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Arteriosclerosis, Thrombosis, and Vascular Biology
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Volume 24, Issue 8; August 1, 2004

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EditorialsBack

A Summary of Implications of Recent Clinical Trials for the National Cholesterol Education Program Adult Treatment Panel III Guidelines

Scott M. Grundy, James I. Cleeman, C. Noel Bairey Merz, H. Bryan Brewer, Jr, Luther T. Clark, Donald B. Hunninghake, Richard C. Pasternak, Sidney C. Smith, Jr, Neil J. Stone for the Coordinating Committee of the National Cholesterol Education Program
Arterioscler Thromb Vasc Biol. 2004;24:1329-1330, doi:10.1161/01.ATV.0000139012.45265.e0
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Aortic Valve: Turning Over a New Leaf(let) in Endothelial Phenotypic Heterogeneity

Peter F. Davies, Anthony G. Passerini, and Craig A. Simmons
Arterioscler Thromb Vasc Biol. 2004;24:1331-1333, doi:10.1161/01.ATV.0000130659.89433.c1
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How Does Mutant Proprotein Convertase Neural Apoptosis-Regulated Convertase 1 Induce Autosomal Dominant Hypercholesterolemia?

Pernilla Jirholt, Martin Adiels, and Jan Borén
Arterioscler Thromb Vasc Biol. 2004;24:1334-1336, doi:10.1161/01.ATV.0000133682.97348.ff
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The Mystery of PCSK9

Alan D. Attie
Arterioscler Thromb Vasc Biol. 2004;24:1337-1339, doi:10.1161/01.ATV.0000137288.82390.04
Extract | Full Text | PDF  

 

Brief ReviewsBack

ATVB In Focus: Diabetic Vascular Disease: Pathophysiological Mechanisms in the Diabetic Milieu and Therapeutic Implications

Richard A. Cohen
Arterioscler Thromb Vasc Biol. 2004;24:1340-1341, doi:10.1161/01.ATV.0000137187.16206.79
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Yoshifumi Naka, Loredana G. Bucciarelli, Thoralf Wendt, Larisse K. Lee, Ling Ling Rong, Ravichandran Ramasamy, Shi Fang Yan, and Ann Marie Schmidt
Arterioscler Thromb Vasc Biol. 2004;24:1342-1349; published online before print May 20 2004, doi:10.1161/01.ATV.0000133191.71196.90
Abstract | Full Text | PDF
Ligand engagement of the receptor for advanced glycation end products (RAGE) evokes vascular inflammation and perturbation. In diabetes, when fueled by oxidation, hyperglycemia, and superimposed stresses, the ligand-RAGE axis accelerates atherosclerosis and neointimal expansion. Studies in rodent models of diabetes suggest that testing the impact of RAGE blockade in human subjects is logical.  

Ken A. Lindstedt, Markus J. Leskinen, and Petri T. Kovanen
Arterioscler Thromb Vasc Biol. 2004;24:1350-1358; published online before print June 10 2004, doi:10.1161/01.ATV.0000135322.78008.55
Abstract | Full Text | PDF
Acute atherothrombotic events relate to erosion and rupture of unstable coronary plaques. Plaque stability critically depends on the integrity of the pericellular matrix (PCM) regulating plaque cell survival. By secreting PCM-degrading proteases, infiltrating macrophages, T-lymphocytes, and mast cells trigger plaque cell apoptosis, linking inflammation-dependent proteolysis with plaque erosion and rupture.  

Jian Liu, Galina K. Sukhova, Jiu-Song Sun, Wei-Hua Xu, Peter Libby, and Guo-Ping Shi
Arterioscler Thromb Vasc Biol. 2004;24:1359-1366; published online before print June 3 2004, doi:10.1161/01.ATV.0000134530.27208.41
Abstract | Full Text | PDF
Atherosclerosis is an inflammatory disease characterized by extensive remodeling of the extracellular matrix architecture of the arterial wall. Although matrix metalloproteinases and serine proteases participate in these pathologic events, recent data from atherosclerotic patients and animals suggest the participation of lysosomal cysteine proteases in atherogenesis.  

