Search:
Advanced Search
ATVB Home
Subscriptions
Archives
Feedback
Authors
Help
AHA Journals Home
« Previous Issue
|
Next Issue »
About This Cover
Volume 25, Issue 11; November 1, 2005
Editorials
Brief Reviews
Vascular Biology
Atherosclerosis and Lipoproteins
Thrombosis
Letters to the Editor
Search This Issue:
Index by Author
Sign up for eTOCs
To see an article, click its "Full Text" or "PDF" link. To review many abstracts, check the boxes to the left of the titles you want, and click the "Get All Checked Abstract(s)" button. To see one abstract at a time, click its "Abstract" link.
article is free immediately upon publication
Editorials
Iron Chelation and Vascular Function: In Search of the Mechanisms
Dardo E. Ferrara and W. Robert Taylor
Arterioscler Thromb Vasc Biol. 2005;25:2235-2237, doi:10.1161/01.ATV.0000189303.45609.1f
Full Text
|
PDF
Beyond Blood Pressure: Subtle Effects of Drug Classes
Michael F. ORourke
Arterioscler Thromb Vasc Biol. 2005;25:2238-2239, doi:10.1161/01.ATV.0000189321.13314.f7
Full Text
|
PDF
Ethnic Differences in Arterial Responses, Inflammation, and Metabolic Profiles: Possible Insights into Ethnic Differences in Cardiovascular Disease and Stroke
Gregory Y.H. Lip and Christopher J. Boos
Arterioscler Thromb Vasc Biol. 2005;25:2240-2242, doi:10.1161/01.ATV.0000188507.89134.ef
Full Text
|
PDF
Metabolic Syndrome Scientific Statement by the American Heart Association and the National Heart, Lung, and Blood Institute
Scott M. Grundy
Arterioscler Thromb Vasc Biol. 2005;25:2243-2244, doi:10.1161/01.ATV.0000189155.75833.c7
Full Text
|
PDF
Brief Reviews
ATVB in Focus: Novel Mediators and Mechanisms in Angiogenesis and Vasculogenesis
Stefanie Dimmeler
Arterioscler Thromb Vasc Biol. 2005;25:2245, doi:10.1161/01.ATV.0000187471.06942.17
Full Text
|
PDF
Mechanisms of Endothelial Differentiation in Embryonic Vasculogenesis
J.E. Ferguson, III, Rusty W. Kelley, and Cam Patterson
Arterioscler Thromb Vasc Biol. 2005;25:2246-2254; published online before print August 25 2005, doi:10.1161/01.ATV.0000183609.55154.44
Abstract
|
Full Text
|
PDF
The formation of new blood vessels in the adult organism not only contributes to the progression of diseases such as cancer and diabetic retinopathy but also can be promoted in therapeutic approaches to various ischemic pathologies. In this review, we describe the current understanding of where endothelial differentiation from pluripotent progenitor cells occurs during development, how this process is controlled at the molecular level, and what model systems can be used to investigate the earliest steps of blood vessel formation.
Consequences and Therapeutic Implications of Macrophage Apoptosis in Atherosclerosis: The Importance of Lesion Stage and Phagocytic Efficiency
Ira Tabas
Arterioscler Thromb Vasc Biol. 2005;25:2255-2264; published online before print September 1 2005, doi:10.1161/01.ATV.0000184783.04864.9f
Abstract
|
Full Text
|
PDF
Whereas macrophage apoptosis in early atherosclerotic lesions appears to decrease lesion cellularity, macrophage apoptosis in advanced lesions may contribute to necrotic core formation. This difference is probably attributable to the relatively incompetence of late lesional phagocytes to safely and efficiently clear apoptotic cells, leading to postapoptotic macrophage necrosis.
Dietary and Genetic Probes of Atherogenic Dyslipidemia
Ronald M. Krauss
Arterioscler Thromb Vasc Biol. 2005;25:2265-2272; published online before print September 15 2005, doi:10.1161/01.ATV.0000186365.73973.f0
Abstract
|
Full Text
|
PDF
Dietary and genetic factors can interact to generate a phenotype characterized by an increase in small dense LDL particles that is a component of the atherogenic dyslipidemia of the metabolic syndrome. Genotypes associated with responses of lipoprotein subspecies to changes in dietary carbohydrate and fat can contribute to interindividual variability in LDL response to diet.
