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About This Cover
Volume 26, Issue 3; March 1, 2006
Brief Reviews
Vascular Biology
Atherosclerosis and Lipoproteins
Thrombosis
Letters to the Editor
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Brief Reviews
Applications of Nanotechnology to Atherosclerosis, Thrombosis, and Vascular Biology
Samuel A. Wickline, Anne M. Neubauer, Patrick Winter, Shelton Caruthers, and Gregory Lanza
Arterioscler Thromb Vasc Biol. 2006;26:435-441; published online before print December 22 2005, doi:10.1161/01.ATV.0000201069.47550.8b.
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Targeted nanotechnologies offer alternative modes of imaging for in vivo diagnosis and selective drug delivery that are expected to dramatically enhance molecular imaging capabilities and clinical prospects for personalized medicine in the near future.
Apolipoprotein E Recycling: Implications for Dyslipidemia and Atherosclerosis
Joerg Heeren, Ulrike Beisiegel, and Thomas Grewal
Arterioscler Thromb Vasc Biol. 2006;26:442-448; published online before print December 22 2005, doi:10.1161/01.ATV.0000201282.64751.47.
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Role of cAMP Response Element Binding Protein in Cardiovascular Remodeling: Good, Bad, or Both?
Toshihiro Ichiki
Arterioscler Thromb Vasc Biol. 2006;26:449-455; published online before print November 17 2005, doi:10.1161/01.ATV.0000196747.79349.d1.
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The cAMP response element binding protein (CREB) is a nuclear transcription factor activated by various extracellular stimuli. The role of CREB in cardiovascular system is incompletely characterized and several controversies remain. A growing body of recent evidence, however, has suggested that CREB plays an important role in the cardiovascular remodeling.
Tissue Factor Encryption
Ronald R. Bach
Arterioscler Thromb Vasc Biol. 2006;26:456-461; published online before print January 5 2006, doi:10.1161/01.ATV.0000202656.53964.04.
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Tissue factor (TF) procoagulant activity (PCA) is not fully expressed by an unperturbed cell. This post-translational suppression of TF PCA is known as TF encryption. TF PCA is decrypted after an influx of calcium into the cytosol and phosphatidylserine exposure on the cell surface. TF self-association, TF binding to lipid rafts, and repressed autoactivation of factor VII may contribute to TF encryption.
Vascular Biology
Effect of Vectors on Human Endothelial Cell Signal Transduction: Implications for Cardiovascular Gene Therapy
Peng H. Tan, Shao-An Xue, Maria Manunta, Sven C. Beutelspacher, Henrieta Fazekasova, A.K.M. Shamsul Alam, Myra O. McClure, and Andrew J.T. George
Arterioscler Thromb Vasc Biol. 2006;26:462-467; published online before print December 15 2005, doi:10.1161/01.ATV.0000200083.95349.9e.
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Viral vectors are efficient at transducing ECs. However, they activate the cells, causing an increased expression of adhesion molecules and cytokines. This is caused by stimulation of intracellular signaling pathways. Blocking these pathways, or cytokines that provide autocrine stimulation, can prevent activation after transduction.
Endothelial EphrinB2 Is Controlled by Microenvironmental Determinants and Associates Context-Dependently With CD31
Thomas Korff, Gudrun Dandekar, Dennis Pfaff, Tim Füller, Winfried Goettsch, Henning Morawietz, Florence Schaffner, and Hellmut G. Augustin
Arterioscler Thromb Vasc Biol. 2006;26:468-474; published online before print December 15 2005, doi:10.1161/01.ATV.0000200081.42064.e7.
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This study shows that arterial ephrinB2 expression in vivo is lost on transfer into culture, contact with SMC or stimulation with VEGF upregulates ephrinB2, quiescent EC express ephrinB2 on their luminal surface, EphB4-Fc activation induces increased junctional ephrinB2 accumulation, and junctional ephrinB2 associates with CD31.
TNF-
Contributes to Endothelial Dysfunction in Ischemia/Reperfusion Injury
Cuihua Zhang, Xiangbin Xu, Barry J. Potter, Wei Wang, Lih Kuo, Lloyd Michael, Gregory J. Bagby, and William M. Chilian
Arterioscler Thromb Vasc Biol. 2006;26:475-480; published online before print December 29 2005, doi:10.1161/01.ATV.0000201932.32678.7e.
