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Arteriosclerosis, Thrombosis, and Vascular Biology
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Volume 26, Issue 8; August 1, 2006

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EditorialsBack

Clopidogrel Pharmacogenetics: Promising Steps Towards Patient Care?

Amber L. Beitelshees and Howard L. McLeod
Arterioscler Thromb Vasc Biol. 2006;26:1681-1683, doi:10.1161/01.ATV.0000232583.51472.73
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The Nine Lives of ACAT Inhibitors

Robert V. Farese, Jr
Arterioscler Thromb Vasc Biol. 2006;26:1684-1686, doi:10.1161/01.ATV.0000227511.35456.90
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Understanding Changes in High Density Lipoproteins During the Acute Phase Response

Brian J. Van Lenten, Srinivasa T. Reddy, Mohamad Navab, and Alan M. Fogelman
Arterioscler Thromb Vasc Biol. 2006;26:1687-1688, doi:10.1161/01.ATV.0000232522.47018.a6
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Soy Protein, Isoflavones, and Cardiovascular Health: A Summary of a Statement for Professionals From the American Heart Association Nutrition Committee

Frank M. Sacks, Alice Lichtenstein, Linda Van Horn, William Harris, Penny Kris-Etherton, Mary Winston for the AHA Nutrition Committee
Arterioscler Thromb Vasc Biol. 2006;26:1689-1692, doi:10.1161/01.ATV.0000227471.00284.ef
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Brief ReviewsBack

Ira J. Goldberg and Hayes M. Dansky
Arterioscler Thromb Vasc Biol. 2006;26:1693-1701; published online before print June 8 2006, doi:10.1161/01.ATV.0000231521.76545.f6
Abstract | Full Text | PDF
Despite a plethora of in vitro data showing toxic effects of hyperglycemia, accelerated atherosclerosis does not always accompany diabetes in animals. This might result from genetic differences, time course, or because risk factors, such as hyperlipidemia, are present and overwhelm any toxic effects of hyperglycemia.  

Kathryn J. Moore and Mason W. Freeman
Arterioscler Thromb Vasc Biol. 2006;26:1702-1711; published online before print May 25 2006, doi:10.1161/01.ATV.0000229218.97976.43
Abstract | Full Text | PDF
Atherosclerosis arises from the deposition and retention of serum lipoproteins in the artery wall. Macrophage scavenger receptors bind modified lipoproteins and promote cellular cholesterol accumulation in the artery wall. This review focuses on recent advances in scavenger receptor regulation and signal transduction, and highlights their roles in lipid accumulation and inflammation.  

Alex Bobik
Arterioscler Thromb Vasc Biol. 2006;26:1712-1720; published online before print May 4 2006, doi:10.1161/01.ATV.0000225287.20034.2c
Abstract | Full Text | PDF
TGF-ßs regulate diverse functions on vascular cells. They participate in atherosclerosis and restenosis regulating T-cell and smooth muscle cell functions. Defective signaling attributable to ALK-1 and endoglin mutations underlies development of hereditary hemorrhagic telangiectasia, whereas type II bone morphogenetic receptor mutations have been linked to primary pulmonary hypertension.  

Kevin D. O’Brien
Arterioscler Thromb Vasc Biol. 2006;26:1721-1728; published online before print May 18 2006, doi:10.1161/01.ATV.0000227513.13697.ac
Abstract | Full Text | PDF
Over the past 10 to 15 years, calcific aortic valve disease, which includes aortic sclerosis and aortic stenosis, has come to be recognized as an active process, based on numerous studies. These studies will be reviewed and organized into a proposed, global hypothesis for the pathogenesis of calcific aortic valve disease.  

James J. Hathcock
Arterioscler Thromb Vasc Biol. 2006;26:1729-1737; published online before print June 1 2006, doi:10.1161/01.ATV.0000229658.76797.30
Abstract | Full Text | PDF
Thrombosis occurs in a dynamic rheological field where flow conditions regulate the transport of coagulation factors, inhibitors, and cells. Hemodynamic forces regulate not only the predilection of specific anatomic sites to thrombosis but strongly influence the biochemical makeup of thrombi and the reaction pathways involved in thrombus formation.  