Tissue-Specific Hemostasis in Mice
Nigel Mackman
Arterioscler Thromb Vasc Biol. 2005;25:2273-2281; published online before print August 25 2005, doi:10.1161/01.ATV.0000183884.06371.52
Abstract
|
Full Text
|
PDF
Formation of a fibrin-rich clot is regulated by the coagulation, anticoagulation, and fibrinolytic pathways. Decreased fibrin is associated with bleeding, whereas increased fibrin leads to thrombosis. Analysis of mice with defects in clot formation suggests that hemostasis is regulated in a tissue-specific manner.
Vascular Biology
Iron Chelation Suppresses Ferritin Upregulation and Attenuates Vascular Dysfunction in the Aorta of Angiotensin IIInfused Rats
Nobukazu Ishizaka, Kan Saito, Ichiro Mori, Gen Matsuzaki, Minoru Ohno, and Ryozo Nagai
Arterioscler Thromb Vasc Biol. 2005;25:2282-2288; published online before print August 11 2005, doi:10.1161/01.ATV.0000181763.57495.2b
Abstract
|
Full Text
|
PDF
We have investigated whether long-term administration of angiotensin (Ang) II causes ferritin induction and iron accumulation in the rat aorta, and their possible relation to regulatory effects on gene expression and vascular function in Ang II-infused animals. Ang II infusion caused ferritin induction and iron deposition in the aortas. These phenomena might have a role in the regulation of gene expression, impairment of vascular function, and arterial remodeling induced by Ang II, which are presumably mediated in part by enhancement of oxidative stress.
High Serum Bilirubin Concentrations Preserve Coronary Flow Reserve and Coronary Microvascular Functions
Hakan Gullu, Dogan Erdogan, Derya Tok, Semra Topcu, Mustafa Caliskan, Taner Ulus, and Haldun Muderrisoglu
Arterioscler Thromb Vasc Biol. 2005;25:2289-2294; published online before print September 8 2005, doi:10.1161/01.ATV.0000185806.61430.7c
Abstract
|
Full Text
|
PDF
We have measured coronary flow reserve of 53 subjects with low serum bilirubin, 55 subjects with intermediate serum bilirubin level, and 52 subjects with high serum bilirubin level. We found that high serum bilirubin values in normal range preserve coronary flow reserve.
IQGAP1 Regulates Reactive Oxygen SpeciesDependent Endothelial Cell Migration Through Interacting With Nox2
Satoshi Ikeda, Minako Yamaoka-Tojo, Lula Hilenski, Nikolay A. Patrushev, Ghulam M. Anwar, Mark T. Quinn, and Masuko Ushio-Fukai
Arterioscler Thromb Vasc Biol. 2005;25:2295-2300; published online before print September 22 2005, doi:10.1161/01.ATV.0000187472.55437.af
Abstract
|
Full Text
|
PDF
|
Data Supplement
Using a monolayer scratch assay of confluent endothelial cells (ECs), we show that IQGAP1, an actin binding scaffold protein, functions to link Nox2 of NAD(P)H oxidase to actin at the leading edge, thereby facilitating ROS production at the site of injury, which may contribute to EC migration.
12/15-Lipoxygenase Regulates Intercellular Adhesion Molecule-1 Expression and Monocyte Adhesion to Endothelium Through Activation of RhoA and Nuclear Factor-
B
David T. Bolick, A. Wayne Orr, Angela Whetzel, Suseela Srinivasan, Melissa E. Hatley, Martin A. Schwartz, and Catherine C. Hedrick
Arterioscler Thromb Vasc Biol. 2005;25:2301-2307; published online before print September 15 2005, doi:10.1161/01.ATV.0000186181.19909.a6
Abstract
|
Full Text
|
PDF
|
Data Supplement
12/15-lipoxygenase (12/15-LO) promotes monocyte:endothelial interactions and atherosclerosis. We report that 12/15-LO activation in endothelium activates the small GTPase RhoA which then activates PKC{alpha} and NF{kappa}B. The activation of this pathway increases endothelial ICAM-1 expression in vivo. ICAM-1 is a primary regulator of monocyte adhesion to endothelium.