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We examined the role of TNF-{alpha} in endothelial dysfunction after myocardial ischemia-reperfusion (I/R) injury. I/R injury compromised endothelium-dependent dilation to acetylcholine (ACh). TNF-{alpha} expression was increased >4-fold after I/R. Anti-TNF-{alpha} restored vasodilation to ACh and reduced xanthine oxidase activity, the production of O2{middle dot}-.
15d-Prostaglandin J
2
Protects Brain From Ischemia-Reperfusion Injury
Teng-Nan Lin, Wai-Mui Cheung, Jui-Sheng Wu, Jean-Ju Chen, Heng Lin, Jin-Jer Chen, Jun-Yang Liou, Song-Kun Shyue, and Kenneth K. Wu
Arterioscler Thromb Vasc Biol. 2006;26:481-487; published online before print December 29 2005, doi:10.1161/01.ATV.0000201933.53964.5b.
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Adv-COX-1 gene transfer increased 15d-PGJ2 in ischemic brain accompanied by reduced infarct volume, activated caspase 3, and enhanced heme oxygenase-1 and peroxisome proliferator activated receptor {gamma} (PPAR{gamma}) expression. 15d-PGJ2 and rosiglitazone inhibited neuronal apoptosis and necrosis in a PPAR{gamma}-dependent manner.
Thromboxane A2/Prostaglandin H2 Receptor Activation Mediates Angiotensin IIInduced Postischemic Neovascularization
Frédéric Michel, Jean-Sébastien Silvestre, Ludovic Waeckel, Stefano Corda, Tony Verbeuren, Jean Paul Vilaine, Michel Clergue, Micheline Duriez, and Bernard I. Levy
Arterioscler Thromb Vasc Biol. 2006;26:488-493; published online before print December 29 2005, doi:10.1161/01.ATV.0000201969.93348.74.
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Endogenous activation of TXA2 receptor by eicosanoids did not modulate spontaneous neovascularization in the setting of ischemia. In contrast, treatments with TP receptor antagonists or aspirin hampered the proangiogenic effect of Ang II and fully abrogated the Ang II-induced increase in VEGF-A protein content and the number of Mac-3-positive cells.
Antioxidants Inhibit the Ability of Lysophosphatidylcholine to Regulate Proteoglycan Synthesis
Mary Y. Chang, Chang-Yeop Han, Thomas N. Wight, and Alan Chait
Arterioscler Thromb Vasc Biol. 2006;26:494-500; published online before print December 15 2005, doi:10.1161/01.ATV.0000200135.61362.27.
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We previously have shown that lysoPC regulates proteoglycan synthesis by vascular smooth muscle cells. Current findings strongly suggest that reactive oxygen species are key mediators in this ability of lysoPC and that these effects can be inhibited by antioxidants.
Counter-Regulatory Function of Protein Tyrosine Phosphatase 1B in Platelet-Derived Growth Factor or Fibroblast Growth FactorInduced Motility and Proliferation of Cultured Smooth Muscle Cells and in Neointima Formation
Yingzi Chang, Bogdan Ceacareanu, Daming Zhuang, Chunxiang Zhang, Qinghua Pu, Alice C. Ceacareanu, and Aviv Hassid
Arterioscler Thromb Vasc Biol. 2006;26:501-507; published online before print December 22 2005, doi:10.1161/01.ATV.0000201070.71787.b8.
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The current study was designed to test the hypothesis that PTP1B attenuates vascular smooth muscle motility and proliferation induced by platelet-derived growth factor or fibroblast growth factor-2 in cultured cells and that PTP1B plays a counter-regulatory role in neointima formation. Our results confirm the aforementioned hypotheses.
Stereospecific and Redox-Sensitive Increase in Monocyte Adhesion to Endothelial Cells by Homocysteine
Otilia Postea, Florian Krotz, Anna Henger, Christiane Keller, and Norbert Weiss
Arterioscler Thromb Vasc Biol. 2006;26:508-513; published online before print December 22 2005, doi:10.1161/01.ATV.0000201039.21705.dc.
