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    850 results match your criteria Arteriosclerosis and Thrombosis[Journal]

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    Hypercatabolism of lipoprotein-free apolipoprotein A-I in HDL-deficient mutant chickens.
    Arterioscler Thromb 1994 Dec;14(12):2053-9
    Department of Biochemistry, University of Wisconsin-Madison 53706-1569.
    The Wisconsin Hypoalpha Mutant (WHAM) chicken has a sex-linked mutation associated with a 90% reduction in high-density lipoprotein (HDL) cholesterol and apolipoprotein A-I (apoA-I). In the present studies, we did not detect a defect in apoA-I synthesis or secretion in liver or intestine. We tested the hypothesis that apoA-I is not binding properly to lipoprotein particles and is undergoing hypercatabolism. Read More

    Cytomegalovirus infection enhances mRNA expression of platelet-derived growth factor-BB and transforming growth factor-beta 1 in rat aortic allografts. Possible mechanism for cytomegalovirus-enhanced graft arteriosclerosis.
    Arterioscler Thromb 1994 Dec;14(12):2043-52
    Transplantation Laboratory, University of Helsinki, Finland.
    We have recently demonstrated that rat cytomegalovirus (RCMV) infection induces an early inflammatory response in the adventitia (perivasculitis) and in the subendothelial space (endothelialitis) as well as doubles smooth muscle cell (SMC) proliferation and intimal thickening of rat aortic allografts performed from the DA (AG-B4, RT1a) to the WF (AG-B2, RT1v) strain. In this study, the impact of RCMV infection on the structure of inflammation in the allograft adventitia and on the expression of SMC growth factors in the allograft vascular wall was investigated. The recipient rats were inoculated with 10(5) plaque-forming U of RCMV Maastricht strain or left noninfected and used as controls. Read More

    Hyperlipidemia accelerates allograft arteriosclerosis (chronic rejection) in the rat.
    Arterioscler Thromb 1994 Dec;14(12):2032-42
    Transplantation Laboratory, University of Helsinki, Finland.
    The relevance of hyperlipidemia in allograft arteriosclerosis (chronic rejection) is controversial. Isolated hypercholesterolemia induced with cholesterol-cholic acid-diet (CC-diet) or hypertriglyceridemia induced with glycerol-diet (G-diet) had no or only a protective effect on aortic allograft arteriosclerosis in the rat. Combined hyperlipidemia with both diets (CC+G-diet) enhanced allograft arteriosclerosis by doubling intimal thickness and cellularity (P < . Read More

    Long-term induction and regression of diet-induced atherosclerotic lesions in rhesus monkeys. II. Morphometric evaluation of lesions by light microscopy in coronary and carotid arteries.
    Arterioscler Thromb 1994 Dec;14(12):2007-16
    Department of Pathology, Louisiana State University Medical Center, New Orleans 70112.
    Atherosclerotic lesions were induced in rhesus monkeys (Macaca mulatta) by feeding them a high-saturated fatty acid and high-cholesterol diet. After 5.4 years the extent of lesions in three major coronary arteries and the right carotid artery was evaluated morphometrically by light microscopy in one group of animals (group P). Read More

    Mechanically induced calcium mobilization in cultured endothelial cells is dependent on actin and phospholipase.
    Arterioscler Thromb 1994 Dec;14(12):2000-6
    Department of Chemical Engineering, State University of New York at Buffalo.
    We sought to evaluate the mechanisms by which mechanical perturbation elevates intracellular calcium in endothelial cells. We report that the transient elevation in intracellular calcium in cultured bovine aortic endothelial cells (BAEC) in response to gentle perturbation with the side of a micropipette was not blocked by depolarization (external K+, 130 mmol/L), nifedipine (10 mumol/L), or Bay K 8644 R(+) (10 mumol/L). Thus, voltage-dependent calcium channels were not involved in the response. Read More

    Antiproliferative activity to vascular smooth muscle cells and receptor binding of heparin-mimicking polyaromatic anionic compounds.
    Arterioscler Thromb 1994 Dec;14(12):1992-9
    Department of Oncology, Hadassah University Hospital, Jerusalem, Israel.
    Proliferation of bovine aortic smooth muscle cells (SMCs) induced by thrombin, basic fibroblast growth factor, or serum is inhibited by anionic, nonsulfated aromatic compounds that mimic many of the effects of heparin. Among these compounds are aurintricarboxylic acid (ATA) and a newly synthesized polymer of 4-hydroxyphenoxy acetic acid (compound RG-13577). Iodinated- or 14C-labeled compound RG-13577 binds to cultured SMCs in a highly specific and saturable manner. Read More

