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Arteriosclerosis, Thrombosis, and Vascular Biology
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Volume 28, Issue 3; March 1, 2008

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EditorialsBack

Wnt Pathway: A New Role in Regulation of Inflammation

Sarah Jane George
Arterioscler Thromb Vasc Biol. 2008;28:400-402, doi:10.1161/ATVBAHA.107.160952
Full Text | PDF  

 

Brief ReviewsBack

David Varga-Szabo, Irina Pleines, and Bernhard Nieswandt
Arterioscler Thromb Vasc Biol. 2008;28:403-412; published online before print January 3 2008, doi:10.1161/ATVBAHA.107.150474
Abstract | Full Text | PDF
At sites of vascular injury, platelets attach to the exposed extracellular matrix by a complex series of events involving different receptors and their signaling pathways, most notably the vWF receptor GPIb-V-IX and the collagen receptor GPVI, which induce the activation of β1 and β3 integrins and subsequent firm adhesion.  

 

Integrative Physiology/Experimental MedicineBack

Robert D. McBane, II, Robert J. Leadley, Jr, Sangita M. Baxi, Krzysztof Karnicki, and Waldemar Wysokinski
Arterioscler Thromb Vasc Biol. 2008;28:413-418; published online before print December 20 2007, doi:10.1161/ATVBAHA.107.158691
Abstract | Full Text | PDF | Additional Material
In a porcine model of iliac venous stenting, the oral direct Factor Xa inhibitor PD0348292 promptly and completely inhibited thrombosis. Aspirin or clopidogrel had no significant effect on stent thrombosis, indicating that platelet accretion in these thrombi appear to involve pathways distinct from arachidonate metabolism or ADP P2Y12 receptor activation.  

Isabelle Marx, Peter J. Lenting, Thure Adler, Ronan Pendu, Olivier D. Christophe, and Cécile V. Denis
Arterioscler Thromb Vasc Biol. 2008;28:419-424; published online before print January 10 2008, doi:10.1161/ATVBAHA.107.159442
Abstract | Full Text | PDF | Additional Materials
To study von Willebrand factor (vWF) structure-function relationship in vivo, we have expressed wild-type and mutant vWF by hydrodynamic injection in vWF-deficient mice. Wild-type vWF and vWF carrying mutations in its collagen and platelet glycoprotein (GP) IIbIIIa binding sites were able to correct bleeding symptoms in the knockout mice.  

Eric Lancelot, Vardan Amirbekian, Irène Brigger, Jean-Sébastien Raynaud, Sébastien Ballet, Christelle David, Olivier Rousseaux, Soizic Le Greneur, Marc Port, Henri R. Lijnen, Patrick Bruneval, Jean-Baptiste Michel, Tanja Ouimet, Bernard Roques, Smbat Amirbekian, Fabien Hyafil, Esad Vucic, Juan Gilberto S. Aguinaldo, Claire Corot, and Zahi A. Fayad
Arterioscler Thromb Vasc Biol. 2008;28:425-432; published online before print February 7 2008, doi:10.1161/ATVBAHA.107.149666
Abstract | Full Text | PDF | Additional Materials
Noninvasively assessing MMPs in atherosclerosis may aid in evaluating plaque stability. In controlled experiments we tested the molecular MRI probe, P947, which specifically targets MMPs. We showed that P947 significantly improved the ability of MRI to delineate atherosclerosis and was associated with higher uptake in MMP-rich versus MMP-poor human plaques.  

Marianna Papaspyridonos, Eileen McNeill, Joe P. de Bono, Alberto Smith, Kevin G. Burnand, Keith M. Channon, and David R. Greaves
Arterioscler Thromb Vasc Biol. 2008;28:433-440; published online before print December 20 2007, doi:10.1161/ATVBAHA.107.159160
Abstract | Full Text | PDF
Galectin-3 was upregulated in advanced human and murine ApoE-/- atherosclerotic plaques. Mediators released in response to Gal-3 treatment in macrophages increased monocyte chemotaxis, and microarray analysis confirmed the upregulation of several key chemoattractant molecules. Gal-3 is an amplifier of inflammation that could be used as a marker of atherosclerotic plaque progression or target for atherosclerosis.  