Frank M. Faraci and Sean P. Didion
Arterioscler Thromb Vasc Biol. 2004;24:1367-1373; published online before print May 27 2004, doi:10.1161/01.ATV.0000133604.20182.cf
Abstract | Full Text | PDF
Recent studies have begun to define the role of specific isoforms of superoxide dismutase (SOD) in vascular biology. This review focuses on the role of SODs in vessels in health and disease. This area is important because reactive oxygen species are thought to play a major role in vascular pathophysiology.  

Marlies Van de Wouwer, Désiré Collen, and Edward M. Conway
Arterioscler Thromb Vasc Biol. 2004;24:1374-1383; published online before print June 3 2004, doi:10.1161/01.ATV.0000134298.25489.92
Abstract | Full Text | PDF  

 

Vascular BiologyBack

Keiko Kawai-Kowase, Hiroko Sato, Yuko Oyama, Hiroyoshi Kanai, Mahito Sato, Hiroshi Doi, and Masahiko Kurabayashi
Arterioscler Thromb Vasc Biol. 2004;24:1384-1390; published online before print June 24 2004, doi:10.1161/01.ATV.0000136548.17816.07
Abstract | Full Text | PDF | Data Supplement
TGFß1 induces SMC gene expression through an increase in SRF gene expression, which activates CArG-dependent transcription, and Src-tyrosine kinase is required for such an induction in 10T1/2 cells and vascular SMC. bFGF antagonizes TGFß1-induced SMC gene expression, although MEK1 activation without interfering with SRF:DNA binding activity and SRF gene expression.  

Natalia Kalinina, Alex Agrotis, Yulia Antropova, Olga Ilyinskaya, Vladimir Smirnov, Eduard Tararak, and Alex Bobik
Arterioscler Thromb Vasc Biol. 2004;24:1391-1396; published online before print May 27 2004, doi:10.1161/01.ATV.0000133605.89421.79
Abstract | Full Text | PDF | Data Supplement
The actions of TGF-ß in human atherosclerotic lesions were defined by examining the expression of Smad proteins in relation to TGF-ß-mediated responses. Expression of Smad proteins was restricted to macrophages of fibrofatty lesions and SMCs of fibrous plaques. Smad-dependent TGF-ß signaling appeared to be impaired SMCs of fibrofatty lesions.  

Gaia Spinetti, Mingyi Wang, Robert Monticone, Jing Zhang, Di Zhao, and Edward G. Lakatta
Arterioscler Thromb Vasc Biol. 2004;24:1397-1402; published online before print June 3 2004, doi:10.1161/01.ATV.0000134529.65173.08
Abstract | Full Text | PDF | Data Supplement
This study demonstrates that MCP-1 and CCR2 are increased within the thickened aortas of older rats. In early-passage VSMCs from young rats, MCP-1 increased migration and invasion, imparting to these cells the characteristics of VSMCs from older rat aorta. Thus, MCP-1/CCR2 may be implicated in age-associated vascular remodeling.  

Lihua Chen, Günter Daum, Kanchan Chitaley, Scott A. Coats, Daniel F. Bowen-Pope, Martin Eigenthaler, Naresh R. Thumati, Ulrich Walter, and Alexander W. Clowes
Arterioscler Thromb Vasc Biol. 2004;24:1403-1408; published online before print June 3 2004, doi:10.1161/01.ATV.0000134705.39654.53
Abstract | Full Text | PDF | Data Supplement
This study investigated the effects of VASP and VASP phosphorylation at serine157 and serine239 on smooth muscle cell proliferation and nitric oxide-mediated growth inhibition. Our data suggest that VASP is a modulator of smooth muscle cell growth by integrating positive and negative signals that target different phosphorylation sites of VASP.  

Hisanori Kosuge, Jun-ichi Suzuki, Tsunekazu Kakuta, Go Haraguchi, Noritaka Koga, Hideki Futamatsu, Ryo Gotoh, Manabu Inobe, Mitsuaki Isobe, and Toshimitsu Uede
Arterioscler Thromb Vasc Biol. 2004;24:1409-1415; published online before print June 3 2004, doi:10.1161/01.ATV.0000134645.53285.02
Abstract | Full Text | PDF | Data Supplement
The role of the LIGHT pathway in the progression of graft arterial disease (GAD) is not yet evaluated. We demonstrate that blockade of the LIGHT pathway plays important roles in the regulation not only of T cell activation but also of smooth muscle cell proliferation, resulting in prevention of GAD.  