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Incubation of endothelial cells with l-homocystein, but not with d-homocysteine, increases reactive oxygen species accumulation, activation of NF-{kappa}B, and expression of ICAM-1, resulting in a time- and dose-dependent increase in monocyte adhesion to endothelial cells. Pretreatment with superoxide scavengers or an inhibitor of NF-{kappa}B activation reversed all these events.
Elevated Concentrations of Nonesterified Fatty Acids Increase Monocyte Expression of CD11b and Adhesion to Endothelial Cells
Wei-Yang Zhang, Eric Schwartz, Yingjie Wang, Jeanne Attrep, Zhi Li, and Peter Reaven
Arterioscler Thromb Vasc Biol. 2006;26:514-519; published online before print December 15 2005, doi:10.1161/01.ATV.0000200226.53994.09.
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This study demonstrates that elevation of NEFA, as frequently occurs in obesity, insulin resistance, and type 2 diabetes, increases monocyte expression of CD11b and adhesion to endothelial cells. These effects appear mediated, in part, through activation of NADPH oxidase and oxidative stress.
Impact of Mouse Strain Differences in Innate Hindlimb Collateral Vasculature
Armin Helisch, Shawn Wagner, Nadeem Khan, Mary Drinane, Swen Wolfram, Matthias Heil, Tibor Ziegelhoeffer, Ulrike Brandt, Justin D. Pearlman, Harold M. Swartz, and Wolfgang Schaper
Arterioscler Thromb Vasc Biol. 2006;26:520-526; published online before print January 5 2006, doi:10.1161/01.ATV.0000202677.55012.a0.
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The purpose of this study was to assess the importance of genetic background for collateral artery development. Genetic differences in preexistent collateral vasculature can profoundly affect outcome and milieu for compensatory collateral artery growth after femoral artery occlusion.
Atherosclerosis and Lipoproteins
Identification of the cAMP-Responsive Enhancer of the Murine ABCA1 Gene: Requirement for CREB1 and STAT3/4 Elements
Wilfried Le Goff, Ping Zheng, Gregory Brubaker, and Jonathan D. Smith
Arterioscler Thromb Vasc Biol. 2006;26:527-533; published online before print December 22 2005, doi:10.1161/01.ATV.0000201042.00725.84.
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The cAMP-responsive enhancer in the murine ABCA1 gene was identified by a shotgun cloning strategy. This enhancer contains 2 required elements, a consensus cAMP-responsive element that binds phospho CREB1, and a nearby element that binds STAT3/4. A dominant-negative CREB expression vector inhibited ABCA1 induction by cAMP analogues.
ABCA1 and ABCG1 Synergize to Mediate Cholesterol Export to ApoA-I
Ingrid C. Gelissen, Matthew Harris, Kerry-Anne Rye, Carmel Quinn, Andrew J. Brown, Maaike Kockx, Sian Cartland, Mathana Packianathan, Leonard Kritharides, and Wendy Jessup
Arterioscler Thromb Vasc Biol. 2006;26:534-540; published online before print December 15 2005, doi:10.1161/01.ATV.0000200082.58536.e1.
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This study tested the acceptor requirements for hABCG1-mediated cholesterol efflux. A range of phospholipid-containing acceptors were efficient in mediating ABCG1-dependent cholesterol export. Acceptors for ABCG1 could be generated via incubation of apoA-I with macrophages or ABCA1-overexpressing cells, suggesting a synergistic relationship between ABCA1 and ABCG1 in facilitating cholesterol export.
Relative Contributions of ABCA1 and SR-BI to Cholesterol Efflux to Serum From Fibroblasts and Macrophages
MyNgan Duong, Heidi L. Collins, Weijun Jin, Ilaria Zanotti, Elda Favari, and George H. Rothblat
Arterioscler Thromb Vasc Biol. 2006;26:541-547; published online before print January 12 2006, doi:10.1161/01.ATV.0000203515.25574.19.
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Hepatic Lipase Deficiency Delays Atherosclerosis, Myocardial Infarction, and Cardiac Dysfunction and Extends Lifespan in SR-BI/Apolipoprotein E Double Knockout Mice
Sharon L. Karackattu, Bernardo Trigatti, and Monty Krieger
Arterioscler Thromb Vasc Biol. 2006;26:548-554; published online before print January 5 2006, doi:10.1161/01.ATV.0000202662.63876.02.