Suzanne J. House and Harold A. Singer
Arterioscler Thromb Vasc Biol. 2008;28:441-447; published online before print December 20 2007, doi:10.1161/ATVBAHA.107.156810
Abstract | Full Text | PDF | Additional Materials
We observed CaMKII isoform modulation in rat carotid artery in response to vascular injury. Attenuating CaMKII{delta}2 upregulation using siRNA significantly decreased neointima formation and adventitial thickening. This finding is significant in that it provides a link whereby alterations in Ca2+ signaling directly contribute to vascular injury and disease.  

Weiqing Tang, Yinyan Ma, Lin Jia, Yiannis A. Ioannou, Joanna P. Davies, and Liqing Yu
Arterioscler Thromb Vasc Biol. 2008;28:448-454; published online before print January 10 2008, doi:10.1161/ATVBAHA.107.160465
Abstract | Full Text | PDF | Additional Materials
T0901317 increased fecal cholesterol excretion but failed to raise plasma HDL cholesterol in mice lacking NPC1L1. Because NPC1L1 is essential for cholesterol absorption and exclusively expressed in intestine in mice, this finding suggests that intestinal cholesterol absorption is required for an LXR agonist to raise plasma HDL cholesterol in mice.  

Mayumi Takahashi, Yaeko Hiyama, Masayoshi Yokoyama, Shuiqing Yu, Yunying Hu, Kristan Melford, André Bensadoun, and Ira J. Goldberg
Arterioscler Thromb Vasc Biol. 2008;28:455-462; published online before print February 7 2008, doi:10.1161/ATVBAHA.107.153239
Abstract | Full Text | PDF | Additional Materials
Expressing human lipoprotein lipase (LpL) in endothelial cells allows for survival of LpL knockout mice. Although under control conditions, expression of this transgene did not alter inflammatory gene expression in arteries, after TNF-{alpha} treatment there was greater expression of inflammatory molecules and reduced arterial vasodilatation.  

Marcel Liberman, Estêvão Bassi, Marina Kamla Martinatti, Fábio Cerqueira Lario, João Wosniak, Jr, Pablo M.A. Pomerantzeff, and Francisco R.M. Laurindo
Arterioscler Thromb Vasc Biol. 2008;28:463-470; published online before print December 27 2007, doi:10.1161/ATVBAHA.107.156745
Abstract | Full Text | PDF | Additional Materials
We investigated whether oxidants contribute to aortic valve (AV) calcification/stenosis progression. In rabbit model and human AV stenosis, superoxide and NADPH oxidase subunits strongly increased around AV-calcifying foci. Nox4mRNA was increased. Lipoic acid decreased, whereas tempol increased calcification progression in vivo and in vitro. Hydrogen peroxide was implicated in calcification progression.  

 

Cell Biology/SignalingBack

Shani Shilo, Sashwati Roy, Savita Khanna, and Chandan K. Sen
Arterioscler Thromb Vasc Biol. 2008;28:471-477; published online before print February 7 2008, doi:10.1161/ATVBAHA.107.160655
Abstract | Full Text | PDF | Additional Materials
A Dicer knockdown approach was used to test the significance of miRNA in regulating the redox state and angiogenic response of human microvascular endothelial cells. This study provides the first evidence that p47phox function and redox signaling in human endothelial cells is subject to regulation by miRNA.  

Johann Kern, Monika Bauer, Kathrin Rychli, Johann Wojta, Andreas Ritsch, Günther Gastl, Eberhard Gunsilius, and Gerold Untergasser
Arterioscler Thromb Vasc Biol. 2008;28:478-484; published online before print January 10 2008, doi:10.1161/ATVBAHA.107.160432
Abstract | Full Text | PDF | Additional Materials
Alternative splicing of the Vasohibin (VASH1) pre-mRNA transcript in endothelial cells generates a potent antiangiogenic protein (VASH1B). VASH1B is predominantly located in the nucleus and cytoplasm and inhibits proliferation, migration, and tube formation of human endothelial cells in vitro and vessel growth in the chicken chorioallantoic membrane in vivo.  

