracorporeal removal of low density lipoproteins (LDL), dextran sulfate cellulose column and double membrane filtration, were comparatively tested in severe familial hypercholesterolemic patients, both acutely and during a continued 3-month treatment. The selective dextran sulfate procedure removed close to 60% of LDL and 16% of high density lipoproteins (HDL) upon each apheresis, vs. 42% and 32%, respectively, in the case of the semi-selective double membrane filtration. Upon long term biweekly treatments, LDL-cholesterol (LDL-C) decreased, with the selective procedure, from a pre-treatment level of 406.0 +/- 40.7 mg/dl to a value fluctuating between 295.4 +/- 33.8 mg/dl and 116.9 +/- 22.0 mg/dl (highest vs. lowest levels) whereas, in the case of double membrane filtration, LDL-C levels ranged between 334.8 +/- 39.8 mg/dl and 192.3 +/- 49.9 mg/dl. HDL-cholesterol levels were somewhat raised, to a higher extent with dextran sulfate apheresis. The LDL/HDL-cholesterol "atherogenic ratio", decreased from a pre-treatment value of 10.27 +/- 3.04 to values ranging between 3.61 and 6.82 with dextran sulfate and between 6.70 and 7.68 with double membrane plasmapheresis.
Atherosclerosis 1988 Oct
PMID:Apheretic treatment of severe familial hypercholesterolemia: comparison of dextran sulfate cellulose and double membrane filtration methods for low density lipoprotein removal. 246 Dec 7

The cuprolinic blue (CB) staining method has been used to visualize and characterize proteoglycans (PG) in the extracellular matrix (ECM) of normal and atherosclerotic human arteries. Arterial tissues of 13 individuals (1-83 years of age) were obtained by autopsy. For electron microscopic visualization of PGs staining with CB was performed in the presence of a critical electrolyte concentration of 0.3 M MgCl2. Under these conditions CB selectively interacts with the polysulfated glycosaminoglycan (GAG) side chains of the molecules. Removal of PG side chains by GAG-degrading enzymes prior to CB staining selectively prevented the formation of chondroitin sulfate (CS)-rich and dermatan sulfate (DS)-rich PG-CB precipitates. The DS-rich type of PG is mainly associated with collagen fibrils, the CS-rich type of PG is preferentially localized in nonfibrous areas of the ECM (soluble matrix). When normal arterial tissues are compared with those affected by atherosclerosis quantitative and qualitative changes of PG-CB precipitates are detected. In fibrous plaques a strong accumulation of a large CS-rich type of precipitate close by smooth muscle cells (SMC) and foam cells is observed. In addition, these precipitates are significantly longer in fibrous plaques than in adjacent normal media (116 nm vs. 100 nm; P less than 0.001). This alteration is independent of the age of the donor. Small DS-rich PG-CB precipitates associated with collagen fibrils show strong variations in their length, but not a significant tendency towards elongated precipitates in atherosclerosis. The present results demonstrate that ultracytochemical and morphometric analysis are useful in providing information on the diverse types, locations, interactions, and possibly of molecular changes of PGs in normal and atherosclerotic human arteries.
Atherosclerosis 1989 Jun
PMID:Cytochemical changes in a human arterial proteoglycan related to atherosclerosis. 247 59

