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9641. Hypercholesterolemia abrogates late preconditioning via a tetrahydrobiopterin-dependent mechanism in conscious rabbits.
作者: Xian-Liang Tang.;Hitoshi Takano.;Yu-Ting Xuan.;Hiroshi Sato.;Eitaro Kodani.;Buddhadeb Dawn.;Yanqing Zhu.;Gregg Shirk.;Wen-Jian Wu.;Roberto Bolli.
来源: Circulation. 2005年112卷14期2149-56页
Although the late phase of ischemic preconditioning (PC) is known to confer cardioprotection in healthy animal models, it is unknown whether this phenomenon exists in the presence of hypercholesterolemia. The goal of this study was to determine whether the infarct-sparing effect of late PC is affected by hypercholesterolemia and, if so, whether a tetrahydrobiopterin (BH4)-dependent mechanism is responsible for the loss of late PC.
9642. Role of the protein kinase C-epsilon-Raf-1-MEK-1/2-p44/42 MAPK signaling cascade in the activation of signal transducers and activators of transcription 1 and 3 and induction of cyclooxygenase-2 after ischemic preconditioning.
作者: Yu-Ting Xuan.;Yiru Guo.;Yanqing Zhu.;Ou-Li Wang.;Gregg Rokosh.;Robert O Messing.;Roberto Bolli.
来源: Circulation. 2005年112卷13期1971-8页
Although Janus kinase (JAK)-mediated Tyr phosphorylation of signal transducers and activators of transcription (STAT) 1 and 3 is essential for the upregulation of cyclooxygenase-2 (COX-2) and the cardioprotection of late preconditioning (PC), the role of Ser phosphorylation of STAT1 and STAT3 in late PC and the upstream signaling mechanisms responsible for mediating Ser phosphorylation of STAT1 and STAT3 remain unknown.
9643. Atorvastatin inhibits hypercholesterolemia-induced calcification in the aortic valves via the Lrp5 receptor pathway.
作者: Nalini M Rajamannan.;Malayannan Subramaniam.;Frank Caira.;Stuart R Stock.;Thomas C Spelsberg.
来源: Circulation. 2005年112卷9 Suppl期I229-34页
Calcific aortic valve disease is the most common indication for surgical valve replacement in the United States. The cellular mechanisms of valve calcification are not well understood. We have previously shown that cellular proliferation and osteoblastogenesis are important in the development of valvular heart disease. Lrp5, a known low-density receptor-related protein, plays an essential role in cellular proliferation and osteoblastogenesis via the beta-catenin signaling pathway. We hypothesize that Lrp5 also plays a role in aortic valve (AV) calcification in experimental hypercholesterolemia.
9644. Gender differences in the risk of ischemic stroke and peripheral embolism in atrial fibrillation: the AnTicoagulation and Risk factors In Atrial fibrillation (ATRIA) study.
作者: Margaret C Fang.;Daniel E Singer.;Yuchiao Chang.;Elaine M Hylek.;Lori E Henault.;Nancy G Jensvold.;Alan S Go.
来源: Circulation. 2005年112卷12期1687-91页
Previous studies provide conflicting results about whether women are at higher risk than men for thromboembolism in the setting of atrial fibrillation (AF). We examined data from a large contemporary cohort of AF patients to address this question.
9645. Mechanisms of ventricular fibrillation in canine models of congestive heart failure and ischemia assessed by in vivo noncontact mapping.
作者: Thomas H Everett.;Emily E Wilson.;Scott Foreman.;Jeffrey E Olgin.
来源: Circulation. 2005年112卷11期1532-41页
Much of the research performed studying the mechanism of ventricular fibrillation (VF) has been in normal ventricles rather than under a pathological condition predisposing to VF. We hypothesized that different ventricular substrates would alter the mechanism and characteristics of VF.
9646. Unmasking of brugada syndrome by lithium.
作者: Dawood Darbar.;Tao Yang.;Keith Churchwell.;Arthur A M Wilde.;Dan M Roden.
来源: Circulation. 2005年112卷11期1527-31页
The characteristic ECG pattern of ST-segment elevation in V1 and V2 in the Brugada syndrome is dynamic; it is often intermittently present in affected individuals and can be unmasked by sodium channel blockers, including antiarrhythmic drugs and tricyclic antidepressants. We report here 2 patients who developed the Brugada ECG pattern after administration of lithium, a commonly used drug not previously reported to block cardiac sodium channels.
9647. Dynamic imaging of allogeneic mesenchymal stem cells trafficking to myocardial infarction.
作者: Dara L Kraitchman.;Mitsuaki Tatsumi.;Wesley D Gilson.;Takayoshi Ishimori.;Dorota Kedziorek.;Piotr Walczak.;W Paul Segars.;Hunter H Chen.;Danielle Fritzges.;Izlem Izbudak.;Randell G Young.;Michelle Marcelino.;Mark F Pittenger.;Meiyappan Solaiyappan.;Raymond C Boston.;Benjamin M W Tsui.;Richard L Wahl.;Jeff W M Bulte.