Si Jin, Yang Zhang, Fan Yi, and Pin-Lan Li
Arterioscler Thromb Vasc Biol. 2008;28:485-490; published online before print December 27 2007, doi:10.1161/ATVBAHA.107.159772
Abstract | Full Text | PDF | Additional Materials
Besides its proapototic effects, EST is also able to induce endothelial dysfunction. This early-stage action of EST is associated with LR clustering and consequent assembling and activation of NADPH oxidase.  

Cindy Gustin, Edouard Delaive, Marc Dieu, Damien Calay, and Martine Raes
Arterioscler Thromb Vasc Biol. 2008;28:491-497; published online before print December 27 2007, doi:10.1161/ATVBAHA.107.158642
Abstract | Full Text | PDF | Additional Materials
Starting from a 2D-gel analytical approach, we demonstrated a LPA-induced pentraxin-3 overexpression in endothelial cells. LPA- but also oxLDL-induced pentraxin-3 upregulation was reduced in the presence of an antagonist of the LPA-receptors and was largely dependent on NF{kappa}B activation. Finally, we demonstrated the chemotactic activity of pentraxin-3 on monocytes THP-1.  

Stefan P. Kastl, Walter S. Speidl, Christoph Kaun, Katharina M. Katsaros, Gersina Rega, Taras Afonyushkin, Valery N. Bochkov, Peter Valent, Afshin Assadian, Georg W. Hagmueller, Martina Hoeth, Rainer de Martin, Yongsheng Ma, Gerald Maurer, Kurt Huber, and Johann Wojta
Arterioscler Thromb Vasc Biol. 2008;28:498-503; published online before print January 10 2008, doi:10.1161/ATVBAHA.107.160580
Abstract | Full Text | PDF
C5a increased the expression of the gp130 ligand oncostatin-M (OSM) in monocytes, monocyte-derived macrophages, and plaque macrophages through the C5a receptor and through a putative AP-1 site in the OSM promoter. This link between the complement system and the gp130 system might impact on the pathology of inflammatory diseases.  

Claudia Pereira, Dominik J. Schaer, Esther B. Bachli, Michael O. Kurrer, and Gabriele Schoedon
Arterioscler Thromb Vasc Biol. 2008;28:504-510; published online before print January 3 2008, doi:10.1161/ATVBAHA.107.157438
Abstract | Full Text | PDF | Additional Materials
Gene expression profiling in human macrophages exposed to LPS and INF-{gamma} in the presence or absence of recombinant APC or IL-10 identified Wnt5A as one of the most prominently regulated transcripts by these mediators. Wnt5A is critically involved in inflammatory macrophage signaling in sepsis.  

Emily A. Van Vré, Hidde Bult, Vicky Y. Hoymans, Viggo F.I. Van Tendeloo, Christiaan J. Vrints, and Johan M. Bosmans
Arterioscler Thromb Vasc Biol. 2008;28:511-518; published online before print January 24 2008, doi:10.1161/ATVBAHA.107.157016
Abstract | Full Text | PDF | Additional Materials
C-reactive protein (CRP), a predictor of cardiovascular disease (CVD), was tested as modulator of dendritic cells (DCs). Exposure to CRP induced DC activation, DC-mediated T-cell proliferation, and IFN-{gamma} production. Immunohistochemistry could demonstrate DC/CRP colocalization in human plaques. This suggests that CRP in CVD patients can influence DC function during atherogenesis.  