    A perfusion chamber developed to investigate thrombus formation and shear profiles in flowing native human blood at the apex of well-defined stenoses.
    Arterioscler Thromb 1994 Dec;14(12):1984-91
    Biotechnology Centre of Oslo, Norway.
    The precipitating event leading to stroke, myocardial infarction, and/or sudden death may be related to the formation of mural thrombus at the site of a ruptured or superficially damaged stenotic plaque. The fluid dynamic properties at atherosclerotic plaques that may be implicated in this thrombus formation have been described in a wide variety of model systems in both the process of plaque rupture and the growth of platelet thrombi. In general, the local fluid dynamic conditions are complex and show major variations from flow in well-defined laminar flow systems. Read More

    Tissue factor-induced coagulation triggers platelet thrombus formation as efficiently as fibrillar collagen at arterial blood flow conditions.
    Arterioscler Thromb 1994 Dec;14(12):1976-83
    Nycomed Bioreg AS, Oslo, Norway.
    The relative importance of vessel wall tissue factor (TF) in initiating thrombogenesis is not well defined. In contrast, vessel wall collagens have been well documented as potent inducers of thrombus formation. We compared the potency of a human TF/phospholipid surface with that of a surface consisting of human type III collagen fibrils in triggering thrombus formation in native human blood at venous and arterial blood flow conditions. Read More

    Oxidation of heparin-isolated LDL by hemin. The effect of serum components.
    Arterioscler Thromb 1994 Dec;14(12):1966-75
    Department of Medicine, University of Otago Medical School, Dunedin, New Zealand.
    Oxidation of low-density lipoprotein (LDL) in the artery wall is probably determined by several factors, some of which may include physiological oxidants such as heme and hydrogen peroxide, blood serum components, and the interaction of the lipoprotein with glycosaminoglycans. Glycosaminoglycans form complexes with LDL that increase its susceptibility to oxidation in vitro. To examine the effect of these factors on oxidation of LDL from serum by using heparin and oxidized the resolubilized lipoprotein (Hep-LDL) with hemin and hydrogen peroxide in the presence of apolipoprotein B lipoprotein-deficient serum (BLPDS). Read More

    Three novel mutations of antithrombin inducing high-molecular-mass compounds.
    Arterioscler Thromb 1994 Dec;14(12):1958-65
    INSERM CJF 91-01, UFR des Sciences Pharmaceutiques et Biologiques (Université Paris V, France.
    We have identified three novel mutations of the antithrombin (AT) gene in patients with thrombotic complications: a Cys 128 --> Tyr mutations, a G --> A mutation in the intervening sequence 4 (IVS4) 14 nucleotide 5' to exon 5, and a 9 bp deletion in the 3' end of exon 6 resulting in a short aberrant sequence after Arg 425. The latter mutation was associated with an Arg 47 --> His mutation in two compound heterozygous brothers. These three mutations led to the expression in the circulation of small amounts of inactive molecules with a high molecular mass in immunoblot analysis. Read More

    13C-NMR spectroscopy of human atherosclerotic lesions. Relation between fatty acid saturation, cholesteryl ester content, and luminal obstruction.
    Arterioscler Thromb 1994 Dec;14(12):1951-7
    Cardiac Unit, Harvard Medical School, Boston, MA.
    Previous investigations have used 13C-nuclear magnetic resonance (NMR) spectroscopy to demonstrate the similarities between lipoproteins and the mobile lipids of atheroma. In this study, we tested the hypothesis that 13C-NMR changes are related to indices of histological severity. We classified 20 human arteries according to their obstruction ratio (OR), defined as the ratio of the plaque area to the area delimited by the external elastic lamina. Read More

    The insulin resistance syndrome in smokers is related to smoking habits.
    Arterioscler Thromb 1994 Dec;14(12):1946-50
    Lundberg Laboratory for Diabetes Research, Department of Internal Medicine, Sahlgrenska University Hospital, Göteborg University, Sweden.
    The relationship between smoking habits, insulin resistance, and related risk factors for cardiovascular disease was examined in 57 middle-aged male smokers whose degree of insulin resistance was quantified by using the euglycemic clamp technique. Smoking habits correlated with degree of insulin resistance and consequently with various manifestations of the insulin resistance syndrome including levels of insulin, high-density lipoprotein cholesterol, triglycerides, and plasminogen activator inhibitor-1 (PAI-1) activity. Smoking habits, independent of degree of insulin resistance, were also related to levels of total cholesterol and low-density lipoprotein cholesterol as well as triglycerides. Read More