Kurt Wallner, Chen Li, Prediman K. Shah, Kai-Jin Wu, Stephen M. Schwartz, and Behrooz G. Sharifi
Arterioscler Thromb Vasc Biol. 2004;24:1416-1421; published online before print June 3 2004, doi:10.1161/01.ATV.0000134299.89599.53
Abstract | Full Text | PDF | Data Supplement
Tenascin-C was found to undergo fragmentation in cultured smooth muscle cells and in human atherosclerotic plaques generating a fragment that contains the epidermal growth factor-like domain of tenascin-C. Recombinant epidermal growth factor-like domain of tenascin-C induces apoptosis of cultured smooth muscle cells, an activity that was blocked by chymotrypsin inhibitor and MMP inhibitor.  

Kousei Tanaga, Hideaki Bujo, Yanjuan Zhu, Tatsuro Kanaki, Satoshi Hirayama, Kazuo Takahashi, Masahiro Inoue, Keiji Mikami, Wolfgang J. Schneider, and Yasushi Saito
Arterioscler Thromb Vasc Biol. 2004;24:1422-1428; published online before print May 27 2004, doi:10.1161/01.ATV.0000133607.80554.09
Abstract | Full Text | PDF
LDL receptor relatives (LRs) in atherosclerosis have gained new focus because of the specific expression of these receptors in the thickened intima. LRP1B modulates the migration of SMCs by increasing the degradation of uPAR and PDGFR. This functional characterization of LRP1B elucidates the (patho)physiological significance of SMC migration in plaques.  

Jonathan T. Butcher, Andrea M. Penrod, Andrés J. García, and Robert M. Nerem
Arterioscler Thromb Vasc Biol. 2004;24:1429-1434; published online before print April 29 2004, doi:10.1161/01.ATV.0000130462.50769.5a
Abstract | Full Text | PDF | Data Supplement
Endothelial cells native to the aortic valve may play an important role in mediating tissue responses to the complex fluid environment, and may therefore respond to fluid flow in a different manner than more characterized vascular endothelial cells. These differences in response to mechanical forces suggest a unique phenotype of valvular endothelial cells not mimicked by vascular endothelial cells, and could have implications for cardiovascular cell biology and cell-source considerations for tissue-engineered valvular substitutes.  

Christian Kupatt, Chantal Dessy, Rabea Hinkel, Philip Raake, Géraldine Daneau, Caroline Bouzin, Peter Boekstegers, and Olivier Feron
Arterioscler Thromb Vasc Biol. 2004;24:1435-1441; published online before print June 3 2004, doi:10.1161/01.ATV.0000134300.87476.d1
Abstract | Full Text | PDF | Data Supplement
Percutaneous liposome-based Hsp90 gene transfer in a pig cardiac infarct model was shown to preserve the myocardium from the deleterious effects of ischemia-reperfusion. The gain in cardiac function was dependent on Hsp90-driven regulation of eNOS phosphorylation by Akt and calcineurin, thereby establishing Hsp90 as a promising target for cardiac diseases.  

Takahisa Kondo, Mutsuharu Hayashi, Kyosuke Takeshita, Yasushi Numaguchi, Koichi Kobayashi, Shigeo Iino, Yasuya Inden, and Toyoaki Murohara
Arterioscler Thromb Vasc Biol. 2004;24:1442-1447; published online before print June 10 2004, doi:10.1161/01.ATV.0000135655.52088.c5
Abstract | Full Text | PDF
We examined the effects of smoking and smoking cessation on endothelial progenitor cell (EPC) levels. Circulating EPCs were quantified by flow cytometry using cell surface markers CD45lowCD34+CD133+VEGFR2+. The EPC levels decreased as the cigarette consumption increased. EPCs increased rapidly after cessation and decreased again after resumption of smoking.  