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SR-BI/apoE double knockout (dKO) mice exhibit occlusive atherosclerotic coronary heart disease (CHD) characterized by myocardial infarctions, cardiac dysfunction, and premature death. Analysis of SR-BI/apoE/hepatic lipase (HL) triple knockout mice demonstrated that HL-deficiency reduces atherosclerosis, improves cardiac structure/function, and extends lifespan in this CHD model.
Atherosclerosis in Mice Is Not Affected by a Reduction in Tissue Factor Expression
Rachel E. Tilley, Brian Pedersen, Rafal Pawlinski, Yuichiro Sato, Jonathan H. Erlich, Yuechun Shen, Sharlene Day, Ying Huang, Daniel T. Eitzman, William A. Boisvert, Linda K. Curtiss, William P. Fay, and Nigel Mackman
Arterioscler Thromb Vasc Biol. 2006;26:555-562; published online before print December 29 2005, doi:10.1161/01.ATV.0000202028.62414.3c.
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We sought to determine whether tissue factor (TF) contributes to the progression of atherosclerotic lesions in mice. A 50% reduction of TF in all cells or a selective reduction of TF in hematopoietic cells does not affect the development of atherosclerotic lesions in 2 mouse models. TF does not contribute to the progression of atherosclerosis in mice.
Leukocyte Transglutaminase 2 Expression Limits Atherosclerotic Lesion Size
W.A. Boisvert, D.M. Rose, A. Boullier, O. Quehenberger, A. Sydlaske, K.A Johnson, L.K. Curtiss, and R. Terkeltaub
Arterioscler Thromb Vasc Biol. 2006;26:563-569; published online before print January 12 2006, doi:10.1161/01.ATV.0000203503.82693.c1.
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Uremia-Specific Effects in the Arterial Media During Development of Uremic Atherosclerosis in Apolipoprotein EDeficient Mice
Susanne Bro, Rehannah Borup, Claus B. Andersen, Flemming Moeller, Klaus Olgaard, and Lars B. Nielsen
Arterioscler Thromb Vasc Biol. 2006;26:570-575; published online before print December 22 2005, doi:10.1161/01.ATV.0000201060.47945.cb.
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To compare the molecular pathophysiology of classical and uremic atherosclerosis, we used high-density oligonucleotide microarray analysis to assess gene expression patterns in aortas from 5/6 nephrectomized and sham-operated apolipoprotein E-deficient mice. The results reveal that uremic vasculopathy, in addition to intimal atherosclerosis, is characterized by specific medial smooth muscle cell degeneration.
OxLDLIgG Immune Complexes Induce Survival of Human Monocytes
Riina Oksjoki, Petri T. Kovanen, Ken A. Lindstedt, Bo Jansson, and Markku O. Pentikäinen
Arterioscler Thromb Vasc Biol. 2006;26:576-583; published online before print December 22 2005, doi:10.1161/01.ATV.0000201041.14438.8d.
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Immune complexes containing oxidatively modified low-density lipoprotein (oxLDL) particles are deposited in human atherosclerotic lesions during atherogenesis. Here we show that OxLDL-IgG immune complexes (OxLDL-IgG ICs) promote the survival of monocytes, independently of produced M-CSF, by cross-linking Fc{gamma} receptor I and activating Akt-dependent survival signaling.
18
F-Choline Images Murine Atherosclerotic Plaques Ex Vivo
Christian M. Matter, Matthias T. Wyss, Patricia Meier, Nicolas Späth, Tobias von Lukowicz, Christine Lohmann, Bruno Weber, Ana Ramirez de Molina, Juan Carlos Lacal, Simon M. Ametamey, Gustav K. von Schulthess, Thomas F. Lüscher, Philipp A. Kaufmann, and Alfred Buck
Arterioscler Thromb Vasc Biol. 2006;26:584-589; published online before print December 15 2005, doi:10.1161/01.ATV.0000200106.34016.18.
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For imaging plaque biology, we compared ex vivo autoradiographies and fat stainings of murine atherosclerotic aortae after injections of 18F-fluorocholine (18F-FCH) or 18F-fluorodeoxyglucose (18F-FDG). En face macroscopical and histological correlations were better for 18F-FCH as compared with 18F-FDG. Thus, 18F-FCH may be a promising compound for imaging plaques in patients.
Apolipoproteins C-III and A-V as Predictors of Very-Low-Density Lipoprotein Triglyceride and Apolipoprotein B-100 Kinetics
Dick C. Chan, Gerald F. Watts, Minh N. Nguyen, and P. Hugh R. Barrett
Arterioscler Thromb Vasc Biol. 2006;26:590-596; published online before print January 12 2006, doi:10.1161/01.ATV.0000203519.25116.54.
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We investigated the associations between plasma VLDL-apoC-III and apoA-V concentrations and the kinetics of VLDL-apoB-100 and VLDL triglyceride in 15 men. Increased VLDL-apoC-III concentrations resulting from an overproduction of VLDL-apoC-III was a predictor of the delayed catabolism of VLDL triglyceride and VLDL-apoB. However, apo-V concentration was not significantly associated with VLDL kinetics.
Atherosclerosis Susceptibility Loci Identified From a Strain Intercross of Apolipoprotein EDeficient Mice via a High-Density Genome Scan
Jonathan D. Smith, Jeffrey M. Bhasin, Julie Baglione, Megan Settle, Yaomin Xu, and John Barnard
Arterioscler Thromb Vasc Biol. 2006;26:597-603; published online before print December 22 2005, doi:10.1161/01.ATV.0000201044.33220.5c.
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A strain intercross was performed between atherosclerosis sensitive DBA/2 and atherosclerosis resistant AKR apoE-deficient mice. Aortic root lesion area was ascertained for male and female F2 progeny. A high-density genome scan was performed using single-nucleotide polymorphism chips. Quantitative trait locus statistical analyses identified novel loci associated atherosclerosis susceptibility.
Pravastatin Inhibits Expression of Lectin-Like Oxidized Low-Density Lipoprotein Receptor-1 (LOX-1) in Watanabe Heritable Hyperlipidemic Rabbits: A New Pleiotropic Effect of Statins
Oliver Hofnagel, Birgit Luechtenborg, Heike Eschert, Gabriele Weissen-Plenz, Nicholas J. Severs, and Horst Robenek
Arterioscler Thromb Vasc Biol. 2006;26:604-610; published online before print December 22 2005, doi:10.1161/01.ATV.0000201073.45862.8b.
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The scavenger receptor LOX-1 seems to play a critical role in foam cell formation of macrophages and smooth muscle cells. Our study demonstrated in vivo inhibition of LOX-1 expression by pravastatin. This new pleiotropic effect of pravastatin might be one mechanism for the lipid core reducing effect of pravastatin in atherogenesis.
Metformin Inhibits Proinflammatory Responses and Nuclear Factor-
B in Human Vascular Wall Cells
Kikuo Isoda, James L. Young, Andreas Zirlik, Lindsey A. MacFarlane, Naotake Tsuboi, Norbert Gerdes, Uwe Schönbeck, and Peter Libby
Arterioscler Thromb Vasc Biol. 2006;26:611-617; published online before print December 29 2005, doi:10.1161/01.ATV.0000201938.78044.75.
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This study tested the hypothesis that metformin modulates inflammation in the atherosclerotic plaque by using cells that comprise these lesions. Metformin reduced elaboration of the pro-inflammatory cytokines IL-6 and IL-8 from activated smooth muscle cells, endothelial cells, and macrophages with concomitant impairment of NF-{kappa}B nuclear activation.
Reduced Immunoregulatory CD31
+
T Cells in Patients With Atherosclerotic Abdominal Aortic Aneurysm
Giuseppina Caligiuri, Patrick Rossignol, Pierre Julia, Emilie Groyer, Dikran Mouradian, Dominique Urbain, Namita Misra, Véronique Ollivier, Marc Sapoval, Pierre Boutouyrie, Srini V. Kaveri, Antonino Nicoletti, and Antoine Lafont
Arterioscler Thromb Vasc Biol. 2006;26:618-623; published online before print December 15 2005, doi:10.1161/01.ATV.0000200380.73876.d9.
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Cell-mediated immunity is considered to contribute to the pathogenesis of abdominal aortic aneurysms (AAA). In particular, infiltrating macrophages and CD8+ T lymphocytes participate in the destruction of the aortic wall extracellular matrix and smooth muscle cells. We surmise that these pathological events are controlled by circulating regulatory lymphocytes. Circulating CD4+/CD31+ T cells regulate macrophage and CD8+ T cell activation and effector function in the arterial wall. Their reduction might promote the development of AAA.
Effects of Rosiglitazone on Lipids, Adipokines, and Inflammatory Markers in Nondiabetic Patients With Low High-Density Lipoprotein Cholesterol and Metabolic Syndrome
Frederick F. Samaha, Philippe O. Szapary, Nayyar Iqbal, Monica M. Williams, LeAnne T. Bloedon, Arshneel Kochar, Megan L. Wolfe, and Daniel J. Rader
Arterioscler Thromb Vasc Biol. 2006;26:624-630; published online before print December 15 2005, doi:10.1161/01.ATV.0000200136.56716.30.
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We performed a 12-week, prospective, double-blinded study of 60 nondiabetic subjects with metabolic syndrome randomized to rosiglitazone or placebo. Rosiglitazone had direct effects on inflammatory markers and adipokines in the absence of favorable lipid effects. These findings may underly the possible antiatherosclerotic effects of rosiglitazone.
Lipoprotein-Associated Phospholipase A2 and Measures of Extracoronary Atherosclerosis: The Rotterdam Study
Isabella Kardys, Hok-Hay S. Oei, Irene M. van der Meer, Albert Hofman, Monique M.B. Breteler, and Jacqueline C.M. Witteman
Arterioscler Thromb Vasc Biol. 2006;26:631-636; published online before print December 22 2005, doi:10.1161/01.ATV.0000201289.83256.cf.
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Within the population-based Rotterdam Study, we investigated the association between lipoprotein-associated phospholipase A2 activity and presence of atherosclerosis as derived from common carotid intima-media thickness, carotid plaques, ankle-arm index, and aortic calcification. Associations were present after adjustment for age and sex. They strongly attenuated or even disappeared after adjustment for cholesterol.
Serum Lipoprotein Lipase Concentration and Risk for Future Coronary Artery Disease: The EPIC-Norfolk Prospective Population Study
Jaap Rip, Melchior C. Nierman, Nicholas J. Wareham, Robert Luben, Sheila A. Bingham, Nicholas E. Day, Joram N.I. van Miert, Barbara A. Hutten, John J.P. Kastelein, Jan Albert Kuivenhoven, Kay-Tee Khaw, and S. Matthijs Boekholdt
Arterioscler Thromb Vasc Biol. 2006;26:637-642; published online before print December 22 2005, doi:10.1161/01.ATV.0000201038.47949.56.
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Lipoprotein lipase (LPL) is associated with coronary artery disease (CAD) risk, but prospective population data are lacking. This study addresses the prospective association between LPL and future CAD through measuring LPL concentration in serum. The data indicated that reduced levels of serum LPL are associated with an increased risk for future CAD.
Occupation, Marital Status, and Low-Grade Inflammation: Mutual Confounding or Independent Cardiovascular Risk Factors?
Gunnar Engström, Bo Hedblad, Maria Rosvall, Lars Janzon, and Folke Lindgärde
Arterioscler Thromb Vasc Biol. 2006;26:643-648; published online before print December 15 2005, doi:10.1161/01.ATV.0000200100.14612.bb.
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We explored the relationships between inflammatory proteins, occupation, and marital status, and their independent associations with incidence of cardiovascular disease (CVD). Although the inflammatory proteins vary greatly by occupational and marital status, this does not confound the relationship between inflammatory proteins and incidence of CVD.
Increased Aortic Intima-Media Thickness in 11-Year-Old Healthy Children With Persistent
Chlamydia pneumoniae
Seropositivity
Iina Volanen, Mikko J. Järvisalo, Raija Vainionpää, Martti Arffman, Katariina Kallio, Susanna Anglé, Tapani Rönnemaa, Jorma Viikari, Jukka Marniemi, Olli T. Raitakari, and Olli Simell
Arterioscler Thromb Vasc Biol. 2006;26:649-655; published online before print January 5 2006, doi:10.1161/01.ATV.0000202664.76816.bb.
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We assessed whether the arterial intima-media thickness (IMT) and endothelial function, 2 measures of preclinical atherosclerosis, are related to Chlamydia pneumoniae (Cpn) seropositivity in healthy children. Eleven-year-old children with persistent Cpn seropositivity showed increased aortic IMT, suggesting that Cpn might contribute to the development of early atherosclerosis.
A Negative Carotid Plaque Area Test Is Superior to Other Noninvasive Atherosclerosis Studies for Reducing the Likelihood of Having Underlying Significant Coronary Artery Disease
Robert D. Brook, Robert L. Bard, Smita Patel, Melvyn Rubenfire, Nicholas S. Clarke, Ella A. Kazerooni, Thomas W. Wakefield, Peter K. Henke, and Kim A. Eagle
Arterioscler Thromb Vasc Biol. 2006;26:656-662; published online before print December 15 2005, doi:10.1161/01.ATV.0000200079.18690.60.
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Carotid plaque area was more sensitive, specific, and had a higher negative predictive value than coronary calcium, C-reactive protein, and carotid intima-media thickness for identifying coronary artery disease defined as a stenosis >=50% by computed tomography angiography.
Thrombosis
Shear Induces a Unique Series of Morphological Changes in Translocating Platelets: Effects of Morphology on Translocation Dynamics
Mhairi J. Maxwell, Sacha M. Dopheide, Samantha J. Turner, and Shaun P. Jackson
Arterioscler Thromb Vasc Biol. 2006;26:663-669; published online before print December 29 2005, doi:10.1161/01.ATV.0000201931.16535.e1.
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In this study we have examined GPIb/V/IX-dependent platelet morphological change during translocation on von Willebrand factor. We demonstrate that platelets undergo a unique series of morphological changes in response to increasing shear stress, which influence translocation dynamics. Alterations in shape may represent a novel mechanism of regulating platelet translocation dynamics under flow.
Glycoprotein Ib
Mediated Platelet Adhesion and Aggregation to Immobilized Thrombin Under Conditions of Flow
Cees Weeterings, Jelle Adelmeijer, Timothy Myles, Philip G. de Groot, and Ton Lisman
Arterioscler Thromb Vasc Biol. 2006;26:670-675; published online before print December 15 2005, doi:10.1161/01.ATV.0000200391.70818.a9.
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Recently, it was shown that platelets are able to adhere to immobilized thrombin under static conditions via GPIb{alpha}. Flow studies reveal that platelets are also able to adhere to thrombin immobilized on fibrin or directly on a glass coverslip, which is dependent on the interaction with GPIb{alpha}.
Letters to the Editor
Physiological Plasma Gas6 Levels Do Not Influence Platelet Aggregation
Sylvain Clauser, Christilla Bachelot-lozat, Pierre Fontana, Pascale Gaussem, Véronique Remones, Martine Aiach, and Delphine Borgel
Arterioscler Thromb Vasc Biol. 2006;26:e22, doi:10.1161/01.ATV.0000201968.72967.f9.
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Generation of an Adult Smooth Muscle CellTargeted Cre Recombinase Mouse Model
Jifeng Zhang, Wei Zhong, Taixing Cui, Maozhou Yang, Xing Hu, Kefeng Xu, Changqing Xie, Changyong Xue, Gary H. Gibbons, Chengyu Liu, Li Li, and Yuqing E. Chen
Arterioscler Thromb Vasc Biol. 2006;26:e23-e24; published online before print March 30 2006, doi:10.1161/01.ATV.0000202661.61837.93.
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Gene Therapy With Lipoprotein Lipase Variant S447X
Robert A. Hegele, Colin J.D. Ross, Jaap Twisk, Jan Albert Kuivenhoven, Jaap Rip, John J. Kastelein, and Michael R. Hayden
Arterioscler Thromb Vasc Biol. 2006;26:e25-e28, doi:10.1161/01.ATV.0000203502.01793.8d.
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In Response:
David Feinbloom and Kenneth A. Bauer
Arterioscler Thromb Vasc Biol. 2006;26:e29, doi:10.1161/01.ATV.0000204348.87254.cc.
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Prevalence and Pathology of Amyloid in Atherosclerotic Arteries
Christoph Röcken, Jörg Tautenhahn, Frank Bühling, Daniela Sachwitz, Steffi Vöckler, Andreas Goette, and Thomas Bürger
Arterioscler Thromb Vasc Biol. 2006;26:676-677, doi:10.1161/01.ATV.0000201930.10103.be.
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