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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Randomly chosen medical charts of 212 elderly subjects in 11 nursing homes were reviewed to determine which characteristics of the subjects were most closely associated with their diet prescriptions. The chart reviews indicated that 104 (49.0%) of the 212 subjects had some type of nutrient-modified diet prescription. Eight patients who were tube fed were not included in subsequent analyses. Sodium restriction was the most common modification (60 [29.4%] of the remaining 204 patients) and calorie-controlled diets were also common (52 [25.5%] of the patients). Of the 55 patients with hypertension, 31 (56.4%) had no sodium restriction. Only 10% of all low-sodium diets limited sodium to 2 g per day. Of the 38 patients with diabetes, 7 (18.4%) had no prescription for calorie control, and there was no indication that increased dietary fiber was encouraged for diabetic patients. Only one of the 121 subjects with a diagnosis of coronary heart disease or atherosclerosis had a prescription for a cholesterol-lowering diet. Characteristics of the subjects not specifically related to diet or diagnosis, such as age, sex, duration of stay, and level of care, had no significant relationship to diet prescription. These findings suggest that the practitioners in our sample were not convinced of the efficacy of modified diets to control disease for most nursing home residents.
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PMID:Use of modified diets in nursing homes. 191 38

The frequent concurrence of other cardiovascular risk factors in hypertensive patients, such as obesity and diabetes mellitus, suggests that overlapping genetic and environmental factors may contribute to the common metabolic and cardiovascular derangements observed in these populations. Hypertension and hyperglycemia accelerate atherosclerosis in diabetics, and play an important role in associated morbidity and mortality. Several abnormalities in blood pressure regulatory systems such as the renin-angiotensin system, the sympathetic nervous system, and sodium/volume control have been described in diabetes mellitus. Sodium retention and cardiovascular hyperreactivity appear to occur early in the course of diabetes mellitus, even at normal blood pressure levels and before onset of renal failure, and could set the stage for the development of hypertension. The relationship between obesity and hypertension is also well-established, and may reflect metabolic and cardiovascular adaptations in obese subjects which predispose to blood pressure elevations. Obese subjects display changes in sympathetic nervous system activity, sodium metabolism, and vascular hemodynamics. Sodium-sensitive blood pressure responses in the obese may be secondary to increased cardiac output or fluid volume, and are directly related to circulating insulin levels. Certain metabolic and vascular characteristics of obesity and diabetes mellitus are found in patients with essential hypertension. It has been suggested that insulin and insulin resistance may be the common link between these risk factors. Improved understanding of metabolic considerations in the treatment of obese and diabetic hypertensives should lead to more careful selection of medications that avoid metabolic complications. Although diuretics and beta-blockers may be useful in some patients, there are several reasons not to recommend their use as initial therapy in obese and diabetic hypertensives. On the other hand, calcium channel blockers and angiotensin converting enzyme inhibitors are highly effective, with minimal effects on metabolic parameters, and are well-suited as first-line therapy in the treatment of obese and diabetic hypertensives.
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PMID:Metabolic considerations in hypertension. 207 23

Patients with chronic renal failure who undergo hemodialysis experience accelerated atherosclerosis and premature death. Since the end-metabolite, oxalic acid, accumulates in plasma in proportion to the severity of renal failure, we studied whether sodium oxalate (0 to 300 microM) is an endothelial toxin and, therefore, might enhance atherogenesis. Exposure to uremic levels of oxalate (greater than 30 microM) for 9 to 28 days depressed endothelial cell replication by 33% to 84% (mean +/- SD, 54% +/- 15.7%, n = 17 experiments, p = 0.002). In contrast, replication of fibroblasts exposed to 200 microM oxalate for 45 days was not inhibited. The inhibitory effect of oxalate on endothelial cell replication was both dose- and time-dependent (both p less than 0.0001) and was first detected 3 to 7 days after the initial exposure to oxalate. Further, the inhibitory effect was fully reversible upon removal of oxalate, but only if exposure was limited to 5 days or less. Sodium salts of other carboxylic acids (citric, succinic, glyoxylic, and malonic; 200 microM) as well as HCl (200 microM) did not suppress endothelial cell replication. Oxalate also inhibited endothelial cell migration but had no effect on basal, thrombin-induced, or arachidonate-induced prostacyclin production by endothelial cells. Exposure of endothelial cells to sodium oxalate (200 microM) for as little as 24 hours-a time period sufficient to induce delayed, transient inhibition of replication not detectable until approximately 1 week after exposure-inhibited incorporation of 3H-leucine into protein by 40% (p = 0.009). We conclude that sodium oxalate acts as a uremic toxin, inhibiting endothelial cell replication and migration, functions which may be important for constitutive inhibition of atherosclerosis.
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PMID:Uremic levels of oxalic acid suppress replication and migration of human endothelial cells. 231 57