    Multivariate analysis of the insulin resistance syndrome in women.
    Arterioscler Thromb 1994 Dec;14(12):1940-5
    Department of Epidemiology, School of Public Health and Community Medicine, University of Washington, Seattle 98195.
    The insulin resistance syndrome (IRS) is characterized by a constellation of interrelated coronary heart disease (CHD) risk factors, including dyslipidemia, obesity, central obesity, elevated systolic blood pressure, and hyperinsulinemia. Factor analysis was used to investigate the clustering of these risk factors in individuals by examining the correlational structure among these variables. Data from 281 genetically unrelated nondiabetic women who participated in exam 2 (1979 to 1980) of the Kaiser Permanente Women Twins Study were used. Read More

    Intraperitoneal insulin therapy corrects abnormalities in cholesteryl ester transfer and lipoprotein lipase activities in insulin-dependent diabetes mellitus.
    Arterioscler Thromb 1994 Dec;14(12):1933-9
    Department of Medicine, Rush Medical College, Chicago, Ill.
    Patients with insulin-dependent diabetes mellitus (IDDM) have proatherogenic disturbances in cholesteryl ester transfer (CET) despite intensive subcutaneous insulin therapy (ISC). Since CET is activated by insulin-sensitive lipoprotein lipase (LPL), which normally increases postprandially, we queried whether iatrogenic hyperinsulinism from ISC stimulated LPL and CET by studying well-controlled IDDM patients after ISC and then 6 months after lowering systemic insulin levels by intraperitoneal (IP) insulin delivery. Although glycemic control (HbA1c IDDM, 6. Read More

    Intraindividual variability of fibrinogen levels and cardiovascular risk profile.
    Arterioscler Thromb 1994 Dec;14(12):1928-32
    Department of Medicine, Rush-Presbyterian-St Luke's Medical Center, Chicago, Ill 60612.
    Prospective population studies have established that fibrinogen is an independent predictor for ischemic heart disease and stroke. These study conclusions have prompted recommendations that fibrinogen determinations be included in the cardiovascular risk profile. The routine availability of fibrinogen measurements may result in widespread screening prior to establishing the validity of a single fibrinogen level as an accurate descriptor for individual subjects. Read More

    Association of factor VII genotype with plasma factor VII activity and antigen levels in healthy Indian adults and interaction with triglycerides.
    Arterioscler Thromb 1994 Dec;14(12):1923-7
    Department of Paediatrics, National University of Singapore.
    Plasma factor VII activity (factor VIIc) is one of the independent risk factors for coronary artery disease and is controlled by both genetic and environmental factors. Several studies in healthy Caucasian subjects have revealed an association of a common genetic polymorphism at residue 353 (Arg-->Gln) of the factor VII gene with plasma factor VIIc. We have investigated the influence of this polymorphism (factor VII Arg/Gln353) on fasting plasma factor VIIc and antigen (factor VIIag) levels and its interaction with triglyceride levels in 185 healthy Dravidian Indians of both sexes (128 men, 57 women). Read More

    A nonsense mutation in the apolipoprotein A-I gene is associated with high-density lipoprotein deficiency and periorbital xanthelasmas.
    Arterioscler Thromb 1994 Dec;14(12):1915-22
    Institut für Arterioskleroseforschung, Westfälische Wilhelms-Universität Münster, FRG.
    Conflicting data from epidemiological trials, genetic family studies, transgenic animal models, and in vitro experiments have created controversy regarding the importance of HDL and apolipoprotein (apo) A-I for reverse cholesterol transport and protection from atherosclerosis. In this study we identified a homozygous nonsense mutation in codon 32 (Q32X) of the apoA-I gene as the molecular basis of apoA-I deficiency in a 31-year-old woman who did not present with clinical signs of atherosclerosis. Despite half-normal plasma concentrations of HDL cholesterol and apoA-I in subjects heterozygous for this mutation, the history of the patient's large family did not indicate any increased prevalence of myocardial infarction. Read More

    Effects of lovastatin on ApoA- and ApoB-containing lipoproteins. Families in a subpopulation of patients participating in the Monitored Atherosclerosis Regression Study (MARS).
    Arterioscler Thromb 1994 Dec;14(12):1906-13
    Lipid and Lipoprotein Laboratory, Oklahoma Medical Research Foundation, Oklahoma City 73104.
    To establish whether lovastatin, an inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase, exhibits a specific effect on apolipoprotein (apo) A- and apoB-containing lipoproteins, 63 subjects, a subset of the 270 Monitored Atherosclerosis Regression Study (MARS) patients with hypercholesterolemia (190 to 295 mg/dL) and documented coronary artery disease, were randomized into either lovastatin 40 mg twice daily or matching placebo tablets twice daily. Both groups consumed a diet containing 27% calories as fat (polyunsaturated fat/saturated fat ratio, 2.85) and a daily cholesterol intake of less than 250 mg. Read More