Xinwen Wang, Dan Liao, Uddalak Bharadwaj, Min Li, Qizhi Yao, and Changyi Chen
Arterioscler Thromb Vasc Biol. 2008;28:519-526; published online before print December 20 2007, doi:10.1161/ATVBAHA.107.159467
Abstract | Full Text | PDF | Additional Materials
The objective of this study was to determine the effects and potential mechanisms of C-reactive protein (CRP) on cholesterol efflux from human macrophage foam cells, which may play a critical role in atherogenesis. CRP inhibits cholesterol efflux from human foam cells derived from THP-1 and PBMCs in vitro though oxidative stress, ERK1/2 activation, and downregulation of intracellular cholesterol transport molecules ABCA-1 and ABCG-1.  

Minjia Zhu, Yi Fu, Yingjian Hou, Nanping Wang, Youfei Guan, Chaoshu Tang, John Y.-J. Shyy, and Yi Zhu
Arterioscler Thromb Vasc Biol. 2008;28:527-533; published online before print December 20 2007, doi:10.1161/ATVBAHA.107.143487
Abstract | Full Text | PDF
The expression of LXRs and their target genes was increased in the atheroprotective area of mouse aorta and in endothelial cells under a laminar flow in vitro. This effect was attenuated by inhibitions of LXR{alpha}, CYP27, and PPAR{gamma}. Thus, laminar flow increases LXR function via a PPAR{gamma}-CYP27-dependent mechanism.  

Robert Pape, Bernhard H. Rauch, Anke C. Rosenkranz, Gernot Kaber, and Karsten Schrör
Arterioscler Thromb Vasc Biol. 2008;28:534-540; published online before print December 27 2007, doi:10.1161/ATVBAHA.107.159483
Abstract | Full Text | PDF | Additional Materials
PAR-1 mediates thrombin-induced mitogenesis in vascular SMCs. This study reports transcriptional downregulation of PAR-1 by the PGI2 mimetic iloprost at low nanomolar concentrations in human vascular SMCs. This may be relevant for the vascular response to injury in vivo to control thrombin-induced neointima formation.  

Rangnath Mishra and Michael S. Simonson
Arterioscler Thromb Vasc Biol. 2008;28:541-547; published online before print December 20 2007, doi:10.1161/ATVBAHA.107.157339
Abstract | Full Text | PDF
Here, we demonstrate that the free fatty acid oleate induces a myofibroblast phenotype in microvascular pericytes. This oleate-induced conversion suggests a mechanism whereby elevated free fatty acids could affect a profibrotic shift in pericyte phenotype and microvascular remodeling.  

James P. Corsetti, Dan Ryan, Arthur J. Moss, David L. Rainwater, Wojciech Zareba, and Charles E. Sparks
Arterioscler Thromb Vasc Biol. 2008;28:548-554; published online before print December 20 2007, doi:10.1161/ATVBAHA.107.155556
Abstract | Full Text | PDF
To provide information generally not available regarding recurrent risk beyond incident myocardial infarction in nonhyperlipidemic postinfarction patients, 37 genetic markers and 17 blood markers associated with CVD were assessed for risk using multivariable modeling. Only the 4G/5G polymorphism in the PAI-1 promoter region was associated with risk.  

 

Letters to the EditorBack

Matrix Metalloproteinase-8 and Tissue Inhibitor of Metalloproteinase-1 in Serum Do Not Reflect the Analytes Circulating in Blood

Klaus Jung
Arterioscler Thromb Vasc Biol. 2008;28:e15-e16; published online before print November 29 2007, doi:10.1161/ATVBAHA.107.158790
Full Text | PDF  

Matrix Metalloproteinase-8 and Tissue Inhibitor of Metalloproteinase-1 in Serum Do Not Reflect the Analytes Circulating in Blood

A.M. Tuomainen, K. Nyyssönen, T. Tervahartiala, T. Sorsa, and P.J. Pussinen
Arterioscler Thromb Vasc Biol. 2008;28:e17, doi:10.1161/ATVBAHA.107.159277
Full Text | PDF  

Dual Therapy With Statins and Antioxidants Is Superior to Statins Alone in Decreasing the Risk of Cardiovascular Disease in a Subgroup of Middle-Aged Individuals With Both Diabetes Mellitus and the Haptoglobin 2-2 Genotype