Ty E. Adams and James A. Huntington
Arterioscler Thromb Vasc Biol. 2006;26:1738-1745; published online before print May 25 2006, doi:10.1161/01.ATV.0000228844.65168.d1
Abstract | Full Text | PDF | Data Supplement
Substrate recognition by thrombin is largely controlled by cofactors, and crystal structures have now been reported for all of the thrombin-cofactor complexes. The purpose of this article is to summarize the features of these structures and to discuss the mechanisms and physiological relevance of cofactor binding in thrombin regulation.  

 

Vascular BiologyBack

Xiang-Yang Zhu, Elena Daghini, Alejandro R. Chade, Martin Rodriguez-Porcel, Claudio Napoli, Amir Lerman, and Lilach O. Lerman
Arterioscler Thromb Vasc Biol. 2006;26:1746-1752; published online before print May 18 2006, doi:10.1161/01.ATV.0000227469.40826.01
Abstract | Full Text | PDF | Data Supplement
The mechanisms of myocardial microvascular remodeling in early hypertension (HT) were investigated in pigs. Increased myocardial microvascular density in experimental HT was accompanied by tissue oxidative stress, inflammation, and altered growth factor expression, and attenuated by antioxidant intervention. This study underscores a role of increased oxidative stress in modulating myocardial microvascular architecture in early HT.  

Matthias Oelze, Ascan Warnholtz, Jörg Faulhaber, Philip Wenzel, Andrei L. Kleschyov, Meike Coldewey, Ulrich Hink, Olaf Pongs, Ingrid Fleming, Sven Wassmann, Thomas Meinertz, Heimo Ehmke, Andreas Daiber, and Thomas Münzel
Arterioscler Thromb Vasc Biol. 2006;26:1753-1759; published online before print June 8 2006, doi:10.1161/01.ATV.0000231511.26860.50
Abstract | Full Text | PDF | Data Supplement
Endothelium-dependent relaxation is compromised in mice lacking the ß1 subunit of the large conductance, Ca2+-activated K+ channel. Expression of the NADPH oxidase subunit p67phox and aortic superoxide are increased, but endothelial NO production is normal. Thus, BKß1 deletion induces endothelial dysfunction, at least in part, via NADPH oxidase-mediated ROS production.  

C.J.M. Loomans, H. Wan, R. de Crom, R. van Haperen, H.C. de Boer, P.J.M. Leenen, H.A. Drexhage, T.J. Rabelink, A.J. van Zonneveld, and F.J.T. Staal
Arterioscler Thromb Vasc Biol. 2006;26:1760-1767; published online before print May 25 2006, doi:10.1161/01.ATV.0000229243.49320.c9
Abstract | Full Text | PDF | Data Supplement
The lineage relationship of EPCs and other blood cells has remained elusive. Using eNOS-GFP transgenic mice, we show that EPCs share phenotypic and functional characteristics with myeloid cells and develop from myeloid precursors in the bone marrow. However, they have unique angiogenic function, providing a rationale for therapeutic neovascularization applications.  

H.-W. Cheng, A.F. James, R.R. Foster, J.C. Hancox, and D.O. Bates
Arterioscler Thromb Vasc Biol. 2006;26:1768-1776; published online before print June 8 2006, doi:10.1161/01.ATV.0000231518.86795.0f
Abstract | Full Text | PDF | Data Supplement
In human microvascular endothelial cells, VEGF activated a 27 pS, gadolinium-sensitive cation current, reversing at 0 mV, that was independent of calcium stores, IP3 receptors, or serine/threonine kinases. A similar current was activated by OAG and, in VEGFR2-TRPC3- and VEGFR2-TRPC6-transfected cells, by VEGF. VEGF activates a receptor-operated cation channel.  

Yabing Chen, Ralph C. Budd, Robert J. Kelm, Jr, Burton E. Sobel, and David J. Schneider
Arterioscler Thromb Vasc Biol. 2006;26:1777-1783; published online before print May 18 2006, doi:10.1161/01.ATV.0000227514.50065.2a
Abstract | Full Text | PDF
We determined that increased expression of PAI-1 increased proliferation of VSMCs. The balance between caspase-8 and FLIP favored proliferation when PAI-1 was increased. Thus, when vascular wall PAI-1 is increased, restenosis after coronary intervention is likely to be potentiated by greater proliferation of VSMCs and resistance to apoptosis.  