    Oxidized lipids in the diet are a source of oxidized lipid in chylomicrons of human serum.
    Arterioscler Thromb 1994 Dec;14(12):1900-5
    Department of Veterans Affairs Medical Center, San Francisco, CA 94121.
    We examined whether oxidized lipids in the diet determine the levels of oxidized lipid in human postprandial serum chylomicrons. After we fed subjects control corn oil containing low quantities of oxidized lipid, the levels of conjugated dienes in the chylomicron fraction were low (9.67 +/- 0. Read More

    LDL oxidation in patients with severe carotid atherosclerosis. A study of in vitro and in vivo oxidation markers.
    Arterioscler Thromb 1994 Dec;14(12):1892-9
    Department of Internal Medicine, University of Pavia, Italy.
    Among the various risk factors involved in the development and progression of carotid atherosclerosis, the oxidation of LDL has been proposed to play a relevant role. LDL oxidation has been investigated in 94 patients with severe carotid atherosclerosis undergoing elective carotid artery endarterectomy and in 42 matched control subjects. LDL oxidation was evaluated in all patients as (1) the susceptibility to in vitro oxidation, (2) vitamin E concentration and its efficiency in LDL, and (3) the presence of autoantibodies against oxidatively modified lipoprotein to monitor the occurrence of the oxidative processes taking place in vivo. Read More

    Common carotid intima-media thickness and lower extremity arterial atherosclerosis. The Rotterdam Study.
    Arterioscler Thromb 1994 Dec;14(12):1885-91
    Department of Epidemiology and Biostatistics, Erasmus University Medical School, Rotterdam, The Netherlands.
    High-resolution B-mode ultrasonography of the carotid arteries is used to investigate the signs of early atherosclerotic vessel wall disease. To assess whether carotid artery findings reflect atherosclerosis elsewhere, we studied the association between common carotid intima-media thickness and lower extremity arterial atherosclerosis among the first 1000 participants of the Rotterdam Study. The Rotterdam Study is a single-center population-based prospective follow-up study of 7983 subjects, > or = 55 years old. Read More

    Lactoferrin binding to heparan sulfate proteoglycans and the LDL receptor-related protein. Further evidence supporting the importance of direct binding of remnant lipoproteins to HSPG.
    Arterioscler Thromb 1994 Dec;14(12):2025-31
    Gladstone Institute of Cardiovascular Disease, Cardiovascular Research Institute, San Francisco, CA 94141-9100.
    Bovine lactoferrin inhibits the clearance of remnant lipoproteins from the plasma and competes with the cell-surface binding of apolipoprotein (apo) E-enriched remnants. We established that lactoferrin inhibits remnant binding and uptake by interacting with both heparan sulfate proteoglycans (HSPG) and the low-density lipoprotein receptor-related protein (LRP). The binding of 125I-lactoferrin was inhibited 45% to 60% in HepG2 hepatocytes and wild-type Chinese hamster ovary (CHO) cells treated with heparinase to remove HSPG. Read More

    Presence of LDL receptor-related protein/alpha 2-macroglobulin receptors in macrophages of atherosclerotic lesions from cholesterol-fed New Zealand and heterozygous Watanabe heritable hyperlipidemic rabbits.
    Arterioscler Thromb 1994 Dec;14(12):2017-24
    Cardiovascular Division, Washington University School of Medicine, St. Louis, MO 63110.
    Atherosclerotic lesions are composed of a complex mixture of cell types that are engorged with lipid and enveloped in extracellular matrix elements. This manifestation probably results from imbalances in the cellular processing of cholesterol-delivering lipoproteins, changes in extracellular matrix deposition, and growth factor elaboration. One receptor class that could modulate these processes is LDL receptor-related protein/alpha 2-macroglobulin receptors (LRP/alpha 2-MR). Read More

    Proceedings of the Nutrition Research/Cardiovascular Disease Conference. American Heart Association, Dallas, Tex.
    • Authors:
    Arterioscler Thromb 1994 Nov;14(11):1880-4
    The AHA, through its Nutrition Committee, can take an active role in working with federal agencies, professional societies, and industry to identify priorities for nutrition research in CVD, to develop coordinated programs and increased support for nutrition research and training, and to highlight the role of nutrition research in addressing the nation's health needs. Read More

    Susceptibility to diet-induced atherosclerosis in transgenic mice expressing a dysfunctional human apolipoprotein E(Arg 112,Cys142).
    Arterioscler Thromb 1994 Nov;14(11):1873-9
    Gladstone Institute of Cardiovascular Disease, University of California, San Francisco.
    Transgenic mice expressing apolipoprotein (apo) E(Cys 142), a human defective variant of apo E, have elevated levels of plasma cholesterol, triglycerides, and very-low-density lipoproteins (VLDL); beta-VLDL, the biochemical hallmark of the human genetic disease type III hyperlipoproteinemia (HLP), is also present in these mice. This study was designed to determine whether these type III HLP mice have an increased susceptibility to spontaneous or diet-induced atherosclerosis. Three 4-month-old male transgenic mice and three male nontransgenic littermates were assessed for the presence of atherosclerotic lesions in the proximal aorta. Read More