 

Atherosclerosis and LipoproteinsBack

Khadija Ouguerram, Maud Chetiveaux, Yassine Zair, Philippe Costet, Marianne Abifadel, Mathilde Varret, Catherine Boileau, Thierry Magot, and Michel Krempf
Arterioscler Thromb Vasc Biol. 2004;24:1448-1453; published online before print May 27 2004, doi:10.1161/01.ATV.0000133684.77013.88
Abstract | Full Text | PDF
Kinetic study using [2H3] leucine was conducted in 2 subjects with PCSK9 mutation and in controls. Patients exhibited a dramatic increase in the production rate of apolipoprotein B100 in VLDL, IDL, and LDL, a decrease in VLDL and IDL conversion rate, and a slight decrease in LDL fractional catabolic rate.  

Geneviève Dubuc, Ann Chamberland, Hanny Wassef, Jean Davignon, Nabil G. Seidah, Lise Bernier, and Annik Prat
Arterioscler Thromb Vasc Biol. 2004;24:1454-1459; published online before print June 3 2004, doi:10.1161/01.ATV.0000134621.14315.43
Abstract | Full Text | PDF
The gene PCSK9, encoding NARC-1, has been implicated recently in autosomal dominant hypercholesterolemia. Using real-time polymerase chain reaction, we showed that PCSK9 is regulated by cholesterol in HepG2 cells and in human primary hepatocytes. PCSK9 promoter contains the typical elements for sterol regulation.  

Hilke Wientgen, Fayanne E. Thorngate, Sabina Omerhodzic, Linda Rolnitzky, John T. Fallon, David L. Williams, and Edward A. Fisher
Arterioscler Thromb Vasc Biol. 2004;24:1460-1465; published online before print June 3 2004, doi:10.1161/01.ATV.0000134297.61979.3c
Abstract | Full Text | PDF | Data Supplement
Using transgenic mice expressing different levels of plasma apoE, we have shown that after arterial injury, subphysiological apoE levels were associated with reduced intima-to-media (I/M) ratios of lesions. Lipid levels were not associated with reduced I/M ratios, consistent with previous mouse studies of apoE and atherosclerosis progression.  

Jiang Yang, Kaori Sato, Tamar Aprahamian, Nathaniel J. Brown, Jack Hutcheson, Ann Bialik, Harris Perlman, and Kenneth Walsh
Arterioscler Thromb Vasc Biol. 2004;24:1466-1473; published online before print June 3 2004, doi:10.1161/01.ATV.0000134402.94963.2f
Abstract | Full Text | PDF
Fas ligand (FasL) can induce apoptosis in cells bearing the Fas receptor. This study examined the function of endothelial FasL during atherosclerosis. Overexpression of endothelial FasL transgene significantly reduced atherosclerotic lesion areas in aortae. Overexpression of endothelial FasL is antiinflammatory and inhibits atherosclerosis under hypercholesterolemic conditions.  

Stéphane Potteaux, Bruno Esposito, Olivia van Oostrom, Valérie Brun, Patrice Ardouin, Hervé Groux, Alain Tedgui, and Ziad Mallat
Arterioscler Thromb Vasc Biol. 2004;24:1474-1478; published online before print June 3 2004, doi:10.1161/01.ATV.0000134378.86443.cd
Abstract | Full Text | PDF | Data Supplement
Here we show that IL-10 deficiency in leukocytes induced 2-fold increase in lesion development in the thoracic aorta of LDLr -/- mice compared with controls. Furthermore, IL-10 deficiency led to a marked increase in the accumulation of both lymphocytes and macrophages, associated with a significant reduction in collagen accumulation. Finally, transfer of IL-10-/- splenocytes to LDLr-/- mice resulted in a 3-fold increase in lesion size in the aortic sinus in comparison with mice transplanted with IL-10+/+ splenocytes.  

Tanya L. Medley, Timothy J. Cole, Anthony M. Dart, Christoph D. Gatzka, and Bronwyn A. Kingwell
Arterioscler Thromb Vasc Biol. 2004;24:1479-1484; published online before print June 10 2004, doi:10.1161/01.ATV.0000135656.49158.95
Abstract | Full Text | PDF
Coronary artery disease patients that carry at least 1 copy of the MMP-9 T allele have stiffer large arteries compared with C/C homozygotes. This relationship may result from increased degradation of important elastic components of the extracellular matrix secondary to elevated MMP-9 gene expression and protein levels in the aorta.  

