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)

(1) The composition of acidic glycosaminoglycans (AGAG) in the pooled human cerebral arteries was investigated by electrophoretic characterization before and after digestion with chondroitinases. Constitution of the chondroitin sulfate (CS) family was determined qualitatively on the basis of the disaccharide subunits of the CS chains after depolymerization with the enzymes. (2) The data obtained indicated that the AGAG in cerebral arteries consisted of, in order of amount, heparan sulfates, chondroitin-6-sulfate, dermatan sulfate, chondroitin-4-sulfate and hyaluronic acid. (3) The existence of oversulfated CS and undersulfated CS in the cerebral AGAG was supported by the detection of unsaturated di-sulfated and non-sulfated disaccharides on paper chromatography. In addition, the presence of hyaluronic acid was indicated by electrophoretic and enzymatic separation. (4) The distribution of the individual AGAG in cerebral arteries was also examined on the basis of molecular weight by gel filtration on a Sephadex G-100 column.
Atherosclerosis 1976 Oct
PMID:Composition of acidic glycosaminoglycans in human cerebral arteries. 98 97

It has been suggested that the glycosaminoglycans (GAG) influence atherogenesis by regulating the permeability of the arterial wall. For this reason, a study has been made of the diffusive transport of Ca2+ and water across the in vitro porcine artery wall, where particular attention was focused on the influence of GAG content and distribution within the wall on the transport properties. The radioisotop-s 45Ca and 3HHO were used to measure the tracer-diffusion flux in a stirred, two chamber diffusion cell. GAG were isolated, fractionated using a cetyl pyridinium chloride-cellulose column procedure, and assayed using a colorimetric carbazole reaction for uronic acid. The biochemical analyses showed that the pulmonary artery contains significantly more hyaluronic acid and dermatan sulfate than found in two locations in the thoracic aorta. In addition, a significant regression was found for the diffusion coefficient of 45Ca2+ (99% level) and 3HHO (95% level) versus specific GAG fractions. The regression indicated an increase in permeability with increase in the ratio of sulfated: nonsulfated GAG.
Atherosclerosis
PMID:Influence of glycosaminoglycan content on mass transfer behavior of porcine artery wall. Part 2. Differences in mass transfer rates related to variations in glycosaminoglycan content. 100 5

Arteriosclerotic plaques were found in the aorta and arteries of rabbits given homocysteine thiolactone, methionine or homocysteic acid, both parenterally and in a synthetic diet. Animals given large doses of parenteral methionine or homocysteine thiolactone died of pulmonary embolism and pulmonary infarct. Pyridoxine prevented thrombosis and pulmonary embolism but did not prevent arteriosclerotic plaques. These findings and previous work, showing a new matabolic pathway for sulfate ester synthesis from methionine, the somatotrophic activity of homocysteic acid, and control of cellular growth and intercellular matrix synthesis by homocysteine derivatives, suggest a theory to explain aspects of the pathogenesis of arteriosclerosis.
Atherosclerosis
PMID:Homocysteine theory of arteriosclerosis. 119 72

The relation of lactation and weaning to the development of early arterial lesions in the female breeder rat was investigated. Changes in aortic hexosamine and 35S-uptake, which are indicative of ground substance metabolism were correlated with changes in aortic calcium, phosphorus, and 45Ca-uptake during lactation and weaning. Lactation was associated with reduced aortic hexosamine content and lowered uptake of [S]sulfate. Further dynamic changes in aortic metabolism of these substances occurred following weaning in conjunction with an intense calcium uptake in the aorta of some, but not all, of the post-lactation animals. These latter changes were associated with the beginning aortic calcifications. Histopathologically, early arterial lesions developing during lactation, consist of intimal accumulations of mucopolysaccharide capped over by collagen. With repeated breeding cycles, these early lesions become exacerbated with extensive medial calcification occurring in areas rich in mucopolysaccharide and collagen particularly around degenerating elastic fibers. The hormones associated with reproduction and lactation may have a conditioning effect on these arterial connective tissue alterations and the development of arterial degenerative changes.
Atherosclerosis
PMID:Aortic hexosamine, [35S]sulfate uptake, and calcium metabolism related to early arterial degenerative changes induced by lactation and forced weaning in breeder rats. 119 74

Rat heart lipoprotein lipase was highly purified by affinity chromatography using heparin-Sepharose 4B. When extracts of acetone powder were applied to columns, lipase activity was firmly bound to the gel matrix and was later eluted with 1.5 M NaCl. At this stage the eluted enzyme was purified 1500-fold. Disc gel electrophoresis yielded a single protein band corresponding with the enzyme activity. The apparent molecular weight was 60,000. The purified enzyme was highly unstable; however, its activity could be partially stabilized by glycerol or ethylene glycol. In studying the purified enzyme we observed: (i) a cofactor in serum was required for full enzymatic activity; ApoLp-Glu could be substituted for this cofactor; (ii) ApoLp-Ser was inhibitory to lipase activity; (iii) NaCl and protamine sulfate also markedly inhibited the lipase activity; (iv) heparin stimulated the enzymatic activity.
Atherosclerosis
PMID:Rat heart lipoprotein lipase. 120 Nov 47

Autoradiographic tests carried out on rats with renal hypertension using 3H-proline resulted in an acclerated collagen synthesis by media cells of aorta and coronary arteries. Electronmicroscopically an increased content of collagen fibers and an enrichment of ruthenium-red-positive substances in the extracellular space were found. The 35S-sulfate-incorporation in aorta and coronary arteries of animals with hypertension is also increased. These changes in the extracellular space of the vascular wall have an atherosclerosis promoting effect, probably caused by a distrubance of the permeability.
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PMID:[Expermental contribution on the genesis of arteriosclerosis caused by hypertension]. 123 18