    Effect of endotoxin and cytokines on lipoprotein lipase activity in mice.
    Arterioscler Thromb 1994 Nov;14(11):1866-72
    Department of Medicine, University of California, San Francisco.
    Endotoxin (lipopolysaccharide [LPS]) stimulates the production of cytokines, which mediate many of the metabolic effects associated with infection. In LPS-sensitive C57B1/6 mice, LPS doses as low as 0.01 micrograms per mouse decreased adipose tissue lipoprotein lipase (LPL) activity by greater than 50%. Read More

    Species difference in cholesteryl ester cycle and HDL-induced cholesterol efflux from macrophage foam cells.
    Arterioscler Thromb 1994 Nov;14(11):1860-5
    Department of Biochemistry, Kumamoto University School of Medicine, Japan.
    The species difference in the turnover rates of the cholesteryl ester (CE) cycle in macrophage foam cells (MFC) was examined in mice and rats. MFC were induced by acetyl-LDL and pulsed with [3H]oleate, followed by a chase with [14C]oleate. The replacement of the initial amount of cholesteryl [3H]oleate by cholesteryl [14C]oleate within 24 hours was 63% in mouse MFC, whereas it was 33% in rat MFC. Read More

    Alterations in basal and serotonin-stimulated calcium permeability and vasoconstriction in atherosclerotic aorta.
    Arterioscler Thromb 1994 Nov;14(11):1854-9
    Department of Physiology, Medical College of Pennsylvania, Philadelphia 19129.
    Hypersensitivity to vasoactive stimuli, a common finding in atherosclerotic arteries, is thought to play an important role in the pathology of arterial and coronary vasospasm and may be a factor in myocardial ischemia and infarction. While this phenomenon is well documented, the underlying mechanism is unknown. The present study used isometric force measurements coupled with 45Ca2+ and Fura 2-AM techniques in aortic smooth muscle to probe transmembrane calcium movements and cytosolic calcium levels in an attempt to determine their relation to altered vasomotion in a rabbit model of dietary atherosclerosis. Read More

    Neointima formation after vascular stent implantation. Spatial and chronological distribution of smooth muscle cell proliferation and phenotypic modulation.
    Arterioscler Thromb 1994 Nov;14(11):1846-53
    First Department of Surgery, Osaka University Medical School, Japan.
    Intravascular stents have proved useful as angioplasty devices, but intimal hyperplasia after stent implantation remains an unsolved problem. In the present study, we analyzed the spatial and chronological distribution of proliferation and phenotypes of smooth muscle cells (SMCs) in rabbit aortas during the process of neointima formation after stent implantation (Gianturco's Z type) by immunohistochemistry for proliferating cell nuclear antigen (PCNA) and myosin heavy chain isoforms (SM1, SM2, and SMemb). Stent implantation induced regional injury in the arterial wall. Read More

    Changes in the caldesmon isoform content and intimal thickening in the rabbit carotid artery induced by a silicone elastomer collar.
    Arterioscler Thromb 1994 Nov;14(11):1837-45
    Cardiac Medicine Department, National Heart and Lung Institute, London, UK.
    The presence of a silicone elastomer collar around one carotid artery of a rabbit induces thickening of the tunica intima. We used immunoblotting to study quantitatively changes in the isoforms of caldesmon, a protein implicated in the regulation of contractility in smooth muscle, while also monitoring the histological changes during 28 days after collaring. Control rabbit carotid arteries (n = 28) contained 245 +/- 6. Read More

    Formation of biologically active autacoids is regulated by calcium influx in endothelial cells.
    Arterioscler Thromb 1994 Nov;14(11):1821-8
    Institut für Prophylaxe und Epidemiologie der Kreislaufkrankheifen, University of Munich, FRG.
    The blocker of receptor-mediated calcium entry SK&F 96365 was used to evaluate the contribution of calcium influx to the formation of biologically active endothelial prostanoids and endothelium-derived relaxing factor (EDRF). SK&F 96365 inhibited histamine-stimulated calcium entry into human umbilical vein endothelial cells but not its discharge from intracellular stores as determined spectrofluorometrically by changes of intracellular calcium concentration in fura-2-loaded cells. Concordantly, SK&F 96365 inhibited histamine-induced endothelial synthesis of 6-keto-prostaglandin F1 alpha and thromboxane B2 in a dose-dependent manner. Read More

    Polar expression of tissue factor in human umbilical vein endothelial cells.
    Arterioscler Thromb 1994 Nov;14(11):1815-20
    Biotechnology Centre of Oslo, University of Oslo, Norway.
    Endothelial cells grown on filters developed junctional complexes that reduced diffusional transport and increased electrical resistance over the cell layer. Induction of tissue factor by recombinant interleukin-1 beta led to a highly polarized tissue factor expression on the apical cell surface only. After prolonged growth to allow deposition of matrix, removal of the endothelial cells by collagenase or by 0. Read More

    Oxidation of LDL to a biologically active form by derivatives of nitric oxide and nitrite in the absence of superoxide. Dependence on pH and oxygen.
    Arterioscler Thromb 1994 Nov;14(11):1808-14
    Department of Medicine, UCLA School of Medicine 90024-1679.
    A key factor in atherogenesis is oxidation of LDL in the subendothelial space. In the normal vessel wall or in the thickened intima of diseased vessels, this space is rich in nitric oxide (NO.) released from endothelial cells, smooth muscle cells, and macrophages. Read More

    Low-density lipoproteins of the postprandial state induce cellular cholesteryl ester accumulation in macrophages.
    Arterioscler Thromb 1994 Nov;14(11):1799-807
    Department of Internal Medicine, University of Innsbruck, Austria.
    Chemically or biologically modified low-density lipoproteins (LDL) but not native unmodified LDL lead to foam cell formation in monocyte-derived macrophages. Since the magnitude of postprandial lipemia after a challenge test seems to be associated with coronary artery disease, we tested the hypothesis that in the course of postprandial lipemia, LDL appear in plasma that are capable of leading to foam cell formation even without prior modification. We incubated the macrophage-like cell line P388 with unmodified postabsorptive and postprandial LDL from 17 healthy donors and measured the cellular cholesterol and triglyceride contents and amounts of exogenous [14C]oleic acid incorporated into the cholesteryl ester fraction. Read More

    Binding of recombinant apolipoprotein(a) to extracellular matrix proteins.
    Arterioscler Thromb 1994 Nov;14(11):1792-8
    Department of Biochemistry, Queen's University, Kingston, Ontario, Canada.
    Elevated levels of lipoprotein(a), which consists of apolipoprotein(a) [apo(a)] covalently linked to a low-density lipoprotein-like moiety, is an independent risk factor for the development of atherosclerosis. We show that a recombinant form of apo(a) [r-apo(a)] binds strongly to fibronectin and fibrinogen, weakly to laminin, and not at all to von Willebrand factor, vitronectin, or collagen type IV. In contrast to the binding of plasminogen to fibronectin, r-apo(a) binding does not appear to be mediated by lysine-dependent interactions, based on the inability of epsilon-aminocaproic acid concentrations up to 0. Read More

    Selective inhibition of platelet macroaggregate formation by a recombinant heparin-binding domain of human thrombospondin.
    Arterioscler Thromb 1994 Nov;14(11):1784-91
    Unité 353 INSERM, Protéines Adhésives et Protéases des Cellules Vasculaires et Sanguines, Hôpital St Louis, Paris, France.
    Thrombospondin (TSP) is a platelet alpha-granule adhesive protein that plays a critical role in the stabilization of thrombus by promoting the formation of platelet macroaggregates. We have recently shown that a monoclonal antibody (mAb) to the NH2-terminal heparin-binding domain of TSP, MAII, inhibits platelet aggregation induced by thrombin in a dose-dependent manner. In this study, we have expressed in Escherichia coli two recombinant proteins comprising residues 1 to 174 (TSP18) and 1 to 242 (TSP28) of TSP. Read More

    HDL and apolipoprotein A-I protect erythrocytes against the generation of procoagulant activity.
    Arterioscler Thromb 1994 Nov;14(11):1775-83
    Department of Biochemistry, McMaster University Health Sciences Centre, Hamilton, Ontario, Canada.
    The appearance of anionic lipids on the extracellular surface of cells is required for the formation of the procoagulant complex that leads to the activation of prothrombin. Procoagulant activity would be expected to be inhibited by substances that stabilize the membrane structure and hence inhibit the transbilayer diffusion of phosphatidylserine from the cytoplasmic to the extracellular surface of the plasma membrane. The generation of procoagulant activity in human erythrocytes by A23187 and Ca2+ is inhibited by apolipoprotein A-I, its amphipathic peptide analogues, and high-density lipoprotein (HDL). Read More