Mahmoud Zureik, Pilar Galan, Sandrine Bertrais, Louise Mennen, Sébastien Czernichow, Jacques Blacher, Pierre Ducimetière, and Serge Hercberg
Arterioscler Thromb Vasc Biol. 2004;24:1485-1491; published online before print June 24 2004, doi:10.1161/01.ATV.0000136648.62973.c8
Abstract | Full Text | PDF | Data Supplement
Limited data exist from randomized trials evaluating, noninvasively, the impact of antioxidant supplementation on vascular structure and function. The results of this large-scale study suggest no beneficial effects of long-term supplementation of antioxidant vitamins and minerals on carotid atherosclerosis and arterial stiffness in 1162 apparently healthy individuals (at baseline) in France.  

Ming-Lin Liu, Kati Ylitalo, Riitta Salonen, Jukka T. Salonen, and Marja-Riitta Taskinen
Arterioscler Thromb Vasc Biol. 2004;24:1492-1497; published online before print June 17 2004, doi:10.1161/01.ATV.0000135982.60383.48
Abstract | Full Text | PDF
Ox-LDL, susceptibility of LDL to oxidation in vitro, plasma 8-isoprostane, and antioxidants, lipids and lipoproteins, LDL particle size, and carotid IMT were measured to investigate the determinants of Ox-LDL and its association with carotid IMT in 150 asymptomatic FCHL family members. Serum LDL cholesterol, apoB, and 8-isoprostane levels were the most important determinants of Ox-LDL. Ox-LDL is independently associated with carotid IMT in asymptomatic FCHL family members and can be used as a marker of early atherosclerosis in FCHL.  

Gunnar Engström, Bo Hedblad, Lars Stavenow, Susanna Jonsson, Peter Lind, Lars Janzon, and Folke Lindgärde
Arterioscler Thromb Vasc Biol. 2004;24:1498-1502; published online before print June 3 2004, doi:10.1161/01.ATV.0000134293.31512.be
Abstract | Full Text | PDF
This population-based study explored whether inflammation-sensitive plasma proteins (ISPs) (ie, fibrinogen, orosomucoid, {alpha}1-antitrypsin, haptoglobin, ceruloplasmin) modify the obesity-associated risk of myocardial infarction and stroke in initially healthy men (n=6075) followed-up over 18 years. The cardiovascular risk varied widely between obese and overweight men with high and low ISPs.  

S. Matthijs Boekholdt, Ron J. G. Peters, C. Erik Hack, Nicholas E. Day, Robert Luben, Sheila A. Bingham, Nicholas J. Wareham, Pieter H. Reitsma, and Kay-Tee Khaw
Arterioscler Thromb Vasc Biol. 2004;24:1503-1508; published online before print June 3 2004, doi:10.1161/01.ATV.0000134294.54422.2e
Abstract | Full Text | PDF
Using a prospective nested case-control study among apparently healthy individuals, we found that high plasma levels of IL-8 were predictive for the risk of future coronary artery disease, independent of traditional risk factors and C-reactive protein levels.  

Sonia S. Anand, Fahad Razak, Qilong Yi, Bonnie Davis, Ruby Jacobs, Vlad Vuksan, Eva Lonn, Koon Teo, Matthew McQueen, and Salim Yusuf
Arterioscler Thromb Vasc Biol. 2004;24:1509-1515; published online before print June 17 2004, doi:10.1161/01.ATV.0000135845.95890.4e
Abstract | Full Text | PDF
CRP varies substantially between people of different ethnic origin. Compared with Europeans, Aboriginals, South Asians, and Chinese have significantly different CRP distributions, which are influenced by metabolic factors including abdominal adiposity, body weight, and HbA1c. CRP is independently associated with CVD across all populations.  