Toll-Like Receptor 2 Mediates Persistent Chemokine Release by
Chlamydia pneumoniae
Infected Vascular Smooth Muscle Cells
Xin Yang, Daniel Coriolan, Kelly Schultz, Douglas T. Golenbock, and Debbie Beasley
Arterioscler Thromb Vasc Biol. 2005;25:2308-2314; published online before print September 22 2005, doi:10.1161/01.ATV.0000187468.00675.a3
Abstract
|
Full Text
|
PDF
|
Data Supplement
TLR2 is expressed constitutively in mouse VSMCs, its expression is inducible in human VSMCs, and it mediates both persistent stimulation of MCP-1 release in SMCs infected with C pneumoniae and acute stimulation by extracellular C pneumoniae. Activation of TLR2 expressed in VSMCs may promote inflammation within the arterial wall.
Integrin
V
ß
3
as a Target for Blocking HIV-1 Tat-Induced Endothelial Cell Activation In Vitro and Angiogenesis In Vivo
Chiara Urbinati, Stefania Mitola, Elena Tanghetti, Chandra Kumar, Johannes Waltenberger, Domenico Ribatti, Marco Presta, and Marco Rusnati
Arterioscler Thromb Vasc Biol. 2005;25:2315-2320; published online before print September 15 2005, doi:10.1161/01.ATV.0000186182.14908.7b
Abstract
|
Full Text
|
PDF
|
Data Supplement
The transactivating factor (Tat) of HIV-1 binds to endothelial {alpha}vß3 integrin triggering focal adhesion kinase and NF-{kappa}B activation that lead to endothelial cell proliferation, membrane ruffling, and motility in vitro and neovascularization in vivo. The RGD-peptidomimetic SCH221153 inhibits these biological activities with high efficiency and specificity.
PAR-1 Activation on Human Late Endothelial Progenitor Cells Enhances Angiogenesis In Vitro With Upregulation of the SDF-1/CXCR4 System
David M. Smadja, Ivan Bièche, Georges Uzan, Heidi Bompais, Laurent Muller, Catherine Boisson-Vidal, Michel Vidaud, Martine Aiach, and Pascale Gaussem
Arterioscler Thromb Vasc Biol. 2005;25:2321-2327; published online before print September 1 2005, doi:10.1161/01.ATV.0000184762.63888.bd
Abstract
|
Full Text
|
PDF
|
Data Supplement
We provide evidence that human late endothelial progenitor cells express PAR-1, and that PAR-1 activation induces proliferation, migration and increased capillary-like structure formation in Matrigel. Analysis of this phenomenon showed that enhancement of the CXCR-4/SDF-1 pathway is a key mechanism underlying PAR-1-induced EPC angiogenesis.
HERP1 Inhibits Myocardin-Induced Vascular Smooth Muscle Cell Differentiation by Interfering With SRF Binding to CArG Box
Hiroshi Doi, Tatsuya Iso, Miki Yamazaki, Hideo Akiyama, Hiroyoshi Kanai, Hiroko Sato, Keiko Kawai-Kowase, Toru Tanaka, Toshitaka Maeno, Ei-ichi Okamoto, Masashi Arai, Larry Kedes, and Masahiko Kurabayashi
Arterioscler Thromb Vasc Biol. 2005;25:2328-2334; published online before print September 8 2005, doi:10.1161/01.ATV.0000185829.47163.32
Abstract
|
Full Text
|
PDF
|
Data Supplement
Myocardin is a potent SRF coactivator for VSMC differentiation. HERP1, a target gene of Notch, is a transcriptional repressor in vascular system. Both factors are coinduced in synthetic VSMCs. HERP1 inhibits myocardin-dependent SMC differentiation by preventing SRF from DNA binding through physical association with SRF.