The glycosaminoglycan (GAG) content of normal and atherosclerotic areas of cerebral arterial tissue isolated from human males was measured. The main trunk and distal branches of the arteries were obtained at autopsy on 12-89-year-old Japanese subjects. The GAG components were analysed by high-performance liquid chromatography (HPLC) after enzymatic digestion, using specific GAG lyases. Both total GAGs and water content were lower in the diseased arteries than those in the normal state. In contrast, the reverse was noted for the lipid content. The main GAG component of the normal cerebral arteries was heparan sulfates (HS), comprising half the total GAGs, followed by dermatan sulfate (DS) and chondroitin 6-sulfate (Ch-6S) constituting 1/5 to 1/9 the total GAGs. Chondroitin 4-sulfate (Ch-4S) comprised approx. 1/10 the total GAGs. Oversulfated chondroitin sulfate isomers were detected as novel peaks of the chondroitin sulfate types G, B, E and H on HPLC analysis. Small amounts of hyaluronic acid (HA) and chondroitin were also detected. The total GAG content decreased with severity of atherosclerosis. The content and proportions of HS to the total GAGs decreased remarkably, and those of Ch-4S, HA and chondroitin showed a moderate decrease. The reverse was the case for those of DS, Ch-6S and oversulfated DS and/or Ch-S. The lipid components, in particular cholesterol ester, in the diseased tissue were significantly greater than in the visibly normal parts while the opposite was the case for the water content. Thus, the GAG species and their contents in human cerebral arteries showed a characteristic distribution. As oversulfated DS and Ch-S isomers have anticoagulant and anti-atherosclerotic activities, they may play a pertinent role in the disease process.
Atherosclerosis 1989 Jul
PMID:Acidic glycosaminoglycans in human atherosclerotic cerebral arterial tissues. 250 94

The concentration of dehydroepiandrosterone sulfate (DHEA-S) in human plasma is higher than any other steroid. Recent evidence has suggested an inverse relationship between plasma DHEA levels and the development of coronary atherosclerosis in humans. We used the cholesterol-fed rabbit model to investigate whether DHEA feeding would diminish aortic fatty streak formation in this model. Fifteen New Zealand White rabbits were fed rabbit chow supplemented with 0.5% cholesterol (wt/wt). Seven animals were, in addition, fed DHEA, 0.5% of diet (wt/wt). Animals were sacrificed after 2 months, and the aortic involvement with fatty streaks was evaluated by computerized planimetry of Sudan IV-stained aortas and by chemical analysis of aortic wall lipids. Compared to controls, DHEA-fed animals had similar plasma levels of total, very low density lipoprotein (VLDL), low density lipoprotein (LDL), and high density lipoprotein (HDL) cholesterol, corticoids, and estrogens. DHEA-fed animals had higher plasma levels of total, VLDL, and LDL triglycerides and lower HDL triglycerides than did controls. DHEA feeding resulted in 30% and 40%, respectively, inhibition of fatty streak formation by chemical analysis and planimetry. We conclude that DHEA feeding inhibits the development of aortic fatty streaks in cholesterol-fed rabbits, independent of changes in plasma total and LDL cholesterol levels of DHEA conversion to estrogens or corticoids.
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PMID:Dehydroepiandrosterone feeding prevents aortic fatty streak formation and cholesterol accumulation in cholesterol-fed rabbit. 252 96

Plasma levels of dehydroepiandrosterone sulfate (DHEA-S), testosterone, dihydrotestosterone (DHT) androstenedione, sex hormone-binding globulin (SHBG), lipoproteins, apolipoproteins and high density lipoprotein (HDL) subfraction were measured in 32 men aged 26-40 years after myocardial infarction (MI) suffered at least 3-4 months prior to the study, who were normocholesterolemic and had angiographically demonstrated coronary occlusion. The control group consisted of 76 healthy men aged 25-40 years. Blood samples were obtained in the morning from fasting subjects. A significant decrease in plasma DHEA-S and DHT levels were found in MI patients. Also, a significant decrease in HDL-cholesterol, HDL2-cholesterol (HDL2-C) and apolipoprotein A-I, an increase in apolipoprotein B and LDL-cholesterol (LDL-C) levels were observed in those patients as compared with healthy men. However, there were no differences in testosterone, androstenedione and SHBG concentrations between the groups. Significant correlations between testosterone and HDL2-C (r = 0.46, P less than 0.01), as well as between DHEA-S and HDL3-C (r = 0.39, P less than 0.05) levels in MI patients were observed. These results suggest that decreased levels of plasma DHEA-S and DHT may promote the development of coronary atherosclerosis in men.
Atherosclerosis 1989 Oct
PMID:Decreased plasma dehydroepiandrosterone sulfate and dihydrotestosterone concentrations in young men after myocardial infarction. 253 16