Kwang Kon Koh, Mi-Seung Shin, Ichiro Sakuma, Jeong Yeal Ahn, Dong Kyu Jin, Hyung Sik Kim, Dae Sung Kim, Seung Hwan Han, Wook-Jin Chung, and Eak Kyun Shin
Arterioscler Thromb Vasc Biol. 2004;24:1516-1521; published online before print May 27 2004, doi:10.1161/01.ATV.0000133683.65877.bc
Abstract | Full Text | PDF
Fifty-seven women received micronized progesterone 100 mg with either conjugated equine estrogen 0.625 mg (C-HRT) or 0.3 mg (L-HRT) daily for 2 months. Compared with C-HRT, L-HRT has comparable effects on lipoproteins, flow-mediated dilation, and PAI-1 antigen levels. However, L-HRT did not increase hsCRP or F1+2 levels.  

Shiro Kitamoto, Kaku Nakano, Yasuhiko Hirouchi, Yoshiro Kohjimoto, Shunichi Kitajima, Makoto Usui, Shujiro Inoue, and Kensuke Egashira
Arterioscler Thromb Vasc Biol. 2004;24:1522-1528; published online before print June 3 2004, doi:10.1161/01.ATV.0000134518.27241.da
Abstract | Full Text | PDF
Treatment with pravastatin reduced plaque size and changed characteristics of plaques to more stable phenotype in cynomolgus monkeys with established atherosclerotic lesion independent of cholesterol lowering. Equivalent inhibitory effects were observed in animals that received anti-MCP-1 therapy. An antiinflammatory mechanism might be involved in the pleiotropic chloesterol-lowering independent antiatherosclerotic effects of pravastatin.  

 

ThrombosisBack

Gordon D.O. Lowe, Ann Rumley, Alex D. McMahon, Ian Ford, Denis St. J. O’Reilly, Christopher J. Packard for the West of Scotland Coronary Prevention Study Group
Arterioscler Thromb Vasc Biol. 2004;24:1529-1534; published online before print June 17 2004, doi:10.1161/01.ATV.0000135995.39488.6c
Abstract | Full Text | PDF
We compared fibrin D-dimer, IL-6, coagulation factors VII and XIIa, and C-reactive protein in prediction of coronary risk in a case-control study from the West of Scotland Coronary Prevention Study. Although D-dimer correlated with IL-6 and C-reactive protein, only D-dimer showed a significant independent relationship with coronary risk.  

 

NCEP ReportBack

Scott M. Grundy, James I. Cleeman, C. Noel Bairey Merz, H. Bryan Brewer, Jr, Luther T. Clark, Donald B. Hunninghake, Richard C. Pasternak, Sidney C. Smith, Jr, Neil J. Stone, for the Coordinating Committee of the National Cholesterol Education Program Endorsed by the National Heart, Lung, and Blood Institute, American College of Cardiology Foundation, and American Heart Association
Arterioscler Thromb Vasc Biol. 2004;24:e149-e161, doi:10.1161/01.ATV.0000133317.49796.0E
Abstract | Full Text | PDF  

 

Letters to the EditorBack

Common Polymorphism in the MTP Promoter Attenuates the Dyslipidemic and Proatherogenic Effects of Excess Body Weight

Andrei C. Sposito, Sophie Gonbert, Gerard Turpin, M. John Chapman, and Joëlle Thillet
Arterioscler Thromb Vasc Biol. 2004;24:e143, doi:10.1161/01.ATV.0000136549.23994.b8
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Associations Among Plasma Lipoprotein Subfractions as Characterized by Analytical Capillary Isotachophoresis, Apolipoprotein E Phenotype, Alzheimer Disease, and Mild Cognitive Impairment

Bo Zhang, Akira Matsunaga, Keijiro Saku, Seigo Nakano, and Tatsuo Yamada
Arterioscler Thromb Vasc Biol. 2004;24:e144, doi:10.1161/01.ATV.0000134391.01498.b8
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Is There Really a Power Shortage in Clinical Trials Testing the "Homocysteine Hypothesis?"

G.J. Hankey, J.W. Eikelboom, K. Loh, Q. Yi, J. Pizzi, M. Tang, S. Hickling, M. Le, C.J. M. Klijn, P. Dusitanond, F. van Bockxmeer, A. Gelavis, R. Baker, and K. Jamrozik
Arterioscler Thromb Vasc Biol. 2004;24:e147, doi:10.1161/01.ATV.0000136385.50973.68
Extract | Full Text | PDF  

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