Statin Protects Endothelial Nitric Oxide Synthase Activity in Hypoxia-Induced Pulmonary Hypertension
Takahisa Murata, Kazuya Kinoshita, Masatoshi Hori, Masayoshi Kuwahara, Hirokazu Tsubone, Hideaki Karaki, and Hiroshi Ozaki
Arterioscler Thromb Vasc Biol. 2005;25:2335-2342; published online before print September 15 2005, doi:10.1161/01.ATV.0000186184.33537.48
Abstract
|
Full Text
|
PDF
|
Data Supplement
We investigated the effect of fluvastatin on endothelial impairment in pulmonary hypertension and revealed that fluvastatin can restore the decrease in endothelial NO production through its protective effects against eNOS-tight coupling with caveolin-1 caused by chronic hypoxia.
Single Perivascular Delivery of Mitomycin C Stimulates p21 Expression and Inhibits Neointima Formation in Rat Arteries
Juan F. Granada, Diana Ensenat, Amit N. Keswani, Grzegorz L. Kaluza, Albert E. Raizner, Xiao-ming Liu, Kelly J. Peyton, Mohammed A. Azam, Hong Wang, and William Durante
Arterioscler Thromb Vasc Biol. 2005;25:2343-2348; published online before print September 1 2005, doi:10.1161/01.ATV.0000184779.01822.9d
Abstract
|
Full Text
|
PDF
|
Data Supplement
We examined the effect of mytomycin C (MMc) on VSMC proliferation. MMc inhibited the growth of cultured VSMCs and neointima formation after rat carotid artery balloon injury, and this was associated with increased p21 expression. MMc represents a potentially new therapeutic agent in preventing vasculoproliferative disorders.
Proteinase-Activated Receptor-2 Mediates Arterial Vasodilation in Diabetes
Fiorentina Roviezzo, Mariarosaria Bucci, Vincenzo Brancaleone, Annarita Di Lorenzo, Pierangelo Geppetti, Silvana Farneti, Luca Parente, Giuseppe Lungarella, Stefano Fiorucci, and Giuseppe Cirino
Arterioscler Thromb Vasc Biol. 2005;25:2349-2354; published online before print September 1 2005, doi:10.1161/01.ATV.0000184770.01494.2e
Abstract
|
Full Text
|
PDF
|
Data Supplement
On diabetes development in NOD mice there is a diminished vasodilatory response to acetylcholine that is counterbalanced by an increased expression of PAR-2 both as protein and message. The expression is mainly localized on the smooth muscle cell component as demonstrated by the immunohistochemistry and functional studies
Novel Mechanism of Vasodilation in Inflammatory Bowel Disease
Ossama A. Hatoum, Kathryn M. Gauthier, David G. Binion, Hiroto Miura, Gordon Telford, Mary F. Otterson, William B. Campbell, and David D. Gutterman
Arterioscler Thromb Vasc Biol. 2005;25:2355-2361; published online before print September 1 2005, doi:10.1161/01.ATV.0000184757.50141.8d
Abstract
|
Full Text
|
PDF
In IBD patients, Ach-mediated dilation in arterioles shifts from endothelial production of NO and EDHF to nonendothelial generation of a PG, likely PGD2. This is a novel dilator mechanism arising from nonendothelial vascular tissue that compensates for loss of endothelium-dependent dilation.
Ethnic Differences in Arterial Responses and Inflammatory Markers in Afro-Caribbean and Caucasian Subjects
Lalit Kalra, Curtis Rambaran, Philip Chowienczyk, David Goss, Ian Hambleton, James Ritter, Ajay Shah, Rainford Wilks, and Terrence Forrester
Arterioscler Thromb Vasc Biol. 2005;25:2362-2367; published online before print August 25 2005, doi:10.1161/01.ATV.0000183887.76087.6a
Abstract
|
Full Text
|
PDF
Small vessel disease is more common in Afro-Caribbeans. A comparison of metabolic variables, inflammatory markers, and arterial function between 78 healthy Afro-Caribbeans and 82 matched Caucasians showed higher diastolic blood pressure, fasting insulin, tumor necrosis factor {alpha}, and interleukin 6 levels in Afro-Caribbeans, which was associated with the attenuation of small, but not large, vessel function.
