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Arteriosclerosis, Thrombosis, and Vascular Biology
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Volume 25, Issue 7; July 1, 2005

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EditorialsBack

Cardioprotective Effects of High-Density Lipoproteins: The Evidence Strengthens

P.J. Barter
Arterioscler Thromb Vasc Biol. 2005;25:1305-1306, doi:10.1161/01.ATV.0000172634.93210.5c
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Return to Ectopia: Stem Cells in the Artery Wall

Linda L. Demer and Yin Tintut
Arterioscler Thromb Vasc Biol. 2005;25:1307-1308, doi:10.1161/01.ATV.0000172633.74942.e6
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Down But Not Out: New Insights Into the Role of {alpha}Vß3 Integrins in Vascular Healing

G.A. Stouffer, A. Pathak, R. Zhao, and J. Huang
Arterioscler Thromb Vasc Biol. 2005;25:1309-1310, doi:10.1161/01.ATV.0000172686.16863.be
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Brief ReviewsBack

Björn Dahlbäck and Bruno O. Villoutreix
Arterioscler Thromb Vasc Biol. 2005;25:1311-1320; published online before print April 28 2005, doi:10.1161/01.ATV.0000168421.13467.82
Abstract | Full Text | PDF
The protein C system provides important control of blood coagulation by regulating the activities of factor VIIIa (FVIIIa) and factor Va (FVa), cofactors in the activation of factor X and prothrombin, respectively. The protein C system is physiologically important, and genetic defects affecting the system are the most common risk factors of venous thrombosis. The molecular recognition of the protein C system is progressively being unraveled, giving us new insights into this fascinating and intricate molecular scenario at the atomic level.  

Denisa D. Wagner
Arterioscler Thromb Vasc Biol. 2005;25:1321-1324; published online before print April 14 2005, doi:10.1161/01.ATV.0000166521.90532.44
Abstract | Full Text | PDF
This article is a summary of the Sol Sherry Lecture of the Council on Arteriosclerosis, Thrombosis, and Vascular Biology, which was presented at the Scientific Sessions of the American Heart Association in November 2004. The article focuses mainly on new aspects of P-selectin and CD40L (CD154) biology and on the interplay of platelets and leukocytes in thrombosis and inflammation.  

Mohamad Navab, G.M. Anantharamaiah, Srinivasa T. Reddy, Susan Hama, Greg Hough, Victor R. Grijalva, Nicholas Yu, Benjamin J. Ansell, Geeta Datta, David W. Garber, and Alan M. Fogelman
Arterioscler Thromb Vasc Biol. 2005;25:1325-1331; published online before print April 14 2005, doi:10.1161/01.ATV.0000165694.39518.95
Abstract | Full Text | PDF
The antiinflammatory properties of different class A amphipathic helical peptides such as D-4F depend on subtle differences in the configuration of the hydrophobic face of the peptides that determine the ability of the peptides to sequester inflammatory lipids.  

Jane A. Leopold and Joseph Loscalzo
Arterioscler Thromb Vasc Biol. 2005;25:1332-1340; published online before print March 24 2005, doi:10.1161/01.ATV.0000163846.51473.09
Abstract | Full Text | PDF
Heritable polymorphisms of pro-oxidant enzymes and antioxidant enzyme deficiencies modulate the risk of atherothrombotic cardiovascular disease. Individually, inheritance of one of these polymorphisms or enzyme deficiencies promotes a state of uncompensated oxidant stress on the vasculature. Collectively, these enzymes polymorphisms and deficiencies are recognized as the oxidative enzymopathies.  

 

Vascular BiologyBack

Monsur Kazi, Chaoyong Zhu, Joy Roy, Gabrielle Paulsson-Berne, Anders Hamsten, Jesper Swedenborg, Ulf Hedin, and Per Eriksson
Arterioscler Thromb Vasc Biol. 2005;25:1341-1346; published online before print April 21 2005, doi:10.1161/01.ATV.0000166601.49954.21
Abstract | Full Text | PDF | Data Supplement
It has been suggested that the intraluminal thrombus of abdominal aortic aneurysms (AAAs) predisposes for AAA rupture. Differences in gene expression pattern revealed that many MMPs were upregulated in the thrombus-free wall. The source of the proteases responsible for the degradation of the thrombus-covered wall needs to be determined.  