Obesity, diet and alcohol consumption constitute major environmental determinations of blood pressure elevation. The long term setting of blood pressure in response to these factors will be determined by genetic susceptibility, and interactions with effects of physical fitness and smoking. Dietary changes which independently influence both atherosclerosis and hypertension are likely to be of greatest value in helping to control morbidity and mortality from hypertensive cardiovascular disease. Recommendations should focus on diets low in total and saturated fat intake and high in fruit and vegetables, containing potassium and fibre, coupled with weight control, alcohol moderation to less than two drinks per day in drinkers and regular physical exercise. Sodium restriction will help lower blood pressure in older hypertensives in particular. The role of dietary calcium or fish oils in blood pressure regulation is still uncertain. Dietary and related recommendations on smoking and exercise should be 'first line' treatment in mild hypertensives, and complimentary to therapy in all patients requiring drugs.
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PMID:Diet, alcohol and hypertension. 255 47

Adhesion of bovine endothelial cells on fibronectin and collagen before and after nonenzymatic glycation in vitro has been studied. Nonenzymatic glycation of these proteins reduced their ability to bind endothelial cells. Furthermore, nonenzymatically glycated fibronectin failed to bind to normal and nonenzymatically glycated gelatin and to fibrin. So gelatin and fibrin Sepharoses can be used to separate highly glycated fibronectins from fibronectins with a low degree of nonenzymatic glucose substitution. Sodium dodecylsulfate polyacrylamide gel electrophoresis did not demonstrate a covalent cross-link between nonenzymatically glycated fibronectins. These results present further evidences for the role of nonenzymatic glycation of proteins in the development of vascular complications in long-term diabetes and of atherosclerosis.
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PMID:Diminished adhesion of endothelial aortic cells on fibronectin and collagen layers after nonenzymatic glycation. 340 68

Sodium spirulan (Na-SP) is a sulfated polysaccharide with M(r) approximately 220,000 isolated from the blue-green alga Spirulina platensis. The polysaccharide consists of two types of disaccharide repeating units, O-hexuronosyl-rhamnose (aldobiuronic acid) and O-rhamnosyl-3-O-methylrhamnose (acofriose) with sulfate groups, other minor saccharides and sodium ion. Since vascular smooth muscle cell proliferation is a crucial event in the progression of atherosclerosis, we investigated the effect of Na-SP on the proliferation of bovine arterial smooth muscle cells in culture. It was found that Na-SP markedly inhibits the proliferation without nonspecific cell damage. Either replacement of sodium ion with calcium ion or depolymerization of the Na-SP molecule to M(r) approximately 14,700 maintained the inhibitory activity, however, removal of sodium ion or desulfation markedly reduced the activity. Heparin and heparan sulfate also inhibited vascular smooth muscle cell growth but their effect was weaker than that of Na-SP; dextran sulfate, chondroitin sulfate, dermatan sulfate and hyaluronan failed to inhibit the cell growth. The present data suggest that Na-SP is a potent inhibitor of arterial smooth muscle cell proliferation, and the inhibitory effect requires a certain minimum sequence of polysaccharide structure whose molecular conformation is maintained by sodium ion bound to sulfate group.
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PMID:Sodium spirulan as a potent inhibitor of arterial smooth muscle cell proliferation in vitro. 1499 20

Since oxidative stress plays an important role in dysregulation of the microcirculation as well as the pathogenesis of atherosclerosis, therapeutic intervention with antioxidants has been speculated to prevent cardiovascular diseases. Ascorbic acid (AA) has been reported to improve endothelial function; however, its intracellular metabolic pathway has not been fully determined. Sodium-dependent vitamin C transporter (SVCT) types 1 and 2 were recently cloned. In the present study, we investigated whether SVCT-2 is functionally expressed in vascular endothelial cells and, if so, what factors modulate its activity. The uptake of AA into human umbilical vein endothelial cells (HUVECs) was examined by incubation with radiolabeled AA (14C-AA). AA was transported into HUVECs in a dose- and time-dependent manner. Replacement of sodium chloride with choline chloride in the medium suppressed the uptake of AA. RT-PCR revealed that HUVECs expressed SVCT-2 mRNA, but not SVCT-1. Transfection of HUVECs with the antisense oligonucleotide of SVCT-2 significantly suppressed the uptake of AA. Furthermore, tumor necrosis factor-alpha and interleukin-1beta inhibited the transport activity of AA. Thus, SVCT-2 is functionally expressed in human endothelial cells, and its activity is negatively regulated by inflammatory cytokines. Our findings might provide a new insight into understanding the treatment of cardiovascular diseases with AA.
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PMID:Functional expression of sodium-dependent vitamin C transporter 2 in human endothelial cells. 1534 Feb 49