    Triglyceride-rich lipoproteins isolated by selected-affinity anti-apolipoprotein B immunosorption from human atherosclerotic plaque.
    Arterioscler Thromb 1994 Nov;14(11):1767-74
    Cardiovascular Research Institute, University of California, San Francisco.
    We isolated and characterized immunoreactive apolipoprotein B (apoB)-containing lipoproteins from human atherosclerotic plaque and plasma to determine whether very-low-density lipoprotein (VLDL) can enter and become incorporated into the atherosclerotic lesion and how plaque apoB-containing lipoproteins differ from apoB-containing lipoproteins isolated from plasma. Atherosclerotic plaques were obtained during aortic surgery and processed immediately. Lipoproteins were extracted from minced plaque in a buffered saline solution (extract A). Read More

    Increased radiosensitivity and radioresistant DNA synthesis in cultured fibroblasts from patients with coronary atherosclerosis.
    Arterioscler Thromb 1994 Nov;14(11):1761-6
    Department of Biological and Medical Research, King Faisal Specialist Hospital and Research Centre, Riyadh, Saudi Arabia.
    Cultured skin fibroblasts from five patients with atherosclerosis who underwent coronary artery bypass graft surgery were compared with those from one ataxia telangiectasia (AT) homozygote, three AT heterozygotes, and five healthy subjects to determine their sensitivity to gamma radiation as determined by a colony survival assay. Fibroblasts from four of these patients were also compared with those from two AT homozygotes, two AT heterozygotes, and three healthy subjects to determine postirradiation [3H]thymidine incorporation, indicating the levels of radioresistant DNA synthesis (RDS). On the basis of colony survival assay, after long-term irradiation (at low dose rate, ie, 0. Read More

    Short-term consumption of a low-fat diet beneficially affects plasma lipid concentrations only when accompanied by weight loss. Hypercholesterolemia, low-fat diet, and plasma lipids.
    Arterioscler Thromb 1994 Nov;14(11):1751-60
    Lipid Metabolism Laboratory, Tufts University, Boston, Mass 02111.
    Study subjects (6 women and 5 men) over the age of 40 years with fasting low-density lipoprotein cholesterol concentrations > 130 mg/dL were studied during three 5-week diet phases and one 10-week phase: baseline (36% fat: 13% saturated fatty acids [SFA], 12% monounsaturated fatty acids [MUFA], 8% polyunsaturated fatty acids [PUFA], and 128 mg cholesterol/1000 kcal); reduced fat (29% fat: 7% SFA, 9% MUFA, 11% PUFA, and 85 mg cholesterol/1000 kcal); and two low fat (15% fat: 5% SFA, 5% MUFA, 3% PUFA, and 73 mg cholesterol/1000 kcal). Body weight was maintained during the first three 5-week phases (baseline, reduced fat, and low fat [-->energy]) and decreased during the last 10-week phase when the low-fat diet was provided such that the subjects determined, in part, their caloric intake (low fat [decreases energy]). Mean body weight declined by 0. Read More

    Fibrinolytic responses to moderate intensity exercise. Comparison of physically active and inactive men.
    Arterioscler Thromb 1994 Nov;14(11):1746-50
    Department of Physical Education, Northern Illinois University, DeKalb 60115.
    The purposes of this study were to compare fibrinolytic responses to moderate intensity exercise in physically active and inactive men and during morning and evening exercise. Fourteen physically inactive men (mean age, 34.7 +/- 4. Read More

    Abnormally high circulation levels of tissue plasminogen activator and plasminogen activator inhibitor-1 in patients with a history of ischemic stroke.
    Arterioscler Thromb 1994 Nov;14(11):1741-5
    Clinica Medica, Universitá di Napoli, Italy.
    We evaluated 106 subjects with and 109 subjects without a history of ischemic stroke. All were attending a metabolic ward. The two groups were compared for major risk factors for ischemic events. Read More

    Correlation of vitamin K-dependent clotting factors with cholesterol and triglycerides in healthy young adults.
    Arterioscler Thromb 1994 Nov;14(11):1737-40
    Department of Medicine, State University of New York at Stony Brook 11794-8151.
    The plasma level of factor VII activity was a risk factor for the development of ischemic heart disease (IHD) in a prospective epidemiological study of hemostatic factors. We have previously reported significant correlations between factor VII clotting activity or antigen and lipid fractions in a group of 132 young men (< 30 years old) at low risk for IHD and concluded that control of the plasma factor VII level may be linked to lipid metabolism in normal male physiology. Because factor VII is one of four vitamin K-dependent procoagulant proteins, we hypothesized that plasma levels of all these proteins would be similarly controlled in normal physiology. Read More

    Plasma Lp(a) levels correlate with number, severity, and length-extension of coronary lesions in male patients undergoing coronary arteriography for clinically suspected coronary atherosclerosis.
    Arterioscler Thromb 1994 Nov;14(11):1730-6
    Hospital of the Westfälische Wilhelms-University of Münster, FRG.
    The relation between lipoprotein(a) [Lp(a)] as an independent risk factor for coronary atherosclerosis and the severity and extension of angiographically detectable coronary atherosclerotic lesions has not been systematically evaluated. In 118 male patients (54.3 +/- 7. Read More