Christina Duftner, Rüdiger Seiler, Peter Klein-Weigel, Heike Göbel, Christian Goldberger, Christian Ihling, Gustav Fraedrich, and Michael Schirmer
Arterioscler Thromb Vasc Biol. 2005;25:1347-1352; published online before print April 21 2005, doi:10.1161/01.ATV.0000167520.41436.c0
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Animal studies and tissue studies suggest a role for interferon (IFN)-{gamma}-producing T cells in the development of abdominal aortic aneurysms (AAAs). This study shows an increased prevalence of circulating IFN-{gamma}-producing CD28- T cells especially in smaller AAAs, and thus supports the concept of a T cell-mediated pathophysiology of AAAs.  

Romain Debret, Frank Antonicelli, Aurore Theill, William Hornebeck, Philippe Bernard, Moncef Guenounou, and Richard Le Naour
Arterioscler Thromb Vasc Biol. 2005;25:1353-1358; published online before print April 28 2005, doi:10.1161/01.ATV.0000168412.50855.9f
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Elastin-derived peptides, as generated during arterial diseases such as AAA, were shown to act as potent T-cell stimuli inducing Th-1 polarization and MMP-9 production.  

Sridevi Devaraj, Terry W. Du Clos, and Ishwarlal Jialal
Arterioscler Thromb Vasc Biol. 2005;25:1359-1363; published online before print April 28 2005, doi:10.1161/01.ATV.0000168573.10844.ae
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In addition to being a risk marker, CRP exerts atherothrombotic effects in endothelial cells. In this study, using flow cytometry and fluorescence microscopy, we show that CRP binds to CD32 and CD64 on HAECs, is internalized, and exerts its biological effects. Antibodies to CD32 and CD64 abrogated the biological effects of CRP, whereas antibodies to CD16 had no effect.  

Endre Dyrøy, Arne Yndestad, Thor Ueland, Bente Halvorsen, Jan Kristian Damås, Pål Aukrust, and Rolf K. Berge
Arterioscler Thromb Vasc Biol. 2005;25:1364-1369; published online before print May 26 2005, doi:10.1161/01.ATV.0000171982.57713.96
Abstract | Full Text | PDF | Data Supplement
We show that tetradecylthioacetic acid attenuates tumor necrosis factor-{alpha}-mediated endothelial cell activation, supporting antiinflammatory effects of this fatty acid. The relevance of our findings to human diseases was suggested by a tetradecylthioacetic acid-mediated downregulation of inflammatory mediators in psoriasis patients.  

Wei Li, Kuniyoshi Tanaka, Koichi Morioka, Takahiko Uesaka, Narihisa Yamada, Atsushi Takamori, Mitsuteru Handa, Sawaka Tanabe, and Akio Ihaya
Arterioscler Thromb Vasc Biol. 2005;25:1370-1375; published online before print May 5 2005, doi:10.1161/01.ATV.0000168914.85107.64
Abstract | Full Text | PDF | Data Supplement
Gene transfer of thymidine phosphorylase (TP) into cultured VSMCs significantly decreased their migration and proliferation. Furthermore, adventitial delivery of TP gene to rat balloon-injured carotid artery significantly reduced neointimal VSMC migration and inhibited neointima formation. TP may be useful in treating vascular obstructive disease.  

Yayoi Honda, Tomoko Kitano, Fumiyo Fukuya, Yuji Sato, Seiji Iwama, Toshiya Morie, and Mitsue Notake
Arterioscler Thromb Vasc Biol. 2005;25:1376-1382; published online before print May 5 2005, doi:10.1161/01.ATV.0000168902.18672.2f
Abstract | Full Text | PDF | Data Supplement
We clarified the essential roles of{alpha}vß3 integrin and endothelial cell (EC) regeneration in neointima formation using a rat balloon injury model. In this model, we demonstrated that systemic administration of BS-1417, a novel{alpha}vß3 integrin antagonist, potently and stably inhibits neointima formation without affecting EC regeneration.  

Chandike M. Mallawaarachchi, Peter L. Weissberg, and Richard C.M. Siow
Arterioscler Thromb Vasc Biol. 2005;25:1383-1387; published online before print April 28 2005, doi:10.1161/01.ATV.0000168415.33812.51
Abstract | Full Text | PDF | Data Supplement
This study investigates whether perivascular adenoviral smad7 gene transfer antagonises TGF-ß1 signaling to decrease adventitial cell migration after balloon injury in rat carotid arteries. Smad7 overexpression attenuated the contribution of adventitial cells to neointima formation after vascular injury, concomitant with reduced luminal loss and adventitial collagen content.  