Sodium ferulate (SF) or 3-methoxy-4-hydroxy-cinamate sodium is an active principle from Angelica sinensis, Cimicifuga heracleifolia, Lignsticum chuangxiong, and other plants. It has been used in traditional Chinese medicine and is approved by State Drugs Administration of China as a drug for treatment of cardiovascular and cerebrovascular diseases. SF has antithrombotic, platelet aggregation inhibitory and antioxidant activities in animals and humans. For several decades SF has been widely used in China to treat cardiovascular and cerebrovascular diseases and to prevent thrombosis. Exciting clinical results have been obtained with SF in coronary heart disease, atherosclerosis, pulmonary heart disease and thrombosis. Its safety and efficacy have been demonstrated in clinical practice. This article briefly reviews basic pharmacology, pharmacokinetics, toxicology and clinical pharmacology of SF. The in vitro and in vivo data support the view that SF is a useful drug for the treatment of cardiovascular diseases.
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PMID:Pharmacological actions of sodium ferulate in cardiovascular system. 1600 32

Elevated blood histamine plays a role in the pathogenesis of atherosclerosis. Calcium signaling mediates histamine action in endothelial cells. Selenium (Se) is a dietary essential trace element for humans. Se compounds in different oxidation states were found to exhibit an opposing effect on the histamine-induced calcium signaling in the ECV304 cell line. When Se in the form of sodium selenite was added in the cell culture, the reactivity of the histamine H(1)-receptor was increased as reported in our previous paper. We here show that as a culture supplement, sodium selenite enhanced the activity of selenoprotein thioredoxin reductase (TrxR) and the calcium response to histamine stimulation, which were reversed by treating the cells with gold thioglucose, a nucleophilic drug that selectively modifies thiolate/selenolate groups. Sodium selenite most likely caused a reductive shift in the thiol/disulfide redox balance through increasing TrxR activity. In contrast, when the cells were treated with Se in the form of ebselen, a thiol oxidant with peroxidase-like activity, histamine-induced calcium release and calcium entry were significantly suppressed. This effect appeared related to the thiol-directed modification rather than the peroxidase-like activity of ebselen, because this inhibitory effect was not replicated by increasing cellular peroxidase activity. Thus, the opposing effects of sodium selenite and ebselen on histamine-induced calcium signaling are achieved, at least in part, through their opposite actions in modulating the thiol/disulfide redox state.
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PMID:Opposing regulation of histamine-induced calcium signaling by sodium selenite and ebselen via alterations of thiol redox status. 1978 65

Oxidized low-density lipoprotein (ox-LDL) is known to trigger vascular injury in atherosclerosis development. Sodium ferulate is an effective component from Chinese medicines with various beneficial cardiovascular pharmacological activities. Here, we investigated the effects of sodium ferulate on the gene expression profile of ox-LDL-stimulated endothelial cells. Cultured human umbilical vein endothelial cells (HUVECs) were treated with ox-LDL (50 microg/mL) in the absence or presence of sodium ferulate (5 micromol/L). Sodium ferulate significantly reduced ox-LDL-induced endothelial cell death as evaluated by cell viability assay. Human oligonucleotide microarray analysis demonstrated that a total of 32 ox-LDL-induced genes were significantly downregulated to control levels by sodium ferulate. These genes included members from families of chemokine, inflammatory factor, growth factor, and nuclear receptor. These data provided an overview of the gene expression profile of endothelial cells in response to ox-LDL and sodium ferulate, and demonstrated that sodium ferulate could regulate the expression of inflammation-related genes in endothelial cells and has the potential to benefit endothelial function in the setting of atherosclerosis.
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PMID:Sodium ferulate modified gene expression profile of oxidized low-density lipoprotein-stimulated human umbilical vein endothelial cells. 1983 69


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