The Experts below are selected from a list of 294 Experts worldwide ranked by ideXlab platform
David A Dichek - One of the best experts on this subject based on the ideXlab platform.
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In Vivo Gene Transfer Into Injured Carotid Arteries Optimization and Evaluation of Acute Toxicity
Circulation, 1995Co-Authors: Andrew H. Schulick, Kurt D. Newman, Renu Virmani, David A DichekAbstract:Background Adenoviral vectors are very attractive agents for use in in vivo arterial gene transfer. In a previous study, we demonstrated high-efficiency adenovirus-mediated gene transfer into medial smooth muscle cells of balloon-injured rat Carotid Arteries. We now further characterize this system by investigating the reproducibility of recombinant gene expression, the presence of acute adenovirus-associated toxicity in the vessel wall, and the optimal virus concentration for transduction. Methods and Results Balloon-injured rat Carotid Arteries were incubated with (1) an adenovirus expressing a β-galactosidase gene (Av1LacZ4), (2) a related adenovirus without the recombinant gene (Addl312), or (3) control solutions. Recombinant gene expression was determined 3 days after gene transfer by measurement of β-galactosidase activity in vessel extracts and by counting of smooth muscle cells in microscopic sections that were histochemically stained to detect recombinant β-galactosidase activity. Adenovirus-asso...
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in vivo adenoviral vector mediated gene transfer into balloon injured rat Carotid Arteries
Circulation Research, 1993Co-Authors: Sung W Lee, Renu Virmani, Bruce C Trapnell, Jeffrey J Rade, David A DichekAbstract:We studied the ability of adenoviral vectors to achieve gene transfer into injured Arteries. A recombinant adenoviral vector expressing a nuclear-targeted beta-galactosidase gene was constructed and infused into balloon-injured rat Carotid Arteries. Three days after gene transfer, recombinant gene expression was assessed quantitatively by (1) measuring beta-galactosidase antigen and activity in tissue extracts and (2) histochemical staining and counting of cells expressing beta-galactosidase. Exposure of injured Carotid Arteries to increasing concentrations of the vector (10(8) to 10(10) plaque-forming units per milliliter) resulted in a dose-responsive increase in beta-galactosidase expression, with peak expression of approximately 43 mU or 25 ng beta-galactosidase per vessel. Microscopic examination of histochemically stained Arteries demonstrated gene transfer limited to the vascular media; transduced cells were identified immunohistochemically as smooth muscle cells. Counting of both histochemically stained and total nuclei in the media revealed that approximately 30% of the cells in the media of the injured vessels were transduced. Calculations based on both counting cells and on the level of beta-galactosidase expression in tissue extracts suggested the presence of 5000 to 10,000 transduced cells per 10 mm of vessel. Arteries infused with either vehicle only, a control adenoviral vector, or liposomes combined with the vector plasmid contained little or no evidence of beta-galactosidase expression. High levels of in vivo beta-galactosidase expression persisted for at least 7 days after gene transfer but declined significantly by day 14. We conclude that adenoviral vector-mediated gene transfer into the injured rat Carotid artery results in efficient gene transfer into the vascular media, with levels of recombinant protein production significantly higher than any previously reported in arterial gene transfer studies. Adenoviral vectors appear to be particularly useful agents for in vivo arterial gene transfer.
M Heller - One of the best experts on this subject based on the ideXlab platform.
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vessel wall damage caused by cerebral protection devices ex vivo evaluation in porcine Carotid Arteries
Radiology, 2005Co-Authors: Stefan Mullerhulsbeck, Paul Stolzmann, Carsten Liess, Jurgen Hedderich, Friedrich Paulsen, T Jahnke, M HellerAbstract:PURPOSE: To determine the extent of vessel wall damage caused by cerebral protection devices designed for Carotid angioplasty by using ex vivo porcine Carotid Arteries. MATERIALS AND METHODS: The local animal experimentation committee did not require its approval for this study. With a benchtop vascular model (flow rate, 470 mL/min; dicrotic pulsatile flow, 76 pulses per minute; pressure, 115/67 mm Hg [mean pressure, 91 mm Hg]) into which 85 porcine internal Carotid Arteries (ICAs) were inserted, five different protection devices (Angioguard [Cordis/Johnson & Johnson, Miami, Fla], Filterwire EX [Boston Scientific, Natick, Mass], Trap [Microvena, White Bear Lake, Minn], Neuroshield [Abbott Laboratories, Redwood City, Calif], and Percusurge [Abbott Laboratories]) were evaluated. Adverse movement (1 cm up, 2 cm down, and 1 cm up again) of the activated devices (deployed filters or inflated balloons [Percusurge only]) was simulated, and the device was retrieved. For each of these steps (deployment, movement, ...
Howard M. Clarke - One of the best experts on this subject based on the ideXlab platform.
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Straightening of aberrant Carotid Arteries with age in velocardiofacial syndrome.