Manu O. Platt, Randall F. Ankeny, and Hanjoong Jo
Arterioscler Thromb Vasc Biol. 2006;26:1784-1790; published online before print May 18 2006, doi:10.1161/01.ATV.0000227470.72109.2b
Abstract | Full Text | PDF
Cathepsins have been implicated in vascular remodeling and atherosclerosis, but it is not known whether shear stress regulates them. Here, we show that atheroprotective laminar shear inhibits elastase and gelatinase activities in endothelial cells in a cathepsin L-dependent manner. This may protect vascular wall matrix integrity and prevent atherosclerosis.  

Satu Helske, Suvi Syväranta, Ken A. Lindstedt, Jani Lappalainen, Katariina Öörni, Mikko I. Mäyränpää, Jyri Lommi, Heikki Turto, Kalervo Werkkala, Markku Kupari, and Petri T. Kovanen
Arterioscler Thromb Vasc Biol. 2006;26:1791-1798; published online before print May 25 2006, doi:10.1161/01.ATV.0000228824.01604.63
Abstract | Full Text | PDF | Data Supplement
Here, we demonstrate increased expression and activity of the elastolytic cathepsins S, K, and V and their endogenous inhibitor cystatin C in stenotic aortic valves. These findings suggest that these cathepsins may participate in the adverse remodeling of the valves and accelerate the progression of aortic stenosis.  

Yasmin, Carmel M. McEniery, Kevin M. O’Shaughnessy, Patrick Harnett, Asif Arshad, Sharon Wallace, Kaisa Maki-Petaja, Barry McDonnell, Mike J. Ashby, John Brown, John R. Cockcroft, and Ian B. Wilkinson
Arterioscler Thromb Vasc Biol. 2006;26:1799-1805; published online before print May 18 2006, doi:10.1161/01.ATV.0000227717.46157.32
Abstract | Full Text | PDF
We examined the influence of known MMP-9 polymorphisms on arterial stiffness and elastases in a large cohort of healthy individuals. Aortic stiffness and serum elastases are significantly influenced by MMP-9 polymorphisms, suggesting that genetic variation in this protein may be involved in the process of large artery stiffening.  

 

Atherosclerosis and LipoproteinsBack

Chang Yeop Han, Tsuyoshi Chiba, Jean S. Campbell, Nelson Fausto, Michelle Chaisson, Gabriela Orasanu, Jorge Plutzky, and Alan Chait
Arterioscler Thromb Vasc Biol. 2006;26:1806-1813; published online before print May 18 2006, doi:10.1161/01.ATV.0000227472.70734.ad
Abstract | Full Text | PDF | Data Supplement
Stimulation of cultured hepatocytes with proinflammatory cytokines increased the expression of SAA and concurrently inhibited apoA-I and PON-1 expression. Thus, changes in the regulation of these HDL apolipoproteins could account for changes in HDL composition during inflammation rather than displacement of apoA-I and PON-1 by SAA.  

Thomas A. Bell, III, J. Mark Brown, Mark J. Graham, Kristina M. Lemonidis, Rosanne M. Crooke, and Lawrence L. Rudel
Arterioscler Thromb Vasc Biol. 2006;26:1814-1820; published online before print May 4 2006, doi:10.1161/01.ATV.0000225289.30767.06
Abstract | Full Text | PDF
Liver-specific inhibition of acyl-CoA:cholesterol acyltransferase 2 using antisense oligonucleotides was found to be effective in reducing plasma cholesterol, increasing plasma triglycerides, and shifting LDL cholesteryl ester fatty acids to become mainly polyunsaturated. These changes resulted in a reduction of aortic atherosclerosis in apoB100-only LDLr-/- mice.  

Roshni R. Singaraja, Bjorn Stahmer, May Brundert, Martin Merkel, Joerg Heeren, Nagat Bissada, Martin Kang, Jenelle M. Timmins, Rajasekhar Ramakrishnan, John S. Parks, Michael R. Hayden, and Franz Rinninger
Arterioscler Thromb Vasc Biol. 2006;26:1821-1827; published online before print May 25 2006, doi:10.1161/01.ATV.0000229219.13757.a2
Abstract | Full Text | PDF | Data Supplement
The role of ABCA1 in HDL metabolism was investigated with doubly radiolabeled HDL. In mice with transgenic expression of ABCA1 or in mice with deletions of this transport protein, it is shown that ABCA1 has a substantial effect on HDL turnover in plasma and on HDL catabolism by the liver.  

Kathy L.E. Klos, Charles F. Sing, Eric Boerwinkle, Sara C. Hamon, Thomas J. Rea, Andrew Clark, Myriam Fornage, and James E. Hixson
Arterioscler Thromb Vasc Biol. 2006;26:1828-1836; published online before print June 8 2006, doi:10.1161/01.ATV.0000231523.19199.45
Abstract | Full Text | PDF | Data Supplement
To identify common gene variations with a consistent influence we evaluated 262 SNPs in 54 genes for association with 6 plasma lipid and apolipoprotein traits. We identified 14 SNPs and 9 gene regions with genotype effects.  

Marianna Papaspyridonos, Alberto Smith, Kevin G. Burnand, Peter Taylor, Soundrie Padayachee, Keith E. Suckling, Christian H. James, David R. Greaves, and Lisa Patel
Arterioscler Thromb Vasc Biol. 2006;26:1837-1844; published online before print June 1 2006, doi:10.1161/01.ATV.0000229695.68416.76
Abstract | Full Text | PDF | Data Supplement
Differential gene expression in stable and unstable plaque was assessed by whole transcriptome analysis. Intraplaque analysis by QT-PCR confirmed the differential expression of 18 genes not associated previously with plaque rupture. These genes may represent novel targets for the treatment of unstable plaque or useful diagnostic markers of plaque instability.  

Tina Raj, Peter Kanellakis, Giovanna Pomilio, Garry Jennings, Alex Bobik, and Alex Agrotis
Arterioscler Thromb Vasc Biol. 2006;26:1845-1851; published online before print May 18 2006, doi:10.1161/01.ATV.0000227689.41288.5e
Abstract | Full Text | PDF | Data Supplement
To assess the significance of fibroblast growth factors (FGFs) and their receptors (FGFRs) for atherosclerosis, we inhibited this system in apoE-/- mice. Such inhibition markedly reduced smooth muscle cell and macrophage accumulation, attenuated atherosclerotic lesion severity, and greatly reduced FGFR-1 phosphorylation. Thus, FGF:FGFR-1 signaling promotes the development of atherosclerotic lesions.  

Ken Kitajima, Dawn H.L. Marchadier, Gwen C. Miller, Guang-ping Gao, James M. Wilson, and Daniel J. Rader
Arterioscler Thromb Vasc Biol. 2006;26:1852-1857; published online before print June 8 2006, doi:10.1161/01.ATV.0000231520.26490.54
Abstract | Full Text | PDF
Intravenous administration of AAV2/7- and AAV2/8-apoE vectors effectively mediated robust and sustained hepatic-specific expression of apoE in apoE-deficient mice, resulting in complete prevention of atherosclerosis at 1 year.  

Stéphane Potteaux, Christophe Combadière, Bruno Esposito, Cedric Lecureuil, Hafid Ait-Oufella, Régine Merval, Patrice Ardouin, Alain Tedgui, and Ziad Mallat
Arterioscler Thromb Vasc Biol. 2006;26:1858-1863; published online before print June 8 2006, doi:10.1161/01.ATV.0000231527.22762.71
Abstract | Full Text | PDF | Data Supplement
CC chemokine receptor CCR5 is expressed by atheroma-associated cells and could mediates leukocyte attraction into developing lesions. We examined the role of bone marrow-derived CCR5 the in the development of atherosclerotic lesions after 8, 12, or 35 weeks of high-fat diet in low-density lipoprotein-receptor-deficient mice. We showed that bone marrow-derived CCR5 favors the development of an inflammatory and collagen-poor plaque phenotype in association with decreased macrophage-derived IL-10 and enhanced T cell-derived TNF-{alpha}. These effects were not sustained in the very advanced stages of atherosclerosis.  

Oscar López-Franco, Purificación Hernández-Vargas, Guadalupe Ortiz-Muñoz, Guillermo Sanjuán, Yusuke Suzuki, Luis Ortega, Julia Blanco, Jesús Egido, and Carmen Gómez-Guerrero
Arterioscler Thromb Vasc Biol. 2006;26:1864-1870; published online before print June 1 2006, doi:10.1161/01.ATV.0000229659.94020.53
Abstract | Full Text | PDF | Data Supplement
PTN inhibits the NF-{kappa}B activation and expression of regulated genes in cultured VSMCs and monocytes. PTN protects against the development of atherosclerosis in apoE mice by inhibition of NF-{kappa}B and reduction of inflammatory cell infiltration. PTN treatment may represent a novel therapeutic approach to atherosclerosis.  

Pontus Boström, Björn Magnusson, Per-Arne Svensson, Olov Wiklund, Jan Borén, Lena M. S. Carlsson, Marcus Ståhlman, Sven-Olof Olofsson, and Lillemor Mattsson Hultén
Arterioscler Thromb Vasc Biol. 2006;26:1871-1876; published online before print June 1 2006, doi:10.1161/01.ATV.0000229665.78997.0b
Abstract | Full Text | PDF | Data Supplement
Exposure of human macrophages to hypoxia resulted in an increased accumulation of cytosolic lipid droplets containing triglycerides. This accumulation was attributable to increased triglyceride biosynthesis, reduced ß-oxidation of fatty acids, and increased expression of ADRP.  

Catharine R. Gale, Benyu Jiang, Sian M. Robinson, Keith M. Godfrey, Catherine M. Law, and Christopher N. Martyn
Arterioscler Thromb Vasc Biol. 2006;26:1877-1882; published online before print May 25 2006, doi:10.1161/01.ATV.0000228819.13039.b8
Abstract | Full Text | PDF
A restricted maternal diet during gestation can lead to endothelial dysfunction in animals. We studied the relation between maternal diet during pregnancy and IMT in children. IMT was greater in children whose mothers had lower energy intakes. Lower maternal energy intake during pregnancy may increase the susceptibility to atherogenesis of children.  

Markus Juonala, Jorma S.A. Viikari, Tapani Rönnemaa, Leena Taittonen, Jukka Marniemi, and Olli T. Raitakari
Arterioscler Thromb Vasc Biol. 2006;26:1883-1888; published online before print May 25 2006, doi:10.1161/01.ATV.0000228818.11968.7a
Abstract | Full Text | PDF
Recent findings have supported the view that inflammation has an integral part in the pathophysiology of atherosclerosis. In the present study, childhood C-reactive protein (CRP) values predict weakly but significantly adult CRP, and this association is independent of other metabolic risk factors. Unlike conventional risk factors measured in childhood, CRP does not predict adult intima-media thickness.  

Lukasz Rzeszutko, Jacek Legutko, Grzegorz L. Kaluza, Marcin Wizimirski, Angela Richter, Michal Chyrchel, Grzegorz Heba, Jacek S. Dubiel, and Dariusz Dudek
Arterioscler Thromb Vasc Biol. 2006;26:1889-1894; published online before print June 15 2006, doi:10.1161/01.ATV.0000232500.93340.54
Abstract | Full Text | PDF
We performed an intracoronary thermography study in 40 arteries responsible for ACS. Temperature gradient between culprit and nonculprit segments was observed only when transient blood flow interruption occurred during thermography. Because of the blood cooling effect on the arterial wall the novel thermography system failed to differentiate lesions at risk.  

 

ThrombosisBack

Dominick J. Angiolillo, Antonio Fernandez-Ortiz, Esther Bernardo, Celia Ramírez, Ugo Cavallari, Elisabetta Trabetti, Manel Sabaté, Rosana Hernández, Raul Moreno, Javier Escaned, Fernando Alfonso, Camino Bañuelos, Marco A. Costa, Theodore A. Bass, Pier Franco Pignatti, and Carlos Macaya
Arterioscler Thromb Vasc Biol. 2006;26:1895-1900; published online before print April 27 2006, doi:10.1161/01.ATV.0000223867.25324.1a
Abstract | Full Text | PDF | Data Supplement
Gene sequence variations of CYP3A4 have been suggested to contribute to clopidogrel responsiveness. Carriers of the IVS10+12A allele had reduced GP IIb/IIIa activation (P=0.025) in the steady phase of treatment and more optimal responsiveness (P=0.003) after loading dose administration. In conclusion, genetic variations of CYP3A4 may contribute clopidogrel response variability.  

Wolfhart Kreuz, Monika Stoll, Ralf Junker, Achim Heinecke, Rosemarie Schobess, Karin Kurnik, Reinhard Kelsch, and Ulrike Nowak-Göttl
Arterioscler Thromb Vasc Biol. 2006;26:1901-1906; published online before print May 18 2006, doi:10.1161/01.ATV.0000227510.36653.ed
Abstract | Full Text | PDF
Case-control study measuring FVIII in children experiencing DVT. FVIII values were elevated in patients. The odds ratio for FVIII above the 90th percentile was increased in DVT patients. The heritable(h2)/household(c2) components were calculated for FVIII:Ag levels (h2, 0.48{+/-}0.15; c2, 0.21), and FVIII:C (h2, 0.61{+/-}0.15; c2, 0.41).  

John V. Mitsios, Maria P. Vini, Dominique Stengel, Ewa Ninio, and Alexandros D. Tselepis
Arterioscler Thromb Vasc Biol. 2006;26:1907-1913; published online before print May 25 2006, doi:10.1161/01.ATV.0000228821.79588.ef
Abstract | Full Text | PDF | Data Supplement
Activated platelets secrete the plasma type of platelet-activating factor acetylhydrolase (PAF-AH) primarily associated with platelet-derived microparticles (PMPs) in vitro. Importantly, the enzyme activity is also detected on circulating PMPs in normolipidemic plasma, suggesting that the PMP-associated PAF-AH may play a role in the dissemination of biological activities mediated by these particles.  

Marlies de Lange, Toby Andrew, Harold Snieder, Dongliang Ge, T. Simon Futers, Kristina Standeven, Tim D. Spector, Peter J. Grant, and Robert A.S. Ariëns
Arterioscler Thromb Vasc Biol. 2006;26:1914-1919; published online before print June 8 2006, doi:10.1161/01.ATV.0000231538.60223.92
Abstract | Full Text | PDF
A joint test of linkage and association of 6 single-nucleotide polymorphisms in the factor XIII-A subunit gene, genotyped in 201 dizygotic female white twin pairs, indicates that a common variant (V34L) in the factor XIII-A subunit gene is the main functional variant influencing factor XIII activation.  

Yoshiji Yamada, Norifumi Metoki, Hidemi Yoshida, Kei Satoh, Sahoko Ichihara, Kimihiko Kato, Takashi Kameyama, Kiyoshi Yokoi, Hitoshi Matsuo, Tomonori Segawa, Sachiro Watanabe, and Yoshinori Nozawa
Arterioscler Thromb Vasc Biol. 2006;26:1920-1925; published online before print June 1 2006, doi:10.1161/01.ATV.0000229694.97827.38
Abstract | Full Text | PDF | Data Supplement
The relations of 202 gene polymorphisms to atherothrombotic cerebral infarction, intracerebral hemorrhage, or subarachnoid hemorrhage were examined. Multivariable logistic regression analysis revealed significant associations of IL6 genotype with both atherothrombotic cerebral infarction and intracerebral hemorrhage and of genotypes for UCP3, TNF, and PKD1-like with subarachnoid hemorrhage.  

 

Letters to the EditorBack

Effect of Atorvastatin on Plasma Osteopontin Levels in Patients With Hypercholesterolemia

Nobukiyo Tanaka, Yukihiko Momiyama, Reiko Ohmori, Atsushi Yonemura, Makoto Ayaori, Masatsune Ogura, Shojiro Sawada, Masatoshi Kusuhara, Haruo Nakamura, and Fumitaka Ohsuzu
Arterioscler Thromb Vasc Biol. 2006;26:e129-e130, doi:10.1161/01.ATV.0000229701.42828.73
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Nox2 Is Determinant for Ischemia-Induced Oxidative Stress and Arterial Vasodilatation: A Pilot Study in Patients With Hereditary Nox2 Deficiency

F. Violi, V. Sanguigni, L. Loffredo, R. Carnevale, B. Buchetti, A. Finocchi, M. Tesauro, P. Rossi, and P. Pignatelli
Arterioscler Thromb Vasc Biol. 2006;26:e131-e132, doi:10.1161/01.ATV.0000229710.13054.2d
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Pioglitazone Reduces Endothelial Microparticles in the Metabolic Syndrome

Katherine Esposito, Miryam Ciotola, and Dario Giugliano
Arterioscler Thromb Vasc Biol. 2006;26:1926, doi:10.1161/01.ATV.0000231512.15115.25
Extract | Full Text | PDF  

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