    Atherosclerotic plaque evolution in the descending thoracic aorta in familial hypercholesterolemic patients. A transesophageal echo study.
    Arterioscler Thromb 1994 Nov;14(11):1723-9
    Department of Medicine, Evanston Hospital, Ill.
    We explored the concept that transesophageal echocardiography can be used as a tool to detect, characterize, and study plaque morphology in the descending thoracic aorta. The pattern of atherosclerotic plaques in the descending thoracic aorta in familial hypercholesterolemic (FH) patients was evaluated. Additionally, evolution of plaque characteristics as a result of therapy was analyzed. Read More

    Effect on plasma lipid levels of different classes of mutations in the low-density lipoprotein receptor gene in patients with familial hypercholesterolemia.
    Arterioscler Thromb 1994 Nov;14(11):1717-22
    Department of Medicine, Rayne Institute, University College of London, Medical School, UK.
    We used the single-strand conformational polymorphism method to screen 311 patients with familial hypercholesterolemia from London lipid clinics and Southampton and South West Hampshire health district for mutations in the 3' part of exon 4 of the low-density lipoprotein (LDL) receptor gene. This part of the gene codes for repeat 5 of the binding domain of the LDL receptor, which is known to be critical for the receptor-mediated removal of both triglyceride-rich lipoprotein remnants and LDL. Six previously described mutations were identified in 29 apparently unrelated individuals (9. Read More

    Plasma lipoproteins in familial dysbetalipoproteinemia associated with apolipoproteins E2(Arg158-->Cys), E3-Leiden, and E2(Lys146-->Gln), and effects of treatment with simvastatin.
    Arterioscler Thromb 1994 Nov;14(11):1705-16
    Department of Cardiology, Medical Faculty, University of Leiden, Netherlands.
    Using a density-gradient ultracentrifugation technique, we analyzed in detail the plasma lipoprotein profiles of 18 patients with familial dysbetalipoproteinemia (FD) who had apolipoprotein (apo) E2(Arg158-->Cys) homozygosity (the E2-158 variant, n = 6), apoE3-Leiden heterozygosity (the E3-Leiden variant, n = 6), or apoE2(Lys146-->Gln) heterozygosity (the E2-146 variant, n = 6), with average plasma cholesterol concentrations of 8.99 +/- 1.34 mmol/L, 9. Read More

    Dysbetalipoproteinemia in a kindred with hypobetalipoproteinemia due to mutations in the genes for ApoB (ApoB-70.5) and ApoE (ApoE2).
    Arterioscler Thromb 1994 Nov;14(11):1695-704
    University Utrecht, The Netherlands.
    We identified the first insertion mutation that specifies an apolipoprotein (apo)B truncation, apoB-70.5, in a father and son with hypobetalipoproteinemia (total and low-density lipoprotein [LDL] cholesterol < 5th percentile, plasma apoB levels approximately one third of normal). The mutation is due to insertion of an adenine (A) into a 7-A repeat between cDNA position 9754 and 9760 of the apoB gene, resulting in a frame shift of 13 new amino acids and a termination codon at amino acid residue 3197. Read More

    Genetic predictors of FCHL in four large pedigrees. Influence of ApoB level major locus predicted genotype and LDL subclass phenotype.
    Arterioscler Thromb 1994 Nov;14(11):1687-94
    Department of Medicine, University of Washington, Seattle.
    The genetic basis of familial combined hyperlipidemia (FCHL) has eluded investigators for 20 years, despite the apparent segregation of FCHL as an autosomal dominant disorder affecting 1% to 2% of individuals. Etiologic heterogeneity and additive effects of traits controlled by other genetic loci have been suggested. Two traits have been implicated in FCHL. Read More

    The omega-3 fatty acid docosahexaenoate reduces cytokine-induced expression of proatherogenic and proinflammatory proteins in human endothelial cells.
    Arterioscler Thromb 1994 Nov;14(11):1829-36
    Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Mass 02115.
    The mechanisms by which dietary fatty acids can modulate atherogenesis and inflammation are poorly understood. Induction in endothelial cells of adhesion molecules for circulating leukocytes and of inflammatory mediators by cytokines probably contributes to the early phases of atherogenesis and inflammation. We report here that incorporation into cellular lipids of docosahexaenoic acid (DHA), a specific fatty acid of the omega 3 family, decreases cytokine-induced expression of endothelial leukocyte adhesion molecules, secretion of inflammatory mediators, and leukocyte adhesion to cultured endothelial cells. Read More

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