Studies on the pathogenesis of atherosclerosis (As) were reviewed in our institute. Clinico-pathological study showed that coronary As lesions appeared early and took a long-time to seriously stenosis the arterial lumen, resulting in coronary heart disease. Studies on human As lesions by light and electron microscopy suggested that injury to and increased permeability of endothelial cells (EC) and proliferation of smooth muscle cells (SMC), together with an increase of proteoglycans(PG) were important in atherogenesis. Morphologic responses of the aortic wall of normally fed rats to intimal injury by an indwelling catheter (in place for 3 weeks) were studied at the time of removal of the catheter and 4, 8, and 26 weeks later. Neointimal thickening with SMC proliferation and a significant increase in chondroitin sulfate (CS)-PG granule concentrations were found. A study on cultured human EC showed that after EC reached confluence, secretion of heparin sulfate (HS)-PG increased and inhibited the proliferation of SMC. The proliferative ability of cultured human SMC was found to decrease after 8 passages. More lipid accumulation was found in SMC's of the 10th passage (T10) than in those of the 4th passage (T4). T10 SMC showed a higher 35S incorporation into dermatan sulfate (DS) CS-PG than did T4 SMC in both the medium and cell layer. The results suggest that SMC senescence may play an important role in the pathogenesis of As.
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PMID:[Studies on the pathogenesis of atherosclerosis]. 253 68

The interactions of LDL with extracellular matrix proteoglycans apparently contribute to the accumulation of apo B-lipoproteins in atherogenesis. Serum LDL forms insoluble complexes with human arterial chondroitin sulfate proteoglycans (CSPG). While the amount of insolubilized LDL varies, serum from survivors of myocardial infarcts and ischaemic subjects shows higher values of CSPG-insolubilized LDL than serum from controls. In this study, we explored the relationship between the formation of LDL-CSPG complexes in serum and some LDL properties, using binding isotherms and characterization of isolated LDL from 12 healthy controls and 12 young myocardial infarct survivors. The amount of LDL insolubilized in serum from solutions of CSPG was found to be a function of the product Bt (total binding) x the amount of serum LDL-cholesterol. Furthermore, the Bt values for the isolated LDL from controls and patients could be predicted with more than 70% certainty by using a multiple regression model which included the cholesterol/protein ratio, protein/triglyceride ratio, isoelectric point and the affinity coefficient of the lipoprotein for CSPG. The results indicate that LDL-CSPG measurements in serum are dependent upon both LDL concentration and structural properties which are related to its tendency to form complexes with arterial CSPG.
Atherosclerosis 1989 Oct
PMID:Binding parameters and concentration modulate formation of complexes between LDL and arterial proteoglycans in serum. 259 22

Primary cultures of typical and modified smooth muscle cells isolated from the intima of human aorta were used to study the mechanism whereby low density lipoprotein (LDL) induces accumulation of intracellular cholesterol. Incubation of intimal cells with native LDL obtained from human plasma did not lead to deposition of total cholesterol. LDL added to the cultures simultaneously with hyaluronic acid, heparin, chondroitin sulfate, fibronectin, and mouse monoclonal antibody against LDL also failed to alter the cellular cholesterol. On the other hand, 24-h incubation of the cells with LDL in the presence of dextran sulfate, gelatin, particles of aortic elastin, particles of collagenase-resistant aortic matrix, goat polyclonal antibodies against LDL or latex beads caused a significant (1.5-7-fold) increase in total cholesterol. The compounds which stimulated cholesterol deposition are able to form precipitating complexes with LDL. On the contrary, the agents which failed to induce cholesterol accumulation were unable to insolubilize LDL. A direct correlation (r = 0.927) was found between the cholesterol content of the insoluble complex and the increment of cholesterol in the cultured cells. To find out whether LDL plays a specific role in the deposition of intracellular cholesterol, very low density lipoproteins and high density lipoproteins were used. These lipoproteins stimulated the accumulation of intracellular cholesterol in the presence of agents capable of forming insoluble associates with them. Our data suggest that insolubilization of lipoproteins is a key event in the LDL-mediated accumulation of intracellular cholesterol induced by various agents.
Atherosclerosis 1989 Sep
PMID:Insolubilization of low density lipoprotein induces cholesterol accumulation in cultured subendothelial cells of human aorta. 280 47


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