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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 variable doses of ethanol on plasma lecithin: cholesterol acyltransferase (LCAT) activity was examined in male, atherosclerosis-susceptible squirrel monkeys over a 12-month period. Primates were divided into three groups: 1) Controls fed isocaloric liquid diet; 2) Low Ethanol monkeys given liquid diet with vodka substituted isocalorically for carbohydrate at 12% of calories; and 3) High Ethanol animals fed diet plus vodka at 24% of calories. There were no significant differences between the treatments in serum glutamate oxaloacetate transaminase (SGOT), a measure of liver function. However, plasma LCAT activity (% esterification/min) measured in vitro was significantly reduced in High Ethanol monkeys while cholesterol esterification was elevated in the Low Ethanol group and intermediate in Controls. Similarly, the in vivo appearance of radiolabeled cholesteryl ester in high density lipoproteins (HDL) following the intravenous injection of 3H mevalonolactone was highest in the Low Ethanol primates, intermediate in Controls and significantly lower in monkeys fed the high alcohol diet. In vitro measurement of LCAT enzyme efficiency was similar for the three groups while substrate efficiency was lower in the High Ethanol treatment. Although LCAT activator (apoprotein A-I) was not markedly altered by dietary ethanol and the concentration of LCAT substrates (HDL free cholesterol and phosphatidyl choline) was significantly elevated in the High Ethanol group, subtle modifications in substrate-product composition may account for the observed reduction in cholesterol esterification. These include potential substrate and/or product LCAT inhibition resulting from increased concentrations of plasma free cholesterol, HDL lysophosphatidyl choline, and higher HDL2/HDL3 subfraction ratios, as well as alterations in HDL phospholipid fatty acid profiles in the High Ethanol group. Results from this study provide the first evidence of an anomalous enhancement in LCAT activity in nonhuman primates fed ethanol at 12% of calories and a marked depression in cholesterol esterification at the 24% dose which may be due to substrate alterations and product inhibition prior to overt biochemical evidence of liver dysfunction.
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PMID:Effect of ethanol on lecithin:cholesterol acyltransferase (LCAT) activity. 399 6

Risk factors for the development and rupture of intracranial saccular (berry) aneurysms were identified in a case-control study of autopsy subjects. The development of berry aneurysms was positively correlated with increased frequencies of systemic arterial hypertension (p less than 0.001), cerebral artery atherosclerosis (p less than 0.05), and marked asymmetry of the cerebral vessels comprising the circle of Willis (p less than 0.005). In addition, patients with berry aneurysms more frequently had histories of persistent headache (p less than 0.001), pregnancy-induced hypertension (p less than 0.01), long-term use of analgesics (p less than 0.001), especially aspirin (p less than 0.05), and a family history of stroke (p less than 0.05). Factors associated with a decreased risk of berry aneurysms included treatment with insulin to control diabetes mellitus (p less than 0.005), leanness (p less than 0.05), chronic pancreatitis (p less than 0.001), malignant tumors (p less than 0.001), and moderate or severe coronary or renal atherosclerosis (p less than 0.05). Rupture of berry aneurysms was positively correlated with size (p less than 0.05) and the presence of multiple aneurysms (p less than 0.005), but also with long-term analgesic usage (p less than 0.05), excessive ethanol consumption (p less than 0.01), and fatty metamorphosis of the liver (p less than 0.01). The factors that predispose to rupture of berry aneurysms are interrelated in the sense that several of them are known to cause a decrease in the synthesis of prostaglandin E, whereas one of the factors that appears to be protective has the opposite effect. Marked and abrupt lowering of serum prostaglandin levels would cause dilatation of cerebral vasculature and increased cerebral blood flow; in the setting of hypertension, focal defects in cerebral arteries could develop, leading to the formation and subsequent rupture of berry aneurysms.
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PMID:Risk factors for the development and rupture of intracranial berry aneurysms. 401 70

Though atherosclerosis may have its origins in childhood, intervention studies on coronary heart disease risk factors have usually begun in older adults. Whether young adults exhibit similar relationships of lifestyle to coronary heart disease risk factors, and therefore might be suitable candidates for appropriate intervention, is poorly understood. The Beaver County Lipid Study is a 9-year follow-up study of a free-living young adult population (mean age 22 years) who were initially screened for hypercholesterolemia as seventh grade school children. This report focuses upon cross-sectional correlates of lipid and lipoprotein concentrations in 561 individuals (males n = 262; females n = 299) in 1981-1982. Body mass index was positively related to low density lipoprotein (LDL) cholesterol and triglycerides in men (r = 0.21; p less than 0.001 and r = 0.41; p less than 0.001) and women (r = 0.16; p less than 0.001 and r = 0.20; p less than 0.001). Cigarette smoking was inversely associated with high density lipoprotein (HDL) cholesterol in men (r = -0.11; p less than 0.001) and women (r = -0.20; p less than 0.001) but positively related to triglycerides in both sexes (r = 0.10; p = 0.05 for men and r = 0.19; p less than 0.01 for women). Alcohol consumption was positively related to HDL cholesterol and triglycerides only among men (r = 0.19; p less than 0.001 and r = 0.12; p less than 0.05, respectively). Educational achievement was also positively related to HDL cholesterol in men (p less than 0.01) and women (p less than 0.001). Multivariate analyses indicate that the sex difference in LDL cholesterol was largely eliminated by controlling for body mass index while significant sex differences in both HDL cholesterol and triglycerides remained after controlling for covariates. Results suggest that the known associations in older adults of body mass index and health-related behavior with lipoproteins are well established by young adulthood. Early intervention particularly for obesity may help ameliorate some of the male excess in cardiovascular disease risk.
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PMID:Lipids and lipoproteins in a young adult population. The Beaver County Lipid Study. 402 95