来源: Circulation. 2005年112卷10期1451-61页
Recent results from animal studies suggest that stem cells may be able to home to sites of myocardial injury to assist in tissue regeneration. However, the histological interpretation of postmortem tissue, on which many of these studies are based, has recently been widely debated.
9648. Subunit interaction determines IKs participation in cardiac repolarization and repolarization reserve.
The role of IKs, the slow delayed rectifier K+ current, in cardiac ventricular repolarization has been a subject of debate.
9649. Characterization of atherosclerotic plaques by laser speckle imaging.
作者: Seemantini K Nadkarni.;Brett E Bouma.;Tina Helg.;Raymond Chan.;Elkan Halpern.;Alexandra Chau.;Milan Singh Minsky.;Jason T Motz.;Stuart L Houser.;Guillermo J Tearney.
来源: Circulation. 2005年112卷6期885-92页
A method capable of determining atherosclerotic plaque composition and measuring plaque viscoelasticity can provide valuable insight into intrinsic features associated with plaque rupture and can enable the identification of high-risk lesions. In this article, we describe a new optical technique, laser speckle imaging (LSI), that measures an index of plaque viscoelasticity. We evaluate the potential of LSI for characterizing atherosclerotic plaque.
9650. Real-time magnetic resonance imaging-guided stenting of aortic coarctation with commercially available catheter devices in Swine.
作者: Amish N Raval.;James D Telep.;Michael A Guttman.;Cengizhan Ozturk.;Michael Jones.;Richard B Thompson.;Victor J Wright.;William H Schenke.;Ranil DeSilva.;Ronnier J Aviles.;Venkatesh K Raman.;Michael C Slack.;Robert J Lederman.
来源: Circulation. 2005年112卷5期699-706页
Real-time MR imaging (rtMRI) is now technically capable of guiding catheter-based cardiovascular interventions. Compared with x-ray, rtMRI offers superior tissue imaging in any orientation without ionizing radiation. Translation to clinical trials has awaited the availability of clinical-grade catheter devices that are both MRI visible and safe. We report a preclinical safety and feasibility study of rtMRI-guided stenting in a porcine model of aortic coarctation using only commercially available catheter devices.
9651. Increased susceptibility to pulmonary hypertension in heterozygous BMPR2-mutant mice.
作者: Yanli Song.;John E Jones.;Hideyuki Beppu.;John F Keaney.;Joseph Loscalzo.;Ying-Yi Zhang.
来源: Circulation. 2005年112卷4期553-62页
Bone morphogenetic protein receptor-2 (BMPR2)-heterozygous, mutant (BMPR2(+/-)) mice have a genetic trait similar to that of certain patients with idiopathic pulmonary arterial hypertension (IPAH). To understand the role of BMPR2 in the development of IPAH, we examined the phenotype of BMPR2(+/-) mice and their response to inflammatory stress.
9652. Cardiac iron determines cardiac T2*, T2, and T1 in the gerbil model of iron cardiomyopathy.
作者: John C Wood.;Maya Otto-Duessel.;Michelle Aguilar.;Hanspeter Nick.;Marvin D Nelson.;Thomas D Coates.;Harvey Pollack.;Rex Moats.
来源: Circulation. 2005年112卷4期535-43页
Transfusional therapy for thalassemia major and sickle cell disease can lead to iron deposition and damage to the heart, liver, and endocrine organs. Iron causes the MRI parameters T1, T2, and T2* to shorten in these organs, which creates a potential mechanism for iron quantification. However, because of the danger and variability of cardiac biopsy, tissue validation of cardiac iron estimates by MRI has not been performed. In this study, we demonstrate that iron produces similar T1, T2, and T2* changes in the heart and liver using a gerbil iron-overload model.
9653. Calcified rheumatic valve neoangiogenesis is associated with vascular endothelial growth factor expression and osteoblast-like bone formation.
作者: Nalini M Rajamannan.;Thomas B Nealis.;Malayannan Subramaniam.;Sanjay Pandya.;Stuart R Stock.;Constatine I Ignatiev.;Thomas J Sebo.;Todd K Rosengart.;William D Edwards.;Patrick M McCarthy.;Robert O Bonow.;Thomas C Spelsberg.
来源: Circulation. 2005年111卷24期3296-301页
Rheumatic heart disease is the most common cause of valvular disease in developing countries. Despite the high prevalence of this disease, the cellular mechanisms are not well known. We hypothesized that rheumatic valve calcification is associated with an osteoblast bone formation and neoangiogenesis.
9654. Rho-kinase mediates hyperglycemia-induced plasminogen activator inhibitor-1 expression in vascular endothelial cells.
Elevated levels of plasminogen activator inhibitor-1 (PAI-1) are associated with myocardial infarction and stroke, especially in patients with diabetes. The induction of PAI-1 expression by hyperglycemia involves oxidative stress and protein kinase C (PKC). However, the mechanism by which hyperglycemia increases PAI-1 expression is unknown.