Atherosclerosis and Lipoproteins
A Comparison of Three Different Methods to Evaluate Endothelium-Dependent Vasodilation in the Elderly: The Prospective Investigation of the Vasculature in Uppsala Seniors (PIVUS) Study
Lars Lind, Nilla Fors, Jan Hall, Kerstin Marttala, and Anna Stenborg
Arterioscler Thromb Vasc Biol. 2005;25:2368-2375; published online before print September 1 2005, doi:10.1161/01.ATV.0000184769.22061.da
Abstract
|
Full Text
|
PDF
|
Data Supplement
In the population-based PIVUS study (1016 subjects aged 70 years), endothelium-dependent vasodilation was evaluated with 3 different methods. The invasive forearm technique with acetylcholine and flow-mediated dilatation were independently associated with the Framingham score, suggesting that conduit artery and resistance artery endothelial function carry different, but important, information in the elderly.
Inhibition of the Renin-Angiotensin System Prevents Free Fatty AcidInduced Acute Endothelial Dysfunction in Humans
Saiko Watanabe, Tatsuya Tagawa, Ken Yamakawa, Michio Shimabukuro, and Shinichiro Ueda
Arterioscler Thromb Vasc Biol. 2005;25:2376-2380; published online before print September 22 2005, doi:10.1161/01.ATV.0000187465.55507.85
Abstract
|
Full Text
|
PDF
We investigated the involvement of the RAS on FFA-induced endothelial dysfunction. An ACE inhibitor or an ARB prevented FFA-induced endothelial dysfunction. Our results suggest that elevated FFAs, which are frequently seen in patients with insulin resistance, cause endothelial dysfunction via RAS activation and presumably the resultant oxidative stress in humans.
Impact of Treatment With Protease Inhibitors on Aortic Stiffness in Adult Patients With Human Immunodeficiency Virus Infection
Giuseppe Schillaci, Giuseppe V.L. De Socio, Matteo Pirro, Gianluca Savarese, Massimo R. Mannarino, Franco Baldelli, Giuliano Stagni, and Elmo Mannarino
Arterioscler Thromb Vasc Biol. 2005;25:2381-2385; published online before print August 25 2005, doi:10.1161/01.ATV.0000183744.38509.de
Abstract
|
Full Text
|
PDF
Aortic stiffness was higher in HIV patients treated with protease inhibitors than in matched controls, also after adjustment for the effect of classic cardiovascular risk factors. Pulse wave velocity increased with longer exposure to treatment. We hypothesize that arteriosclerosis is a side effect of antiretroviral treatment including a protease inhibitor.
The Lamina Adventitia Is the Major Site of Immune Cell Accumulation in Standard Chow-Fed Apolipoprotein EDeficient Mice
Michael P.W. Moos, Nicole John, Rolf Gräbner, Silke Noßmann, Bernd Günther, Rüdiger Vollandt, Colin D. Funk, Brigitte Kaiser, and Andreas J.R. Habenicht
Arterioscler Thromb Vasc Biol. 2005;25:2386-2391; published online before print September 22 2005, doi:10.1161/01.ATV.0000187470.31662.fe
Abstract
|
Full Text
|
PDF
|
Data Supplement
Progression of atherosclerosis in apoE-/- mice is associated with a large increase in adventitial T cells, formation of T/B cell clusters, and of lymphoid-like follicles in the aged aorta. Thus, the lamina adventitia is a major location of adaptive immunity during atherogenesis in apoE-/- mice.