In short-term experiments, healthy fasting persons were given a basic dose of 0.5 g of ethanol/kg body weight, followed by hourly maintenance doses of 0.15 g of ethanol/kg body weight. After 10 h there was a significant increase of triglycerides in the VLDL, LDL, and HDL, the main rise (from 42 to 92 mg/dl) being found in the VLDL triglycerides. Other subjects, who received nourishment isocaloric with ethanol, likewise showed a significant rise of triglycerides in all lipoprotein fractions. Chylomicron triglycerides increased from 9.3 to 35.5 mg/dl. There was no significant change in postheparin HTGL, but postheparin LPL activity decreased after 10 h from 17.9 to 12.2 mmol FFA/ml/h in the fasting subjects, and from 28.5 to 10.2 mmol/FFA/ml/h in the persons receiving food. In long-term experiments after 4 weeks of 70 - 80 g of ethanol and isocaloric food daily, triglycerides increased, especially in the VLDL (from 50 to 82 mg/dl). The increase in the HDL, however, was also significant. After 4 weeks of ethanol, the chylomicron triglycerides in the plasma of the fasting subjects reached a value of 29.3 mg/100 ml, LDL cholesterol decreased, and HDL cholesterol increased. After 4 weeks of ethanol there was an increase in the lipoprotein lipase of the adipose tissue.
Atherosclerosis 1985 Nov
PMID:Lipoprotein fractions, lipoprotein lipase and hepatic triglyceride lipase during short-term and long-term uptake of ethanol in healthy subjects. 408 59

The fluorescent cholesterol probe filipin has been used in this study to histochemically examine the morphology and cholesterol composition of intra- and extracellular Sudanophilic lipid deposits which accumulate in human atherosclerotic lesions. Because filipin reacts with unesterified but not esterified cholesterol, detection of cholesteryl esters was carried out by first extracting native unesterified cholesterol with ethanol, and then enzymatically converting esterified to unesterified cholesterol before filipin staining. The size and structure of particles comprising extracellular cholesteryl ester-rich lipid deposits was different in regions of necrosis as detected using filipin compared with the Sudan lipid-soluble dye oil red 0. Whereas oil red 0 staining often indicated that extracellular cholesteryl ester in these regions occurred in amorphous and spherical particles of varying sizes, filipin staining revealed that extracellular cholesteryl ester occurred in spherical particles more uniform in size than indicated by oil red 0 staining. Also, the majority of extracellular cholesteryl ester-rich particles in necrotic regions were smaller than intracellular cholesteryl ester-containing lipid droplets. In addition, the use of filipin to detect intracellular cholesteryl ester allowed distinction of 2 subpopulations of oil red 0-stained cells which did and did not contain detectable cholesteryl ester.
Atherosclerosis
PMID:Histochemical detection of esterified cholesterol within human atherosclerotic lesions using the fluorescent probe filipin. 620 52

Rats fed a diet low in fibre and provided with ethanol for 4 weeks showed a higher concentration of cholesterol in the serum, liver and heart, but not in the aorta when compared with control rats not provided with ethanol. Animals maintained on a diet of blackgram fibre (30%) and provided with ethanol had significantly lower concentration of cholesterol in these tissues and in the aorta. The concentration of triglyceride was also raised in the serum, liver and heart in rats fed a diet low in fibre + ethanol. A diet of blackgram fibre caused a significant decrease in serum and liver triglyceride. Fecal excretion of neutral sterols and bile acids decreased in rats fed a diet low in fibre + ethanol, whereas blackgram fibre caused an increase in such fecal excretion.
Atherosclerosis 1982 Feb
PMID:Effect of blackgram fibre on ethanol-induced hyperlipidemia in rats. 627 23

Ethanol (88-880 mmol/l) inhibited the formation of proaggregatory, vasoconstricting thromboxane A2 (TxA2) during whole blood clotting and during thrombin-induced aggregation of platelet rich plasma. This inhibition was counteracted by the addition of exogenous arachidonic acid, which suggested that ethanol suppressed the liberation of arachidonic acid, evidently by inhibiting phospholipase A2. Ethanol had no effect on the formation of prostacyclin (PGI2, epoprostenol), the endogenous antagonist of TxA2, by human lung. Thus our results suggest that ethanol may shift the balance between TxA2 and PGI2 to the dominance of antiaggregatory, vasodilating PGI2 by suppressing the release of arachidonic acid in platelets. This finding might partly explain why ethanol protects against atherosclerosis and also the increased risk of subarachnoidal haemorrhage after heavy ethanol intake.
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PMID:Ethanol inhibits platelet thromboxane A2 production but has no effect on lung prostacyclin synthesis in humans. 636 50

The typical occupational cohort study includes all causes of mortality. However, emphasis is usually placed on the presence or absence of excess cancer mortality. A systematic review of completed occupational cohort studies to assess the findings and patterns of cardiovascular mortality would be useful. Although many of these studies will illustrate the "healthy worker effect" with deficits in mortality, particularly from cardiovascular causes, a thorough review should indicate certain exposures needing further research. A recently published study of heart disease mortality in the rubber industry illustrates the potential use of such a literature review with subsequent follow up. Production workers in the rubber industry have shown small excesses in CAHD mortality. A follow-up study at one plant confirmed the known association between carbon disulfide and atherosclerosis, as well as suggested two new causal associations between CAHD and the use of phenol and ethanol as solvents. What additional techniques can be used to generate hypotheses on heart disease and occupation? Some possibilities include: A recent article describes the use of the results of occupational disease surveillance systems for occupational cancer research. A review of such systems for heart disease would be equally useful. It would be useful to review the quality and quantity of occupational data that has been collected in prospective cohort studies, such as those in Framingham and Evans County. The importance of examining the association between occupational exposures and heart disease include: Assessing whether adequate protection is afforded by current limits on exposure to substances known to cause heart disease (carbon disulfide, nitrates, and carbon monoxide).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cardiovascular disease and work place exposures. 638 Apr 27

The serum concentration of lipoprotein Lp(a) and of other lipoproteins of 64 individuals consuming more than 200 g of ethanol per day for several years was measured. 42 of the propositi with no clinical signs of alcoholic liver cirrhosis (ALC) had an apoAI/apoAII ratio twice as high as the control group. The apoAI values of the consumers of alcohol were higher and the HDL-C and Lp(a) levels were lower than those of the control group. 22 alcohol drinkers with ALC exhibited strikingly reduced values of all serum lipids and lipoproteins and the lowest Lp(a) concentrations of all. It is suggested that alcohol drinking lowers serum Lp(a) what might be an additional reason why this group of people seems to be a lower risk of atherosclerosis.
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PMID:Serum concentrations of Lp(a) and other lipoprotein parameters in heavy alcohol consumers. 646

The low density lipoprotein (LDL) receptor pathway was studied in aortic smooth muscle cells from atherosclerosis-susceptible White Carneau pigeons and compared with rhesus monkey cells whose LDL receptor pathway has been previously characterized. Pigeon LDL was bound with high affinity in a saturable manner to both pigeon and monkey aortic smooth muscle cells. The kinetics of binding were different, however. LDL binding to pigeon cells exhibited positive cooperativity at low LDL concentrations and at least two classes of binding sites. The same pigeon LDL bound to monkey cells in a manner consistent with a single class of binding sites. Thus, these differences were a property of the pigeon cells and not the result of differences in the LDL. On the average, pigeon cells bound less than 50% the amount of LDL as monkey cells. Despite the surface binding to pigeon cells, little of the LDL was internalized, whereas pigeon LDL was actively internalized by monkey cells. Consistent with this observation, chloroquine and leupeptin had no effect on accumulation of LDL or on LDL degradation by pigeon cells, and incubation of pigeon cells with LDL produced no increase in cellular cholesteryl ester content. Binding of LDL to pigeon cells also differed from that of monkey cells by being unaffected by pretreatment with the proteolytic enzyme pronase, and by not requiring calcium. Binding was not specific for LDL since acetyl-LDL, and to a lesser degree HDL, were able to compete for LDL binding. Incubation with lipoprotein-deficient serum decreased LDL binding in pigeon cells while 25-OH cholesterol caused an increase in binding; both effects are opposite of that seen with the same LDL in mammalian cells. Preincubation with LDL or cholesterol dissolved in ethanol were without effect on LDL binding in pigeon cells, even though they produced significant increases in cellular free cholesterol content. In spite of the failure to internalize LDL, there was considerable degradation of LDL. This apparently occurred on the cell surface rather than by internalization and degradation within the lysosomes as occurs in mammalian cells. The functional significance of LDL binding to pigeon smooth muscle cells is unclear. The characteristics of binding resemble that of a nonspecific lipoprotein receptor referred to by others as the "lipoprotein receptor" or the "EDTA-insensitive receptor." It is apparent, however, that White Carneau pigeon aortic smooth muscle cells lack a functional LDL receptor pathway and in this way resemble cells from human beings with homozygous familial hypercholesterolemia or from Watanabe rabbits.
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PMID:Pigeon aortic smooth muscle cells lack a functional low density lipoprotein receptor pathway. 649 36


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