Satoshi Murasawa, Atsuhiko Kawamoto, Miki Horii, Shuko Nakamori, and Takayuki Asahara
Arterioscler Thromb Vasc Biol. 2005;25:1388-1394; published online before print April 28 2005, doi:10.1161/01.ATV.0000168409.69960.e9
Abstract | Full Text | PDF
Ex vivo expanded EPC transplantation has shown therapeutic potential for myocardial ischemia. We observed the expression of human-specific cardiac, vascular smooth muscle, and endothelial markers in niche-dependent expression profiles of EPCs via mainly transdifferentiation. EPCs could contribute to not only vasculogenesis but also myogenesis in the ischemic myocardium.  

Xiao Ping Yang, Kaikobad Irani, Subhendra Mattagajasingh, Anthony DiPaula, Firdous Khanday, Michitaka Ozaki, Karen Fox-Talbot, William M. Baldwin, III, and Lewis C. Becker
Arterioscler Thromb Vasc Biol. 2005;25:1395-1400; published online before print April 28 2005, doi:10.1161/01.ATV.0000168428.96177.24
Abstract | Full Text | PDF | Data Supplement
Stat3{alpha} was found to upregulate the ICAM-1 gene in ischemia-reperfusion by a novel mechanism. After Rac1-dependent phosphorylation of Stat3, Stat3{alpha} bound to Sp1, and the resulting transcriptional complex bound to a GAS sequence in the ICAM-1 proximal promoter. Specific inhibition of Stat3 and/or Sp1 significantly reduced ICAM-1 transcription in hypoxic-reoxygenated endothelial cells.  

Giuseppina Basta, Guido Lazzerini, Serena Del Turco, Gian Michele Ratto, Ann Marie Schmidt, and Raffaele De Caterina
Arterioscler Thromb Vasc Biol. 2005;25:1401-1407; published online before print April 21 2005, doi:10.1161/01.ATV.0000167522.48370.5e
Abstract | Full Text | PDF | Data Supplement
We investigated the role of distinct sources of reactive oxygen species (ROS), including the mitochondrial electron transport chain, NADPH oxidase, xanthine oxidase, and arachidonic acid metabolism, in advanced glycation end product (AGE)-induced VCAM-1 expression. ROS generated both by NAD(P)H oxidase and the mitochondrial electron transport system are involved in AGE signaling.  

Wolfgang Utz, Jens Jordan, Thoralf Niendorf, Mandy Stoffels, Friedrich C. Luft, Rainer Dietz, and Matthias G. Friedrich
Arterioscler Thromb Vasc Biol. 2005;25:1408-1413; published online before print May 12 2005, doi:10.1161/01.ATV.0000170131.13683.d7
Abstract | Full Text | PDF
We used muscle blood oxygen level-dependent MRI (BOLD MRI) to study tissue Hb oxygenation in relation to postischemic hyperemia and endothelial stimulation. We found uncoupling of tissue Hb oxygenation from blood flow changes and conclude that BOLD MRI may provide additional information in assessing endothelial function.  

Jan T. Kielstein, Stefanie M. Bode-Böger, Gerrit Hesse, Jens Martens-Lobenhoffer, Attila Takacs, Danilo Fliser, and Marius M. Hoeper
Arterioscler Thromb Vasc Biol. 2005;25:1414-1418; published online before print April 28 2005, doi:10.1161/01.ATV.0000168414.06853.f0
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We explored the role of the endogenous NO synthase inhibitor asymmetrical dimethylarginine (ADMA) in idiopathic pulmonary arterial hypertension (IPAH). Plasma ADMA levels correlated significantly with right atrial pressure, cardiac index, and mixed-venous oxygen saturation. Moreover, ADMA was an independent predictor of survival in patient with IPAH.  