Selective Insulin Resistance Affecting Nitric Oxide Release But Not Plasminogen Activator Inhibitor-1 Synthesis in Fibroblasts From Insulin-Resistant Individuals
Assunta Pandolfi, Anna Solini, Giuliana Pellegrini, Gabriella Mincione, Sara Di Silvestre, Paola Chiozzi, Annalisa Giardinelli, Maria Carmela Di Marcantonio, Alessandro Piccirelli, Fabio Capani, and Agostino Consoli
Arterioscler Thromb Vasc Biol. 2005;25:2392-2397; published online before print September 8 2005, doi:10.1161/01.ATV.0000185831.13559.a2
Abstract
|
Full Text
|
PDF
|
Data Supplement
We investigated insulin pro- and antiatherogenic properties in fibroblasts derived from insulin-resistant (IR) subjects. In IR fibroblasts, insulin-dependent NO release and Akt phosphorylation were impaired, whereas insulin ability to stimulate MAPK activity and PAI-1 release was unaffected.
Transcription Factor SOX18 Is Expressed in Human Coronary Atherosclerotic Lesions and Regulates DNA Synthesis and Vascular Cell Growth
Marta García-Ramírez, José Martínez-González, Josep O. Juan-Babot, Cristina Rodríguez, and Lina Badimon
Arterioscler Thromb Vasc Biol. 2005;25:2398-2403; published online before print September 22 2005, doi:10.1161/01.ATV.0000187464.81959.23
Abstract
|
Full Text
|
PDF
|
Data Supplement
|
Data Supplement
We analyzed the involvement of SOX18 in vascular cell growth. SOX18 is expressed in human coronary advanced atherosclerotic lesions (ECs and VSMCs), and it is associated with cell proliferation and wound repair. Therefore, SOX18 could play a role in atherosclerosis.
Trichostatin A Exacerbates Atherosclerosis in Low Density Lipoprotein ReceptorDeficient Mice
Jae-Hoon Choi, Ki-Hoan Nam, Jiyun Kim, Min Won Baek, Jeong-Euy Park, Hyun-Young Park, Ho Jeong Kwon, Oh-Seung Kwon, Dae-Yong Kim, and Goo Taeg Oh
Arterioscler Thromb Vasc Biol. 2005;25:2404-2409; published online before print September 1 2005, doi:10.1161/01.ATV.0000184758.07257.88
Abstract
|
Full Text
|
PDF
|
Data Supplement
We investigated the effect of trichostatin A, a specific histone deacetylase inhibitor, on atherosclerosis of LDL receptor-deficient mice. TSA significantly increased the formation of fatty streak lesion and macrophage infiltration possibly by enhancing the expression of CD36 and other proatherogenic molecules, suggesting the role of histone acetylation in atherogenesis.
Enhanced Conversion of Triglyceride-Rich Lipoproteins and Increased Low-Density Lipoprotein Removal in LPLS447X Carriers
Melchior C. Nierman, Berthil H.C.M.T. Prinsen, Jaap Rip, Robert Jan Veldman, Jan Albert Kuivenhoven, John J.P. Kastelein, Monique G.M. de Sain-van der Velden, and Erik S.G. Stroes
Arterioscler Thromb Vasc Biol. 2005;25:2410-2415; published online before print September 29 2005, doi:10.1161/01.ATV.0000188506.79946.ce
Abstract
|
Full Text
|
PDF
|
Data Supplement
We evaluated apoB100 kinetics in homozygous LPLS447X carriers using an L-[1-13C]-valine infusion to test the hypothesis of improved apoB100 metabolism in carriers. Enhanced TRL conversion and enhanced LDL removal with increased preheparin LPL concentration in carriers suggest increased enzymatic as well as nonenzymatic consequences of LPL in LPLS447X carriers.
Impact of Short-Term Administration of High-Density Lipoproteins and Atorvastatin on Atherosclerosis in Rabbits
Stephen J. Nicholls, Belinda Cutri, Stephen G. Worthley, Patrick Kee, Kerry-Anne Rye, Shisan Bao, and Philip J. Barter
Arterioscler Thromb Vasc Biol. 2005;25:2416-2421; published online before print September 1 2005, doi:10.1161/01.ATV.0000184760.95957.d6
Abstract
|
Full Text
|
PDF
|
Data Supplement
Atherosclerosis was established in rabbit aortas by balloon denudation and 17 weeks of cholesterol feeding. Infusing HDL during the last 5 days reduced lesion size, increased the ratio of smooth muscle cells to macrophages, and reduced metalloproteinase while increasing thrombomodulin expression in the lesions, consistent with stabilization of plaques by HDL.