Shany Blum, Uzi Milman, Chen Shapira, Rachel Miller-Lotan, Lawrence Bennett, Maria Kostenko, Michele Landau, Shlomo Keidar, Yishai Levy, Alexander Khemlin, Arman Radan, and Andrew P. Levy
Arterioscler Thromb Vasc Biol. 2008;28:e18-e20, doi:10.1161/ATVBAHA.107.159905
Full Text | PDF  

Circulating Endothelial Progenitor Cells Exhibit Diurnal Variation

Honey E. Thomas, Rachael Redgrave, Michael S. Cunnington, Peter Avery, Bernard D. Keavney, and Helen M. Arthur
Arterioscler Thromb Vasc Biol. 2008;28:e21-e22, doi:10.1161/ATVBAHA.107.160317
Full Text | PDF  

 

Venous Thromboembolism: Mechanisms, Treatment and Public AwarenessBack

Venous Thromboembolism: A Need for More Public Awareness and Research Into Mechanisms

Stephan Moll and Nigel Mackman
Arterioscler Thromb Vasc Biol. 2008;28:367-369, doi:10.1161/ATVBAHA.108.163097
Full Text | PDF Free Article  

The Epidemiology of Venous Thromboembolism in the Community

John A. Heit
Arterioscler Thromb Vasc Biol. 2008;28:370-372, doi:10.1161/ATVBAHA.108.162545
Full Text | PDF Free Article  

A Clinical Perspective of Venous Thromboembolism

Stephan Moll
Arterioscler Thromb Vasc Biol. 2008;28:373-379, doi:10.1161/ATVBAHA.108.162818
Full Text | PDF Free Article  

Peter L. Gross and Jeffrey I. Weitz
Arterioscler Thromb Vasc Biol. 2008;28:380-386, doi:10.1161/ATVBAHA.108.162677
Abstract | Full Text | PDF Free Article  

Thomas W. Wakefield, Daniel D. Myers, and Peter K. Henke
Arterioscler Thromb Vasc Biol. 2008;28:387-391, doi:10.1161/ATVBAHA.108.162289
Abstract | Full Text | PDF Free Article  

National Heart, Lung, and Blood Institute Programs for Deep Vein Thrombosis

Rebecca P. Link
Arterioscler Thromb Vasc Biol. 2008;28:392-393, doi:10.1161/ATVBAHA.108.162461
Full Text | PDF Free Article  

CDC Division of Blood Disorders: Public Health Research Activities in Venous Thromboembolism

Michele G. Beckman, Sara E. Critchley, W. Craig Hooper, Althea M. Grant, and Roshni Kulkarni
Arterioscler Thromb Vasc Biol. 2008;28:394-395, doi:10.1161/ATVBAHA.108.162453
Full Text | PDF Free Article  

Patient Advocacy to Promote Public Awareness About Thrombosis and Thrombophilia

Randolph Fenninger
Arterioscler Thromb Vasc Biol. 2008;28:396-397, doi:10.1161/ATVBAHA.107.161802
Full Text | PDF Free Article  

Awareness and Politics of Venous Thromboembolism in the United Kingdom

Beverley J. Hunt
Arterioscler Thromb Vasc Biol. 2008;28:398-399, doi:10.1161/ATVBAHA.108.162586
Full Text | PDF Free Article  

 

Translational Therapeutics at the Platelet Vascular Interface: A CME-Certified ActivityBack

CME Information and Table of Contents.


Arterioscler Thromb Vasc Biol. 2008;28:s0-s2, doi:10.1161/ATVBAHA.108.162701
PDF Free Article  

Introduction

Garret A. FitzGerald
Arterioscler Thromb Vasc Biol. 2008;28:s3-s4, doi:10.1161/ATVBAHA.108.162198
Full Text | PDF Free Article  

Andreas E. May, Peter Seizer, and Meinrad Gawaz
Arterioscler Thromb Vasc Biol. 2008;28:s5-s10; published online before print January 3 2008, doi:10.1161/ATVBAHA.107.158915
Abstract | Full Text | PDF Free Article  

Jane E. Freedman
Arterioscler Thromb Vasc Biol. 2008;28:s11-s16; published online before print January 3 2008, doi:10.1161/ATVBAHA.107.159178
Abstract | Full Text | PDF Free Article  

Guy A. Zimmerman and Andrew S. Weyrich
Arterioscler Thromb Vasc Biol. 2008;28:s17-s24, doi:10.1161/ATVBAHA.107.160218
Abstract | Full Text | PDF Free Article  

Carlo Patrono and Bianca Rocca
Arterioscler Thromb Vasc Biol. 2008;28:s25-s32; published online before print January 3 2008, doi:10.1161/ATVBAHA.107.160481
Abstract | Full Text | PDF Free Article  

Alan D. Michelson
Arterioscler Thromb Vasc Biol. 2008;28:s33-s38; published online before print January 3 2008, doi:10.1161/ATVBAHA.107.160689
Abstract | Full Text | PDF Free Article  

Hyung-Hwan Kim and James K. Liao
Arterioscler Thromb Vasc Biol. 2008;28:s39-s42; published online before print January 3 2008, doi:10.1161/ATVBAHA.107.160226
Abstract | Full Text | PDF Free Article  

Lawrence F. Brass, Li Zhu, and Timothy J. Stalker
Arterioscler Thromb Vasc Biol. 2008;28:s43-s50; published online before print January 3 2008, doi:10.1161/ATVBAHA.107.161026
Abstract | Full Text | PDF Free Article  

Summary

Garret A. FitzGerald
Arterioscler Thromb Vasc Biol. 2008;28:s51-s52, doi:10.1161/ATVBAHA.108.162206
Full Text | PDF Free Article  

CME Post-Test, Evaluation, and Request for Credit.


Arterioscler Thromb Vasc Biol. 2008;28:s53-s56, doi:10.1161/ATVBAHA.108.162784
PDF Free Article  

 

Clinical and Population StudiesBack

Zehra Pamuklar, Jin Sun Lee, Hsin-Yuan Cheng, Manikandan Panchatcharam, Steve Steinhubl, Andrew J. Morris, Richard Charnigo, and Susan S. Smyth
Arterioscler Thromb Vasc Biol. 2008;28:555-561; published online before print January 17 2008, doi:10.1161/ATVBAHA.107.151837
Abstract | Full Text | PDF | Additional Materials
The bioactive lipid mediator lysophosphatidic acid stimulates actin reorganization and aggregation of human platelets. We report that LPA may trigger an inhibitory response in platelets from {approx}20% of healthy individuals. Furthermore, we provide evidence that the presence of coronary artery disease may attenuate this inhibitory pathway.  

Marc S. Sabatine, Lynn Ploughman, Katy L. Simonsen, Olga A. Iakoubova, Todd G. Kirchgessner, Koustubh Ranade, Zenta Tsuchihashi, Kim E. Zerba, Diane U. Long, Carmen H. Tong, Christopher J. Packard, Marc A. Pfeffer, James J. Devlin, James Shepherd, Hannia Campos, Frank M. Sacks, and Eugene Braunwald
Arterioscler Thromb Vasc Biol. 2008;28:562-567; published online before print January 3 2008, doi:10.1161/ATVBAHA.107.156653
Abstract | Full Text | PDF | Additional Materials
In men not on pravastatin, those homozygous for the 227Pro allele of the ADAMTS1 metalloproteinase gene had a nearly 2-fold increased risk of death or MI compared with noncarriers. In this high-risk group, treatment with pravastatin was highly efficacious, reducing the odds of death or MI by approximately 75%, as compared with 25% in noncarriers or heterozygotes.  

Fabian Bamberg, Nina Dannemann, Michael D. Shapiro, Sujith K. Seneviratne, Maros Ferencik, Javed Butler, Wolfgang Koenig, Khurram Nasir, Ricardo C. Cury, Ahmed Tawakol, Stephan Achenbach, Thomas J. Brady, and Udo Hoffmann
Arterioscler Thromb Vasc Biol. 2008;28:568-574; published online before print January 3 2008, doi:10.1161/ATVBAHA.107.155010
Abstract | Full Text | PDF | Additional Materials
We assessed the association between cardiovascular risk factors and noncalcified- (NCAP) and calcified coronary atherosclerotic plaque (CAP). A small proportion of individuals have exclusively NCAP (6%) but the relation of NCAP and CAP changes with age. Only family history of CAD and hyperlipidemia may be associated with the extent of NCAP.  

Stefania Lamon-Fava, David M. Herrington, David M. Reboussin, Michelle Sherman, Katalin V. Horvath, L. Adrienne Cupples, Charles White, Serkalem Demissie, Ernst J. Schaefer, and Bela F. Asztalos
Arterioscler Thromb Vasc Biol. 2008;28:575-579; published online before print January 3 2008, doi:10.1161/ATVBAHA.107.157123
Abstract | Full Text | PDF
We measured plasma levels of remnant lipoproteins and HDL subpopulations in 256 postmenopausal women with angiographic evidence of coronary heart disease. The degree of coronary atherosclerosis was positively associated with both remnant lipoprotein levels and preβ1 HDL levels and inversely associated with {alpha}2 HDL levels, but not with TG or HDL cholesterol. Subpopulations of TG-rich and HDL lipoproteins are better predictors of CHD severity than TG and HDL-cholesterol levels.  

Mireia Junyent, Rosa Gilabert, Daniel Zambón, Miguel Pocoví, Miguel Mallén, Montserrat Cofán, Isabel Núñez, Fernando Civeira, Diego Tejedor, and Emilio Ros
Arterioscler Thromb Vasc Biol. 2008;28:580-586; published online before print December 20 2007, doi:10.1161/ATVBAHA.107.153841
Abstract | Full Text | PDF | Additional Materials
Femoral intima-media thickness (IMT) was assessed in 146 patients with molecularly defined familial hypercholesterolemia (FH) and 193 controls. IMT was increased in FH patients versus controls. Compared with receptor-defective or APOB defects, receptor-negative genotype showed higher IMT, independently of LDL cholesterol. Genetic testing is useful in FH beyond securing diagnosis.  

Philippe Giral, Nelly Jacob, Caroline Dourmap, Boris Hansel, Alain Carrié, Eric Bruckert, Xavier Girerd, and M. John Chapman
Arterioscler Thromb Vasc Biol. 2008;28:587-593; published online before print January 17 2008, doi:10.1161/ATVBAHA.107.157891
Abstract | Full Text | PDF
We evaluated components of the plasma redox system in dyslipidemic patients with metabolic syndrome as a function of the number of qualifying criteria. Our findings suggest that metabolic syndrome is characterized by elevated GGT activity which is in turn associated with a cascade of abnormalities in the thiol redox system.  

Giuliana Fortunato, Maria Donata Di Taranto, Umberto Marcello Bracale, Luca Del Guercio, Francesca Carbone, Cristina Mazzaccara, Alberto Morgante, Francesco Paolo D’Armiento, Maria D’Armiento, Massimo Porcellini, Lucia Sacchetti, Giancarlo Bracale, and Francesco Salvatore
Arterioscler Thromb Vasc Biol. 2008;28:594-600; published online before print February 7 2008, doi:10.1161/ATVBAHA.107.154658
Abstract | Full Text | PDF | Additional Materials
We measured the expression of the PON2, 5-LO, and FLAP genes in carotid atherosclerotic plaques. PON2 mRNA and protein progressively decreased with plaque severity, whereas 5LO and FLAP mRNA increased. We also show that oxidative stress downregulates PON2 mRNA expression, thus suggesting its role in atherosclerotic process.  

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