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Arteriosclerosis, Thrombosis, and Vascular Biology
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Volume 27, Issue 1; January 1, 2007

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EditorialsBack

Arteriosclerosis, Thrombosis, and Vascular Biology, 1999–2007

Donald D. Heistad for the Editors
Arterioscler Thromb Vasc Biol. 2007;27:1-3, doi:10.1161/01.ATV.0000254152.71507.89.
Full Text | PDF  

Gamma-Glutamyl Transferase: Another Biomarker for Metabolic Syndrome and Cardiovascular Risk

Scott M. Grundy
Arterioscler Thromb Vasc Biol. 2007;27:4-7, doi:10.1161/01.ATV.0000253905.13219.4b.
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Homocysteinylation of Metallothionein Impairs Intracellular Redox Homeostasis: The Enemy Within!

Stephen M. Colgan and Richard C. Austin
Arterioscler Thromb Vasc Biol. 2007;27:8-11, doi:10.1161/01.ATV.0000254151.00086.26.
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Nox 4 Regulation of Vascular Smooth Muscle Cell Differentiation Marker Gene Expression

Hamid Deliri and Coleen A. McNamara
Arterioscler Thromb Vasc Biol. 2007;27:12-14, doi:10.1161/01.ATV.0000254154.43871.50.
Full Text | PDF  

 

Brief ReviewsBack

Wolfgang Koenig and Natalie Khuseyinova
Arterioscler Thromb Vasc Biol. 2007;27:15-26; published online before print November 2 2006, doi:10.1161/01.ATV.0000251503.35795.4f.
Abstract | Full Text | PDF
Basic research over the last two decades has identified a large number of biomarkers of atherosclerotic plaque destabilization and rupture, which carry important prognostic information and might be useful in improving risk stratification in the future. To date, however, none of them can be recommended for routine clinical use.  

Katsuya Hirano
Arterioscler Thromb Vasc Biol. 2007;27:27-36; published online before print November 9 2006, doi:10.1161/01.ATV.0000251995.73307.2d.
Abstract | Full Text | PDF
Proteinase-activated receptors (PARs) play critical roles in vascular physiology and pathophysiology. The receptor upregulation is considered to be a key step in contributing to vascular lesion development and pathophysiology of vascular diseases. Elucidating the molecular mechanism regulating PARs expression is thus the next important step in PARs research.  

Yasufumi Sato and Hikaru Sonoda
Arterioscler Thromb Vasc Biol. 2007;27:37-41; published online before print November 9 2006, doi:10.1161/01.ATV.0000252062.48280.61.
Abstract | Full Text | PDF
Genomic regulation of angiogenesis inhibition remains to be established. We recently isolated a novel endothelium-derived angiogenesis inhibitor and named it vasohibin. Our discovery of vasohibin as an endothelium-derived VEGF-inducible angiogenesis inhibitor should shed light on the genomic basis of he negative regulation of angiogenesis.  

 

Vascular BiologyBack

Roza E. Clempus, Dan Sorescu, Anna E. Dikalova, Lily Pounkova, Patricia Jo, George P. Sorescu, Bernard Lassègue, and Kathy K. Griendling
Arterioscler Thromb Vasc Biol. 2007;27:42-48; published online before print November 2 2006, doi:10.1161/01.ATV.0000251500.94478.18.
Abstract | Full Text | PDF | Data Supplement
The mechanisms responsible for maintaining the differentiated phenotype of adult vascular smooth muscle cells (VSMCs) are incompletely understood. Reactive oxygen species (ROS) have been implicated in VSMC differentiation, but the responsible sources are unknown. In this study, we investigated the role of Nox1 and Nox4-derived ROS in this process.  

John C. Barbato, Otilia Catanescu, Kelsey Murray, Patricia M. DiBello, and Donald W. Jacobsen
Arterioscler Thromb Vasc Biol. 2007;27:49-54; published online before print November 2 2006, doi:10.1161/01.ATV.0000251536.49581.8a.
Abstract | Full Text | PDF
We hypothesized that metallothionein, a ubiquitous intracellular zinc-chaperone and superoxide anion radical scavenger, reacts with L-homocysteine and that homocysteinylated-metallothionein suffers loss of function. These studies provide the first evidence that L-homocysteine targets intracellular metallothionein by forming a mixed-disulfide conjugate and that loss of function occurs after homocysteinylation. The data support a novel mechanism for disruption of zinc and redox homeostasis.  

Andreas Schäfer, Christian Schulz, Daniela Fraccarollo, Piet Tas, Meike Leutke, Martin Eigenthaler, Stefan Seidl, Peter Heider, Georg Ertl, Steffen Massberg, and Johann Bauersachs
Arterioscler Thromb Vasc Biol. 2007;27:55-62; published online before print November 2 2006, doi:10.1161/01.ATV.0000251535.30191.60.
Abstract | Full Text | PDF | Data Supplement
We investigated direct effects of fractalkine on vascular function. We demonstrate increased superoxide formation and decreased nitric oxide bioavailability in rat aorta by fractalkine. Induction of vascular dysfunction could provide an alternate mechanism by which fractalkine exerts its pro-atherosclerotic effects.  

Laura Piqueras, Andrew R. Reynolds, Kairbaan M. Hodivala-Dilke, Arántzazu Alfranca, Juan M. Redondo, Toshihisa Hatae, Tadashi Tanabe, Timothy D. Warner, and David Bishop-Bailey
Arterioscler Thromb Vasc Biol. 2007;27:63-69; published online before print October 26 2006, doi:10.1161/01.ATV.0000250972.83623.61.
Abstract | Full Text | PDF | Data Supplement
PPARß/{delta} is expressed in vascular endothelial cells; however, its roles remain unclear. The PPARß/{delta} ligand GW501516 induced endothelial proliferation and angiogenesis. The clinical use of GW501516 in dyslipidemia may therefore need to be monitored for angiogenic processes.  

Peter F. Bodary, Yuechun Shen, Miina Öhman, Kristina L. Bahrou, Fernando B. Vargas, Sarah S. Cudney, Kevin J. Wickenheiser, Martin G. Myers, Jr, and Daniel T. Eitzman
Arterioscler Thromb Vasc Biol. 2007;27:70-76; published online before print November 9 2006, doi:10.1161/01.ATV.0000252068.89775.ee.
Abstract | Full Text | PDF
Elevated levels of leptin have been associated with increased risk for cardiovascular disease. We demonstrate that mice deficient in leptin or leptin receptor are protected from neointimal formation. This effect is mediated by a non-bone marrow-derived leptin receptor pool and by signaling pathways independent of those responsible for energy balance.  

Mingyu Liang and Jennifer L. Pietrusz
Arterioscler Thromb Vasc Biol. 2007;27:77-83; published online before print October 26 2006, doi:10.1161/01.ATV.0000251006.54632.bb.
Abstract | Full Text | PDF | Data Supplement
There is emerging evidence that cellular thiols may be importantly involved in diabetic complications. We systematically determined the expression level of 11 thiol-related genes in streptozotocin-induced diabetes. Thioredoxin 2, a mitochondrion thioredoxin suppressed in the aorta by diabetes, was found to protect human endothelial cells from high ambient glucose.  

Takayoshi Suganami, Kanami Tanimoto-Koyama, Junko Nishida, Michiko Itoh, Xunmei Yuan, Shinji Mizuarai, Hidehito Kotani, Shoji Yamaoka, Kensuke Miyake, Seiichiro Aoe, Yasutomi Kamei, and Yoshihiro Ogawa
Arterioscler Thromb Vasc Biol. 2007;27:84-91; published online before print November 2 2006, doi:10.1161/01.ATV.0000251608.09329.9a.
Abstract | Full Text | PDF | Data Supplement
Using an in vitro coculture system composed of adipocytes and macrophages, we demonstrate that saturated FAs, which are released in large quantities from hypertrophied adipocytes via the macrophage-induced adipocyte lipolysis, serve as a naturally occurring ligand for TLR4, thereby inducing the inflammatory changes in both adipocytes and macrophages through NF-{kappa}B activation.  

Sei Nakata, Masato Tsutsui, Hiroaki Shimokawa, Takahiro Yamashita, Akihide Tanimoto, Hiromi Tasaki, Kiyoshi Ozumi, Ken Sabanai, Tsuyoshi Morishita, Osamu Suda, Hideyasu Hirano, Yasuyuki Sasaguri, Yasuhide Nakashima, and Nobuyuki Yanagihara
Arterioscler Thromb Vasc Biol. 2007;27:92-98; published online before print November 2 2006, doi:10.1161/01.ATV.0000251615.61858.33.
Abstract | Full Text | PDF | Data Supplement
HMG-CoA reductase inhibitors (statins) are known to enhance vascular expression of endothelial and inducible nitric oxide synthase. Here we report that atorvastatin also upregulates vascular neuronal nitric oxide synthase through Akt/NF-{kappa}B pathway, demonstrating a novel nNOS-mediated vascular effect of the statin.  

Natsuo Inoue, Takahisa Kondo, Koichi Kobayashi, Mika Aoki, Yasushi Numaguchi, Masabumi Shibuya, and Toyoaki Murohara
Arterioscler Thromb Vasc Biol. 2007;27:99-105; published online before print November 2 2006, doi:10.1161/01.ATV.0000251504.61247.d5.
Abstract | Full Text | PDF | Data Supplement
Vascular endothelial growth factor-A (VEGF-A) promotes angiogenesis but causes adverse side effects such as edema or tissue inflammation. VEGF-E, found in the genome of the Orf virus, specifically binds to VEGF receptor-2 and shows mitotic activity on endothelial cells. Recently, we created two forms of VEGF-E and human placental growth factor (PlGF) chimera genes (VEGF-E chimera #9 and VEGF-E chimera #33), which are humanized genes with VEGF-E function but showing less antigenicity  

Martin K.C. Ng, Jenny Wu, Edwin Chang, Bing-yin Wang, Regina Katzenberg-Clark, Akiko Ishii-Watabe, and John P. Cooke
Arterioscler Thromb Vasc Biol. 2007;27:106-112; published online before print November 2 2006, doi:10.1161/01.ATV.0000251517.98396.4a.
Abstract | Full Text | PDF | Data Supplement
Nicotine induces nicotinic acetylcholine receptor (nAChR)-dependent endothelial cell migration (ECM). nAChR antagonism also suppresses bFGF- and VEGF-induced ECM. ECM induced by nicotine, VEGF, or bFGF requires nAChR-dependent induction of thioredoxin activity via repression of the thioredoxin inhibitor, TXNIP. Therefore growth factor-induced ECM, a key angiogenesis event, requires nAChR activation.  

Shoukang Zhu, Xialin Liu, Ying Li, Pascal J. Goldschmidt-Clermont, and Chunming Dong
Arterioscler Thromb Vasc Biol. 2007;27:113-119; published online before print November 9 2006, doi:10.1161/01.ATV.0000252035.12881.d0.
Abstract | Full Text | PDF | Data Supplement
A group of cells (simple little cells or SLCs) were markedly decreased in the marrow of old wild-type and apoE-/- mice, relative to their young counterparts. Lineage negative cKit-/Sca-1- cells, the predominant cell type in the SLC population, displayed efficient conversion to a mature endothelial phenotype in vitro.  

Nadina Stadler, Juliane Eggermann, Stefan Vöö, Andrea Kranz, and Johannes Waltenberger
Arterioscler Thromb Vasc Biol. 2007;27:120-126; published online before print October 19 2006, doi:10.1161/01.ATV.0000250614.97896.4c.
Abstract | Full Text | PDF
This study investigated the negative effects of smoking on monocyte migratory responsiveness to VEGF-A and the usefulness of vitamin C to prevent smoking-induced monocyte dysfunction. Stimulation of monocyte migration by VEGF-A was severely attenuated in smokers, and the deficit observed was surmounted by vitamin C supplementation. The negative effects of smoking on monocyte function may translate into adverse impacts on VEGF-A-dependent repair processes such as arteriogenesis. These results propose a causative role of oxidative stress in smoking-induced monocyte dysfunction.  

 

Atherosclerosis and LipoproteinsBack

Douglas S. Lee, Jane C. Evans, Sander J. Robins, Peter W. Wilson, Irene Albano, Caroline S. Fox, Thomas J. Wang, Emelia J. Benjamin, Ralph B. D’Agostino, and Ramachandran S. Vasan
Arterioscler Thromb Vasc Biol. 2007;27:127-133; published online before print November 9 2006, doi:10.1161/01.ATV.0000251993.20372.40.
Abstract | Full Text | PDF | Data Supplement
To determine if serum {gamma}-glutamyl transferase (GGT) is a predictor of cardiovascular disease (CVD) morbidity and mortality, we conducted time-dependent analysis accounting for temporal changes in CVD risk factors. Increased serum GGT predicted incident CVD and death. The highest GGT quartile experienced a 67% increase in CVD incidence.  

Andrew P. Levy, Joanne E. Levy, Shiri Kalet-Litman, Rachel Miller-Lotan, Nina S. Levy, Roy Asaf, Julia Guetta, Chingwen Yang, K. Raman Purushothaman, Valentin Fuster, and Pedro R. Moreno
Arterioscler Thromb Vasc Biol. 2007;27:134-140; published online before print October 26 2006, doi:10.1161/01.ATV.0000251020.24399.a2.
Abstract | Full Text | PDF | Data Supplement
We tested the hypothesis that the Hp genotype is a determinant of oxidative and inflammatory activity in atherosclerotic plaques. Plaques from Hp 2-2 mice were associated with increased iron, lipid peroxidation, and macrophage infiltration as compared with plaques from Hp 1-1 mice.  

David J. Moser, Robert G. Robinson, Stephanie M. Hynes, Rebecca L. Reese, Stephan Arndt, Jane S. Paulsen, and William G. Haynes
Arterioscler Thromb Vasc Biol. 2007;27:141-146; published online before print October 26 2006, doi:10.1161/01.ATV.0000250973.93401.2d.
Abstract | Full Text | PDF
Forearm vascular function was found to be significantly and positively associated with neuropsychological performance in individuals with atherosclerotic vascular disease, after controlling for individual vascular risk factors and other potential confounding variables. With additional research, measures of vascular function might be useful in identifying individuals at greatest risk for vascular cognitive impairment.  

Hidenori Koyama, Tetsuo Shoji, Shinya Fukumoto, Kayo Shinohara, Takuhito Shoji, Masanori Emoto, Katsuhito Mori, Hideki Tahara, Eiji Ishimura, Ryusuke Kakiya, Tsutomu Tabata, Hiroshi Yamamoto, and Yoshiki Nishizawa
Arterioscler Thromb Vasc Biol. 2007;27:147-153; published online before print November 2 2006, doi:10.1161/01.ATV.0000251502.88818.4b.
Abstract | Full Text | PDF
Plasma endogenously secretory receptor for AGEs (esRAGE), an alternatively spliced form of RAGE, is closely associated with metabolic syndrome and atherosclerosis. We showed here that low circulating plasma esRAGE is a predictor of cardiovascular mortality in a cohort of 206 patients with end-stage renal diseases.  

Petra Ijäs, Krista Nuotio, Jani Saksi, Lauri Soinne, Eija Saimanen, Marja-Liisa Karjalainen-Lindsberg, Oili Salonen, Seppo Sarna, Jarno Tuimala, Petri T. Kovanen, Markku Kaste, and Perttu J. Lindsberg
Arterioscler Thromb Vasc Biol. 2007;27:154-160; published online before print November 9 2006, doi:10.1161/01.ATV.0000251991.64617.e7.
Abstract | Full Text | PDF | Data Supplement
We showed that HO-1 and CD163 were overexpressed in symptomatic carotid plaques. Their expression correlated with iron deposition but iron itself was not associated with symptom status. Symptomatic plaques might show a more pronounced induction of CD163 and HO-1 in response to plaque hemorrhages.  

Kenji Inoue, Akira Sugiyama, Patrick C. Reid, Yukio Ito, Katsumi Miyauchi, Sei Mukai, Mina Sagara, Kyoko Miyamoto, Hirokazu Satoh, Isao Kohno, Takeshi Kurata, Hiroshi Ota, Alberto Mantovani, Takao Hamakubo, Hiroyuki Daida, and Tatsuhiko Kodama
Arterioscler Thromb Vasc Biol. 2007;27:161-167; published online before print November 9 2006, doi:10.1161/01.ATV.0000252126.48375.d5.
Abstract | Full Text | PDF | Data Supplement
Pentraxin 3 (PTX3) are increased in patients with acute myocardial infarction, yet its involvement in unstable angina (UAP) remains unclear. We developed a high sensitivity ELISA system for the detection of PTX3. PTX3 were increased in patients with UAP. This ELISA system will be useful for the prediction of UAP.  

Luis M. Blanco-Colio, Jose L. Martín-Ventura, Eduardo de Teresa, Csaba Farsang, Allan Gaw, GianFranco Gensini, Lawrence A. Leiter, Anatoly Langer, Pierre Martineau, Gonzalo Hérnandez, Jesús Egido on behalf of the ACTFAST investigators
Arterioscler Thromb Vasc Biol. 2007;27:168-174; published online before print October 19 2006, doi:10.1161/01.ATV.0000250616.26308.d7.
Abstract | Full Text | PDF
1078 statin-free subjects with coronary heart disease (CHD), CHD-equivalent, or a 10-year CHD risk>20% were assigned to atorvastatin (10 to 80 mg/day) based on LDL-C at screening. At baseline, sFas concentrations are increased whereas sFasL are decreased compared with healthy subjects. Atorvastatin reduces sFas supporting the antiinflammatory effects in high-cardiovascular risk patients.  

Sotirios Tsimikas, Masanori Aikawa, Francis J. Miller, Jr, Elizabeth R. Miller, Michael Torzewski, Steven R. Lentz, Claes Bergmark, Donald D. Heistad, Peter Libby, and Joseph L. Witztum
Arterioscler Thromb Vasc Biol. 2007;27:175-181; published online before print November 2 2006, doi:10.1161/01.ATV.0000251501.86410.03.
Abstract | Full Text | PDF | Data Supplement
Oxidized phospholipids (OxPL) are pro-inflammatory. We evaluated whether changes in plasma levels of OxPL associated with apolipoprotein B-100 (apoB-100) reflect changes in OxPL content in atherosclerotic plaques during dietary-induced atherosclerosis progression and regression. In the setting of overall reduction of plasma OxPL levels after dietary lipid-lowering, increases in the OxPL/apoB ratio reflect reduced content of OxPL in atherosclerotic plaques. These data suggest that changes in the OxPL/apoB ratio may reflect early atherosclerosis regression.  

Michael Joner, Andrew Farb, Qi Cheng, Aloke V. Finn, Eduardo Acampado, Allen P. Burke, Kristi Skorija, Wendy Creighton, Frank D. Kolodgie, Herman K. Gold, and Renu Virmani
Arterioscler Thromb Vasc Biol. 2007;27:182-189; published online before print October 26 2006, doi:10.1161/01.ATV.0000251021.28725.e8.
Abstract | Full Text | PDF | Data Supplement
Although emerging data from preclinical and clinical studies suggests a reduction of in-stent restenosis with peroxisome proliferator-activated receptor (PPAR)-{gamma} agonists, the reduction of neointimal growth via anti-inflammatory mechanisms have not been explored. Oral pioglitazone suppresses in-stent neointimal growth by limiting local inflammatory pathways and may be useful as an adjunctive therapy in patients undergoing percutaneous interventions.  

Ruijie Liu, Mohammad R. Hojjati, Cecilia M. Devlin, Inge H. Hansen, and Xian-Cheng Jiang
Arterioscler Thromb Vasc Biol. 2007;27:190-196; published online before print October 12 2006, doi:10.1161/01.ATV.0000249721.96666.e5.
Abstract | Full Text | PDF
Macrophage PLTP deficiency causes a significant reduction of apoE secretion from the cells, and this in turn promotes the accumulation of cholesterol in the circulation and accelerates the development of atherosclerosis.  

Jinyu Wang, Xunde Xian, Wei Huang, Li Chen, Liling Wu, Yi Zhu, Jianglin Fan, Colin Ross, Michael R. Hayden, and George Liu
Arterioscler Thromb Vasc Biol. 2007;27:197-203; published online before print October 12 2006, doi:10.1161/01.ATV.0000249683.80414.d9.
Abstract | Full Text | PDF | Data Supplement
Expression of LPL in endothelial-intact carotid arteries results in lipid deposition and VCAM-1 upregulation in both LPL- and ApoE-deficient mice, suggesting endothelial cell associated LPL in the arterial wall as a strong proatherosclerotic factor.  

Eva J.A van Wanrooij, Gijs H.M van Puijvelde, Paula de Vos, Hideo Yagita, Theo J.C. van Berkel, and Johan Kuiper
Arterioscler Thromb Vasc Biol. 2007;27:204-210; published online before print October 26 2006, doi:10.1161/01.ATV.0000251007.07648.81.
Abstract | Full Text | PDF | Data Supplement
Tnfrsf4 (OX40) and Tnfsf4 (OX40 ligand) are members of the TNF and TNF receptor family and the OX40/OX40L pathway is an important co-activator of T cells. Anti-OX40 ligand antibody administration reduced atherogenesis by inhibiting IL-4 induced IgG1 isotype switching, and increased anti-oxLDL specific IgM serum levels.  

Julie Tsai, Wei Qiu, Rita Kohen-Avramoglu, and Khosrow Adeli
Arterioscler Thromb Vasc Biol. 2007;27:211-218; published online before print October 12 2006, doi:10.1161/01.ATV.0000249861.80471.96.
Abstract | Full Text | PDF | Data Supplement
Inhibition of the overactive ras-MEK-ERK pathway in HepG2 cells was found to correct the defect in VLDL assembly (that normally secrete immature triglyceride-poor LDL-sized apoB particles) leading to the secretion of large, VLDL-sized particles, similar to primary hepatocytes. Our data implicate the MEK-ERK pathway in regulating the VLDL assembly process in HepG2 cells.  

Akio Kawakami, Masanori Aikawa, Noriko Nitta, Masayuki Yoshida, Peter Libby, and Frank M. Sacks
Arterioscler Thromb Vasc Biol. 2007;27:219-225; published online before print October 12 2006, doi:10.1161/01.ATV.0000249620.68705.0d.
Abstract | Full Text | PDF | Data Supplement
This study showed that apoCIII alone or VLDL containing apoCIII activates PKC{alpha} through the PTX-sensitive G protein pathway in human monocytic cells, leading to NF-{kappa}B activation and increased ß1-integrin expression. Leukocyte NF-{kappa}B activation contributes importantly to inflammatory aspects of atherogenesis. Thus, apoCIII may stimulate diverse inflammatory responses through monocyte activation.  

Christian Cappello, Bernd Saugel, Karin C. Huth, Andreas Zwergal, Martina Krautkrämer, Christophe Furman, Mustapha Rouis, Bianca Wieser, Heike W. Schneider, Dieter Neumeier, and Korbinian Brand
Arterioscler Thromb Vasc Biol. 2007;27:226-232; published online before print October 19 2006, doi:10.1161/01.ATV.0000250615.27795.85.
Abstract | Full Text | PDF | Data Supplement
Evidence suggests that ozone plays a role in atherosclerosis. We demonstrated that ozone-modified LDL (ozLDL) selectively and reversibly inhibited the NF-{kappa}B system, with an accompanying reduction in IRAK-1 phosphorylation/proteolysis. Cholesterol ozonization products were identified as active components. Such inhibition may impair immune function and induce apoptosis.  

 

ThrombosisBack

Katina M. Wilson, Ryan B. McCaw, Lorie Leo, Erland Arning, Sárka Lhoták, Teodoro Bottiglieri, Richard C. Austin, and Steven R. Lentz
Arterioscler Thromb Vasc Biol. 2007;27:233-240; published online before print November 2 2006, doi:10.1161/01.ATV.0000251607.96118.af.
Abstract | Full Text | PDF
We tested the hypothesis that hyperhomocysteinemia and hypercholesterolemia promote thrombosis. Carotid artery thrombosis was accelerated and endothelium-dependent relaxation of carotid artery rings was impaired in apolipoprotein E-deficient mice fed either high fat or hyperhomocysteinemic diets. We conclude that hyperhomocysteinemia and hypercholesterolemia produce endothelial dysfunction and increased susceptibility to arterial thrombosis.  

C. Strassel, C. Nonne, A. Eckly, T. David, C. Leon, M. Freund, J.-P. Cazenave, C. Gachet, and F. Lanza
Arterioscler Thromb Vasc Biol. 2007;27:241-247; published online before print November 9 2006, doi:10.1161/01.ATV.0000251992.47053.75.
Abstract | Full Text | PDF | Data Supplement
Mouse models of Bernard-Soulier bleeding disorder were generated by targeting the GP GPIbß. These mice displayed, in addition to their defective hemostasis, decreased thrombotic responses in different models of arterial and systemic thrombosis.  

 

Letters to the EditorBack

Neointimal Cracks (Plaque Rupture?) and Thrombosis in Wrapped Arteries Without Flow

Erling Falk, Stephen M. Schwartz, Zorina S. Galis, and Michael E. Rosenfeld
Arterioscler Thromb Vasc Biol. 2007;27:248-249, doi:10.1161/01.ATV.0000249644.86759.81.
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Neointimal Cracks (Plaque Rupture?) and Thrombosis in Wrapped Arteries Without Flow

Christopher L. Jackson
Arterioscler Thromb Vasc Biol. 2007;27:250-251, doi:10.1161/01.ATV.0000249645.02230.fe.
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Neointimal Cracks (Plaque Rupture?) and Thrombosis in Wrapped Arteries Without Flow

Masafumi Kuzuya and Takeshi Sasaki
Arterioscler Thromb Vasc Biol. 2007;27:252, doi:10.1161/01.ATV.0000249619.75202.1e.
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Endogenous Secretory Receptor for Advanced Glycation Endproducts Levels Are Correlated With Serum Pentosidine and CML in Patients With Type 1 Diabetes

Junnosuke Miura, Yasuhiko Yamamoto, Mari Osawa, Takuo Watanabe, Hideto Yonekura, Yasuko Uchigata, Hiroshi Yamamoto, and Yasuhiko Iwamoto
Arterioscler Thromb Vasc Biol. 2007;27:253-254, doi:10.1161/01.ATV.0000251533.18013.67.
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Circulating Platelet-Derived Microparticles Are Associated With Atherothrombotic Events

Masashi Namba, Atsushi Tanaka, Kenei Shimada, Yasushi Ozeki, Shigeru Uehata, Tsunemori Sakamoto, Yukio Nishida, Shosaku Nomura, and Junichi Yoshikawa
Arterioscler Thromb Vasc Biol. 2007;27:255-256, doi:10.1161/01.ATV.0000252064.97632.2c.
Full Text | PDF | Data Supplement  

 

Acknowledgment of ReviewersBack

Acknowledgment of Reviewers


Arterioscler Thromb Vasc Biol. 2007;27:e1-e7.
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News From the American Heart AssociationBack

News From the American Heart Association


Arterioscler Thromb Vasc Biol. 2007;27:B1, doi:10.1161/CIRCULATIONAHA.107.180480.
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Meetings CalendarBack

Meetings Calendar


Arterioscler Thromb Vasc Biol. 2007;27:B2-B4, doi:10.1161/CIRCULATIONAHA.107.180481.
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