9655. Conditional mineralocorticoid receptor expression in the heart leads to life-threatening arrhythmias.
作者: Antoine Ouvrard-Pascaud.;Yannis Sainte-Marie.;Jean-Pierre Bénitah.;Romain Perrier.;Christelle Soukaseum.;Aurelie Nguyen Dinh Cat.;Anne Royer.;Khai Le Quang.;Flavien Charpentier.;Sophie Demolombe.;Fatima Mechta-Grigoriou.;Ahmed T Beggah.;Pierre Maison-Blanche.;Marie-Edith Oblin.;Claude Delcayre.;Glenn I Fishman.;Nicolette Farman.;Brigitte Escoubet.;Frederic Jaisser.
来源: Circulation. 2005年111卷23期3025-33页
Life-threatening cardiac arrhythmia is a major source of mortality worldwide. Besides rare inherited monogenic diseases such as long-QT or Brugada syndromes, which reflect abnormalities in ion fluxes across cardiac ion channels as a final common pathway, arrhythmias are most frequently acquired and associated with heart disease. The mineralocorticoid hormone aldosterone is an important contributor to morbidity and mortality in heart failure, but its mechanisms of action are incompletely understood.
9656. Changes in false lumen after transluminal stent-graft placement in aortic dissections: six years' experience.
作者: Hitoshi Kusagawa.;Takatsugu Shimono.;Masaki Ishida.;Tomoaki Suzuki.;Fuyuhiko Yasuda.;Uhito Yuasa.;Koji Onoda.;Isao Yada.;Tadanori Hirano.;Kan Takeda.;Noriyuki Kato.
来源: Circulation. 2005年111卷22期2951-7页
Transluminal stent-graft placements (TSGPs) are a new, less invasive procedure now recognized as the choice for aortic disease repair. Treatment of aortic dissections with TSGPs has resulted in good early results, but the long-term results and changes in the false lumen have not been elucidated in detail.
9657. Development of occlusive neointimal lesions in distal pulmonary arteries of endothelin B receptor-deficient rats: a new model of severe pulmonary arterial hypertension.
作者: D Dunbar Ivy.;Ivan F McMurtry.;Kelley Colvin.;Masatoshi Imamura.;Masahiko Oka.;Dong-Seok Lee.;Sarah Gebb.;Peter Lloyd Jones.
来源: Circulation. 2005年111卷22期2988-96页
Human pulmonary arterial hypertension (PAH) is characterized by proliferation of vascular smooth muscle and, in its more severe form, by the development of occlusive neointimal lesions. However, few animal models of pulmonary neointimal proliferation exist, thereby limiting a complete understanding of the pathobiology of PAH. Recent studies of the endothelin (ET) system demonstrate that deficiency of the ET(B) receptor predisposes adult rats to acute and chronic hypoxic PAH, yet these animals fail to develop neointimal lesions. Herein, we determined and thereafter showed that exposure of ET(B) receptor-deficient rats to the endothelial toxin monocrotaline (MCT) leads to the development of neointimal lesions that share hallmarks of human PAH.
9658. Cellular mechanisms underlying the development of catecholaminergic ventricular tachycardia.
作者: Gi-Byoung Nam.;Alexander Burashnikov.;Charles Antzelevitch.
来源: Circulation. 2005年111卷21期2727-33页
Mutations in the ryanodine 2 receptor (RyR2) gene have been identified in patients with catecholaminergic polymorphic ventricular tachycardia. We examined the cellular basis for the ECG features and arrhythmia mechanisms using low-dose caffeine to mimic the defective calcium homeostasis encountered under these conditions.
9659. Cardiac dyssynchrony analysis using circumferential versus longitudinal strain: implications for assessing cardiac resynchronization.
作者: Robert H Helm.;Christophe Leclercq.;Owen P Faris.;Cengizhan Ozturk.;Elliot McVeigh.;Albert C Lardo.;David A Kass.
来源: Circulation. 2005年111卷21期2760-7页
QRS duration is commonly used to select heart failure patients for cardiac resynchronization therapy (CRT). However, not all patients respond to CRT, and recent data suggest that direct assessments of mechanical dyssynchrony may better predict chronic response. Echo-Doppler methods are being used increasingly, but these principally rely on longitudinal motion (epsilonll). It is unknown whether this analysis yields qualitative and/or quantitative results similar to those based on motion in the predominant muscle-fiber orientation (circumferential; epsiloncc).
9660. On mice, rabbits, and human heart failure.
Sarcomeres, bundled into thick and thin filaments, are the units of contraction in the striated muscle. The thick filaments comprise several hundred hexameric myosin molecules, composed of 2 myosin heavy chain (MyHC) proteins, the molecular motor of contraction, and 2 regulatory and 2 essential light chains. The globular head of MyHC contains the binding domains for cardiac α-actin and adenosine triphosphate (ATP) and is attached to a hinge region, which when flexed, moves the globular head over the thin filaments. The thin filaments comprise the cardiac troponin C (cTnC), T (cTnT), and I (cTnI) complex, α-tropomyosin dimers, and cardiac α-actin, maintained in a tight 1:1:7 stoichiometry. Several additional sarcomeric proteins, such as myosin-binding protein C, titin, obscurin, and telethonin contribute to the stabilization and function of the sarcomeres.
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