 

Atherosclerosis and LipoproteinsBack

P.S. Olofsson, K. Jatta, D. Wågsäter, S. Gredmark, U. Hedin, G. Paulsson-Berne, C. Söderberg-Nauclér, G.K. Hansson, and A. Sirsjö
Arterioscler Thromb Vasc Biol. 2005;25:e113-e116; published online before print May 12 2005, doi:10.1161/01.ATV.0000170130.85334.38
Abstract | Full Text | PDF
We explored the vascular transcriptional response to inflammation. Gene arrays identified the cytomegalovirus-inducible gene 5 (cig5) among the most induced by LPS. Cig5 expression was high in atherosclerosis. We show that the cig5 protein is expressed in atherosclerotic arteries and strongly induced in vascular cells by pathogens and inflammatory stimuli.  

Marcello Rattazzi, Brian J. Bennett, Florian Bea, Elizabeth A. Kirk, Jerry L. Ricks, Mei Speer, Stephen M. Schwartz, Cecilia M. Giachelli, and Michael E. Rosenfeld
Arterioscler Thromb Vasc Biol. 2005;25:1420-1425; published online before print April 21 2005, doi:10.1161/01.ATV.0000166600.58468.1b
Abstract | Full Text | PDF | Data Supplement
Advanced atherosclerotic lesions in the innominate arteries of chow-fed apolipoprotein E-deficient mice become highly calcified. The cell types associated with calcification were investigated. The cells mediating the calcification have a chondrocyte-like phenotype. The process of calcification within advanced lesions of apoE-/- mice may recapitulate endochondral bone formation.  

Mohamad Navab, G.M. Anantharamaiah, Susan Hama, Greg Hough, Srinivasa T. Reddy, Joy S. Frank, David W. Garber, Shaila Handattu, and Alan M. Fogelman
Arterioscler Thromb Vasc Biol. 2005;25:1426-1432; published online before print April 21 2005, doi:10.1161/01.ATV.0000167412.98221.1a
Abstract | Full Text | PDF
D-4F and pravastatin when given in combination at oral doses that were ineffective when given as single agents rendered HDL antiinflammatory in mice and monkeys and prevented atherosclerosis in young and caused regression of established lesions in old apoE null mice.  

Sergei Ragozin, Andreas Niemeier, Alexander Laatsch, Britta Loeffler, Martin Merkel, Ulrike Beisiegel, and Joerg Heeren
Arterioscler Thromb Vasc Biol. 2005;25:1433-1438; published online before print April 21 2005, doi:10.1161/01.ATV.0000166616.86723.d0
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Here we describe the application of RNA interference in vivo by using an adenoviral vector to elucidate the liver-specific role of ABCA1 with regard to its influence on systemic lipoprotein metabolism. Knockdown of hepatic ABCA1 leads to a reduction of both plasma HDL levels and postprandial lipemia.  

Heiko Methe, Jong-Oh Kim, Sieglinde Kofler, Michael Nabauer, and Michael Weis
Arterioscler Thromb Vasc Biol. 2005;25:1439-1445; published online before print April 28 2005, doi:10.1161/01.ATV.0000168410.44722.86
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Statin influences on expression and downstream signaling of Toll-like receptor 4 on CD14+ monocytes were assessed. Statins induced a dose-dependent downregulation of TLR4 with subsequent reduction in IRAK activity and cytokine and B7-1 expression. These effects were mediated via inhibition of protein geranylgeranylation and farnesylation. These observations imply a novel mechanism of pleiotropic statin effects.  

Nadine Brodala, Elizabeth P. Merricks, Dwight A. Bellinger, Damrong Damrongsri, Steven Offenbacher, James Beck, Phoebus Madianos, Daniela Sotres, Yu-Ling Chang, Gary Koch, and Timothy C. Nichols
Arterioscler Thromb Vasc Biol. 2005;25:1446-1451; published online before print April 21 2005, doi:10.1161/01.ATV.0000167525.69400.9c
Abstract | Full Text | PDF | Data Supplement
To determine whether recurrent intravenous injections with Porphyromonas gingivalis promotes coronary artery and aortic atherosclerosis, pigs fed low- or high-fat chow were divided into P gingivalis-challenged or control groups. P gingivalis-challenged pigs developed significantly greater amount of atherosclerosis in the normocholesterolemic group and nearly significant in the hypercholesterolemic group.  

Guillermo Zalba, Oscar Beloqui, Gorka San José, María U. Moreno, Ana Fortuño, and Javier Díez
Arterioscler Thromb Vasc Biol. 2005;25:1452-1457; published online before print April 28 2005, doi:10.1161/01.ATV.0000168411.72483.08
Abstract | Full Text | PDF | Data Supplement
Oxidative stress plays a critical role in the pathogenesis of atherosclerosis. In a population sample of 184 adults without clinically overt atherosclerotic disease, increased NADPH oxidase-derived superoxide production from phagocytic cells associated with enhanced carotid intima-media thickness, thus suggesting a relationship between phagocytic NADPH oxidase and the development of atherosclerosis.  

Hiroshi Yamagami, Kazuo Kitagawa, Taku Hoshi, Shigetaka Furukado, Hidetaka Hougaku, Yoji Nagai, and Masatsugu Hori
Arterioscler Thromb Vasc Biol. 2005;25:1458-1462; published online before print April 28 2005, doi:10.1161/01.ATV.0000168417.52486.56
Abstract | Full Text | PDF
With the use of B-mode ultrasound, this study examined the relationships of serum IL-18 levels with carotid intima-media thickness (IMT). We have found that higher IL-18 levels are associated with greater IMT, suggesting the link between IL-18 and atherosclerosis.  

Anand V. Doobay and Sonia S. Anand
Arterioscler Thromb Vasc Biol. 2005;25:1463-1469; published online before print May 5 2005, doi:10.1161/01.ATV.0000168911.78624.b7
Abstract | Full Text | PDF
The ankle-brachial index (ABI) has been shown to be a marker of cardiovascular risk. This systematic review of the literature shows that the ABI does indeed have a high specificity for predicting cardiovascular events. This simple noninvasive test should be incorporated into cardiovascular risk assessment of certain patient populations.  

Michael Loew, Michael M. Hoffmann, Wolfgang Koenig, Hermann Brenner, and Dietrich Rothenbacher
Arterioscler Thromb Vasc Biol. 2005;25:1470-1474; published online before print April 28 2005, doi:10.1161/01.ATV.0000168416.74206.62
Abstract | Full Text | PDF
The major haplotype -82G/-5G/+4A of the cystatin C gene was found to be associated with plasma concentration of cystatin C but not with prognosis of patients with CHD.  

Angelique C.M. Jansen, Emily S. van Aalst-Cohen, Michael W.T. Tanck, Suzanne Cheng, Marcel R. Fontecha, Jia Li, Joep C. Defesche, and John J.P. Kastelein
Arterioscler Thromb Vasc Biol. 2005;25:1475-1481; published online before print May 5 2005, doi:10.1161/01.ATV.0000168909.44877.a7
Abstract | Full Text | PDF | Data Supplement
We investigated the contribution of 65 polymorphisms in 36 candidate genes to CVD risk in FH patients and found that the G20210A polymorphism in the prothrombin gene was associated with CVD risk. Our results constitute a step forward in the unraveling of the hereditary propensity toward CVD in FH.  

Richard M. Martin, Shah Ebrahim, Maura Griffin, George Davey Smith, Andrew N. Nicolaides, Niki Georgiou, Simone Watson, Stephen Frankel, Jeff M.P. Holly, and David Gunnell
Arterioscler Thromb Vasc Biol. 2005;25:1482-1488; published online before print May 12 2005, doi:10.1161/01.ATV.0000170129.20609.49
Abstract | Full Text | PDF | Data Supplement
We investigated the association between breastfeeding in infancy and later atherosclerosis among 405 participants in a 65-year follow-up study. Breastfeeding was inversely associated with intima-media thickness and carotid and femoral plaque prevalence, even after controlling for socioeconomic and behavioral factors. Breastfeeding may lower atherosclerosis risk in later life.  

 

ThrombosisBack

L. Almasy, J.M. Soria, J.C. Souto, D.M. Warren, A. Buil, M. Borrell, X. Muñoz, N. Sala, M. Lathrop, J. Fontcuberta, and J. Blangero
Arterioscler Thromb Vasc Biol. 2005;25:1489-1492; published online before print April 21 2005, doi:10.1161/01.ATV.0000166602.04711.2e
Abstract | Full Text | PDF
This is the first genome-wide screen for genes influencing levels of TFPI. Linkage (LOD=3.52, genome-wide P=0.01) was observed on chromosome 2q, near the TFPI structural gene. These results suggest that polymorphisms in and around the TFPI gene are the major genetic determinants of variation in TFPI levels.  

Elena M. Egorina, Mikhail A. Sovershaev, Geir Bjørkøy, Franz X.E. Gruber, Jan O. Olsen, Behnaz Parhami-Seren, Kenneth G. Mann, and Bjarne Østerud
Arterioscler Thromb Vasc Biol. 2005;25:1493-1498; published online before print April 28 2005, doi:10.1161/01.ATV.0000168413.29874.d7
Abstract | Full Text | PDF | Data Supplement
In the present ex vivo study, we report several novel observations characterizing the distribution of TF antigen between the interior and the surface of MNCs from HRs and LRs. MNCs from HRs and LRs exhibit distinct patterns of intracellular accumulation, externalization and shedding of TF in LPS-stimulated conditions.  

Jeffrey F.W. Keuren, Simone J.H. Wielders, Hans Ulrichts, Tilman Hackeng, Johan W.M. Heemskerk, Hans Deckmyn, Edouard M. Bevers, and Theo Lindhout
Arterioscler Thromb Vasc Biol. 2005;25:1499-1505; published online before print April 21 2005, doi:10.1161/01.ATV.0000167526.31611.f6
Abstract | Full Text | PDF | Data Supplement
Our study demonstrates that the interaction of thrombin with PAR-1 mediates a synergistic effect on collagen-induced platelet procoagulant activity by inducing a sustained elevation in [Ca2+]i in a subpopulation of platelets.  

Tatsuya Yufu, Katsuya Hirano, Dan Bi, Mayumi Hirano, Junji Nishimura, Yukihide Iwamoto, and Hideo Kanaide
Arterioscler Thromb Vasc Biol. 2005;25:1506-1511; published online before print April 28 2005, doi:10.1161/01.ATV.0000168418.10276.f0
Abstract | Full Text | PDF | Data Supplement
We provided evidence that Rac1 regulates the surface expression of thrombin receptor PAR1 in vascular smooth muscle. Inhibition of Rac1 by hydroxy-3-methyl-glutaryl coenzyme A reductase inhibitor, a Rac1/Cdc42 inhibitory fragment, and an RNA interference technique reduced the surface expression of PAR1 and the responsiveness to thrombin.  

Sebastian F. Mause, Philipp von Hundelshausen, Alma Zernecke, Rory R. Koenen, and Christian Weber
Arterioscler Thromb Vasc Biol. 2005;25:1512-1518; published online before print May 12 2005, doi:10.1161/01.ATV.0000170133.43608.37
Abstract | Full Text | PDF
Platelet activation mediates multiple cellular responses, including secretion of chemokines such as RANTES, and formation of platelet microparticles (PMPs). We studied the role of PMPs in delivering RANTES and promoting monocyte recruitment. Circulating PMPs may serve as a finely tuned transcellular delivery system for RANTES, triggering monocyte arrest to inflamed and atherosclerotic endothelium, introducing a novel mechanism for platelet-dependent monocyte recruitment in inflammation and atherosclerosis.  

J.A. Zeller, A. Lenz, C.C. Eschenfelder, P. Zunker, and G. Deuschl
Arterioscler Thromb Vasc Biol. 2005;25:1519-1523; published online before print April 21 2005, doi:10.1161/01.ATV.0000167524.69092.16
Abstract | Full Text | PDF
Platelet leukocyte aggregation and platelet activation were investigated in 58 acute stroke patients. Patients following previous infection showed significantly more platelet leukocyte aggregates and increased activation compared with the remaining patients. This difference disappeared at day seven. Intercellular platelet leukocyte interaction may contribute to the pathophysiology of acute cerebral ischemia.  

 

Letters to the EditorBack

Nonalcoholic Fatty Liver Disease and Atherosclerosis

Giovanni Targher, Angel Brea, and Emilio Ros
Arterioscler Thromb Vasc Biol. 2005;25:e117-e118, doi:10.1161/01.ATV.0000170132.91268.a2
Extract | Full Text | PDF  

Simvastatin Given for 3 Days Can Inhibit Thrombin Generation and Activation of Factor V and Enhance Factor Va Inactivation in Hypercholesterolemic Patients

Anetta Undas, Magdalena Celinska-Löwenhoff, Kathleen E. Brummel-Ziedins, Jan Brozek, Andrew Szczeklik, and Kenneth G. Mann
Arterioscler Thromb Vasc Biol. 2005;25:1524-1525, doi:10.1161/01.ATV.0000168913.25278.38
Extract | Full Text | PDF  

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