1. Effects of various drugs on cholesterol-induced atherosclerosis in rabbits during the progression phase have been studied. The drugs tested are antimetabolites (mercaptopurine, hydroxyurea), surface active agents (sodiumdodecyl sulfate), inhibitor of adrenocoritcal steroid synthesis (o, p'-DDD), lysosome stablizers (chloroquine, acetylsalicylic acid) with antihistaminic (chlorpheniramine) and cholesterol binder (nystatin). 2. Mercaptopurine treatment showed marekd reduction in both atherosclerotic lesions and cholesterol concentrations of the serum and aorta. 3. Hydroxyurea reduced both the aortic cholesterol concentration and the lesions, but the serum cholesterol concentration remained high. 4. Sodiumdodecyl sulfate and o, o'-DDD showed slight inhibition of the development of atherosclerosis. 5. Pyridinocarbamate showed a slight beneficial effect on the prevention of atherosclerosis only when it was administered prior to the meal. 6. Nystatin, chloroquine and acetylsalicylic acid + chlorpheniramine showed little effect.
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PMID:Study of drugs affecting cholesterol-induced atherosclerosis in rabbits. 127 88

Experiments were designed to examine the effect of oxidized low density lipoproteins (Ox-LDLs) on the expression and the release of endothelin from cultured endothelial cells and intact blood vessels. Ox-LDLs (30-300 micrograms/ml), but not native low density lipoproteins (200 micrograms/ml), stimulated the expression of preproendothelin mRNA in porcine and human endothelial cells, leading to a time- and concentration-dependent release of the peptide into the culture medium. The Ox-LDL-stimulated release of endothelin was mimicked by acetylated low density lipoprotein and abolished by downregulation of protein kinase C by phorbol ester. In the intact porcine aorta, Ox-LDLs, but not native low density lipoproteins, also increased the release of peptide in an endothelium- and concentration-dependent manner. The maximal effect was observed at a concentration of 100 micrograms/ml. Incubation of the intact porcine aorta with the scavenger receptor antagonist dextran sulfate decreased the formation of endothelium evoked by Ox-LDLs. The Ox-LDL-stimulated production of the peptide was further augmented in the presence of thrombin (4 units/ml) and was unaffected by nitric oxide-generating compound 3-morpholinosydnonimine (10(-5) M). These results suggest that Ox-LDL may be an endogenous mediator of the augmented release of endothelin observed in hyperlipidemia and atherosclerosis. The increased production of the peptide could contribute to vasospastic events and may promote vascular smooth muscle proliferation and progression of atherosclerotic vascular disease.
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PMID:Oxidized low density lipoproteins induce mRNA expression and release of endothelin from human and porcine endothelium. 131 34

The effects of oxidized human plasma low density lipoproteins (Ox-LDL) on the proliferation of cultured aortic smooth muscle cells was studied, employing viable cell counting, [3H] thymidine incorporation into DNA, and the release of lactate dehydrogenase (LDH) into the medium. Oxidized LDL (prepared by incubation of LDL with copper sulfate) exerted a concentration-dependent stimulation (2 fold, compared to control) of aortic smooth muscle cell proliferation at low concentrations (0.1 micrograms-10 micrograms/ml medium). On the other hand, at high concentrations (25-200 micrograms/ml), Ox-LDL produced a pronounced decrease in viable cells, a decrease in the incorporation of [3H] thymidine into DNA, and an increase in the release of LDH in the medium. In this report, the previously postulated biological roles of oxidized-LDL in atherosclerosis are discussed in view of these findings.
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PMID:Role of oxidized human plasma low density lipoproteins in atherosclerosis: effects on smooth muscle cell proliferation. 158 38

We evaluated the safety and efficacy of dextran sulfate low-density lipoprotein (LDL) apheresis in the treatment of three children (aged 6, 7, and 10 years) with severe familial homozygous hypercholesterolemia and undetectable LDL receptor activity. A total of 35 double plasma volume procedures were performed. The ranges of the mean decreases of the three patients in plasma lipid concentrations after LDL apheresis (p less than 0.0001) were as follows: total cholesterol, 76% to 79%; LDL-cholesterol, 78% to 81%; very low density lipoprotein cholesterol, 69% to 75%; high-density lipoprotein cholesterol, 27% to 40%; and triglycerides, 34% to 68%. There were statistically significant but clinically and biologically irrelevant changes in hematologic indexes, serum chemistry values, immunoglobulin levels, complement activity, and plasma concentrations of fat-soluble vitamins. Simple correlation analysis of the variables affecting total cholesterol removal showed significant correlation coefficients (r values) for preapheresis total cholesterol values (r = 0.70; p less than 0.01) and preapheresis LDL-cholesterol values (r = 0.61; p less than 0.01). A multiple regression model explained 82% of the variance based on the preapheresis cholesterol concentration, volume of whole blood processed, and the serum albumin concentration. Side effects of the LDL-apheresis treatments were rare and included abdominal cramping and urticaria. Two procedures were aborted because of intravenous access problems in the younger children. This study confirms that LDL apheresis using a dextran sulfate affinity column is efficacious in rapidly lowering total and LDL-cholesterol concentrations. Furthermore, the procedure is safe and well tolerated by children as young as 6 years of age. This treatment may prevent the progression of atherosclerosis in children with homozygous familial hypercholesterolemia and may therefore avert early death.
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PMID:Treatment of children with homozygous familial hypercholesterolemia: safety and efficacy of low-density lipoprotein apheresis. 159 49


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