Plastic and Reconstructive Surgery, 1999Co-Authors: Richard A. Hopper, Derek Armstrong, Howard M. ClarkeAbstract:: Two cases of velocardiofacial syndrome demonstrated spontaneous straightening over a 4-year period of previously deviated Carotid Arteries on contrast enhanced computed tomography. Based on this finding, uncomplicated traditional pharyngeal flaps were performed on both patients. It is unknown whether straightening of aberrant vessels with age is the rule or the exception in this patient population.
Matthew D Robson - One of the best experts on this subject based on the ideXlab platform.
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in vivo quantitative t2 mapping of Carotid Arteries in atherosclerotic patients segmentation and t2 measurement of plaque components
Journal of Cardiovascular Magnetic Resonance, 2013Co-Authors: Luca Biasiolli, Alistair C Lindsay, Joshua T Chai, Robin P Choudhury, Matthew D RobsonAbstract:Background: Atherosclerotic plaques in Carotid Arteries can be characterized in-vivo by multicontrast cardiovascular magnetic resonance (CMR), which has been thoroughly validated with histology. However, the non-quantitative nature of multicontrast CMR and the need for extensive post-acquisition interpretation limit the widespread clinical application of in-vivo CMR plaque characterization. Quantitative T2 mapping is a promising alternative since it can provide absolute physical measurements of plaque components that can be standardized among different CMR systems and widely adopted in multi-centre studies. The purpose of this study was to investigate the use of in-vivo T2 mapping for atherosclerotic plaque characterization by performing American Heart Association (AHA) plaque type classification, segmenting Carotid T2 maps and measuring in-vivo T2 values of plaque components. Methods: The Carotid Arteries of 15 atherosclerotic patients (11 males, 71 ± 10 years) were imaged at 3 T using the conventional multicontrast protocol and Multiple-Spin-Echo (Multi-SE). T2 maps of Carotid Arteries were generated by mono-exponential fitting to the series of images acquired by Multi-SE using nonlinear least-squares regression. Two reviewers independently classified Carotid plaque types following the CMR-modified AHA scheme, one using multicontrast CMR and the other using T2 maps and time-of-flight (TOF) angiography. A semi-automated method based on Bayes classifiers segmented the T2 maps of Carotid Arteries into 4 classes: calcification, lipid-rich necrotic core (LRNC), fibrous tissue and recent IPH. Mean ± SD of the T2 values of voxels classified as LRNC, fibrous tissue and recent IPH were calculated. Results: In 37 images of Carotid Arteries from 15 patients, AHA plaque type classified by multicontrast CMR and by T2 maps (+ TOF) showed good agreement (76% of matching classifications and Cohen’s κ = 0.68). The T2 maps of 14 normal Arteries were used to measure T2 of tunica intima and media (T2 = 54 ± 13 ms). From 11865 voxels in the T2 maps of 15 Arteries with advanced atherosclerosis, 2394 voxels were classified by the segmentation algorithm as LRNC (T2 = 37 ± 5 ms) and 7511 voxels as fibrous tissue (T2 = 56 ± 9 ms); 192 voxels were identified as calcification and one recent IPH (236 voxels, T2 = 107 ± 25 ms) was detected on T2 maps and confirmed by multicontrast CMR. Conclusions: This Carotid CMR study shows the potential of in-vivo T2 mapping for atherosclerotic plaque characterization. Agreement between AHA plaque types classified by T2 maps (+TOF) and by conventional multicontrast CMR was good, and T2 measured in-vivo in LRNC, fibrous tissue and recent IPH demonstrated the ability to discriminate plaque components on T2 maps.
James T Willerson - One of the best experts on this subject based on the ideXlab platform.
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thromboresistance of balloon injured porcine Carotid Arteries after local gene transfer of human tissue factor pathway inhibitor
Circulation, 2000Co-Authors: Pierre Zoldhelyi, Janice Mcnatt, Harnath Shelat, Yasutaka Yamamoto, Zhiqiang Chen, James T WillersonAbstract:Background —Tissue factor pathway inhibitor (TFPI) is an endogenous inhibitor of factor Xa and the coagulant initiator complex tissue factor/factor VIIa. Methods and Results —To study the effects of TFPI gene transfer on thrombus formation, balloon-injured porcine Carotid Arteries were treated locally with an adenovirus encoding human TFPI (Ad-TFPI) or control virus. Gene transfer of TFPI was confirmed by detection of human TFPI in the conditioned medium of porcine Carotid Arteries kept in culture after in vivo transduction. When Carotid flow was measured with Doppler probe 5 days after surgery, cyclic flow variations (CFVs) developed in 7 of 8 control pigs after constriction of the injured Carotid artery by 40%, and all control-treated Arteries occluded after 70% constriction. In contrast, CFVs were observed in only 1 of 8 Ad-TFPI–treated pigs after 40% constriction, and only 3 of 8 occluded after constriction by 70% ( P =0.0027 and P =0.007, respectively). None of the 5 TFPI-transduced Arteries open after 70% constriction developed CFVs during an incremental epinephrine infusion. Conclusions —Compared with baseline, systemic hemostatic variables and platelet aggregation were unimpaired, suggesting that TFPI gene transfer can prevent arterial thrombosis in the presence of severe shear stress and without detectable hemostatic impairment.