Probucol Enhances the Expression of Human Hepatic Scavenger Receptor Class B Type I, Possibly Through a Species-Specific Mechanism
Ken-ichi Hirano, Chiaki Ikegami, Ken-ichi Tsujii, Zhongyan Zhang, Fumihiko Matsuura, Yumiko Nakagawa-Toyama, Masahiro Koseki, Daisaku Masuda, Takao Maruyama, Iichiro Shimomura, Yukihiko Ueda, and Shizuya Yamashita
Arterioscler Thromb Vasc Biol. 2005;25:2422-2427; published online before print September 8 2005, doi:10.1161/01.ATV.0000185834.98941.3d
Abstract
|
Full Text
|
PDF
|
Data Supplement
Probucol increases hepatic SR-BI, which seems to be attributable to a species-specific stabilization of the protein. Data of host-swap experiments indicate that this effect is unlikely to be the result of a direct interaction between probucol and SR-BI protein, but rather may be related to certain factors in human hepatocytes.
Thrombosis
CD40 Ligand Influences Platelet Release of Reactive Oxygen Intermediates
Subrata Chakrabarti, Sonia Varghese, Olga Vitseva, Kahraman Tanriverdi, and Jane E. Freedman
Arterioscler Thromb Vasc Biol. 2005;25:2428-2434; published online before print September 1 2005, doi:10.1161/01.ATV.0000184765.59207.f3
Abstract
|
Full Text
|
PDF
|
Data Supplement
The role of sCD40L in platelet function and RONS formation was examined. Soluble CD40L enhances platelet activation, aggregation, and platelet-leukocyte conjugation, as well as increases stimulation-induced platelet release of RONS through activation of Akt and p38 MAP kinase signaling pathways. sCD40L influences platelet-dependent thrombotic and inflammatory responses contributing to atherothrombosis.
Angiotensin-Converting Enzyme Inhibition Increases Basal Vascular Tissue Plasminogen Activator Release in Women But Not in Men
Mias Pretorius, James M. Luther, Laine J. Murphey, Douglas E. Vaughan, and Nancy J. Brown
Arterioscler Thromb Vasc Biol. 2005;25:2435-2440; published online before print September 15 2005, doi:10.1161/01.ATV.0000186185.13977.94
Abstract
|
Full Text
|
PDF
|
Data Supplement
This study tests the hypothesis that gender influences the effect of ACE inhibition on vascular t-PA release. Enalaprilat increased basal t-PA release in premenopausal (P=0.023) and postmenopausal women (P=0.010) but not in young or older men. During enalaprilat, basal t-PA release was significantly greater in women compared with men (P=0.028).
Letters to the Editor
Circulating Human Heat Shock Protein 60 in the Blood of Healthy Teenagers: A Novel Determinant of Endothelial Dysfunction and Early Vascular Injury?
Julian P.J. Halcox, John Deanfield, Alireza Shamaei-Tousi, Brian Henderson, Andrew Steptoe, Anthony R.M. Coates, Atul Singhal, and Alan Lucas
Arterioscler Thromb Vasc Biol. 2005;25:e141-e142, doi:10.1161/01.ATV.0000185832.34992.ff
Full Text
|
PDF
Inflammation Warms Up the Metabolic Syndrome
Katherine Esposito, Miryam Ciotola, and Dario Giugliano
Arterioscler Thromb Vasc Biol. 2005;25:e143, doi:10.1161/01.ATV.0000185830.17528.e3
Full Text
|
PDF
Spotlight
TOC Spotlight File
Advertisement
ATVB Home
|
Subscriptions
|
Archives
|
Feedback
|
Authors
|
Help
|
AHA Journals Home
|
Search
Copyright © 2008 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited.