OBJECTIVES: We used optical coherence tomography, which has a resolution of |20 microm, to analyze thin layers of neointima in rapamycin-eluting coronary stents. BACKGROUND: Lack of neointimal coverage has been implicated in the pathogenesis of drug-eluting coronary stent thrombosis. Angiography and intracoronary ultrasound lack the resolution to examine this. METHODS: We conducted a randomized trial in patients receiving polymer-coated rapamycin-eluting stents (Cypher, Cordis, Johnson & Johnson, Miami, Florida) and nonpolymer rapamycin-eluting stents (Yukon, Translumina, Hechingen, Germany) to examine neointimal thickness, stent strut coverage, and protrusion at 90 days. Twenty-four patients (n = 12 for each group) underwent stent deployment and invasive follow-up at 90 days with optical coherence tomography. The primary end point was binary stent strut coverage. Coprimary end points were neointimal thickness and stent strut luminal protrusion. RESULTS: No patient had angiographic restenosis. For

TY - JOUR. T1 - The APOSTEL recommendations for reporting quantitative optical coherence tomography studies. AU - Cruz-Herranz, Andrés. AU - Balk, Lisanne J.. AU - Oberwahrenbrock, Timm. AU - Saidha, Shiv. AU - Martinez-Lapiscina, Elena H.. AU - Lagreze, Wolf A.. AU - Schuman, Joel S.. AU - Villoslada, Pablo. AU - Calabresi, Peter. AU - Balcer, Laura. AU - Petzold, Axel. AU - Green, Ari J.. AU - Paul, Friedemann. AU - Brandt, Alexander U.. AU - Albrecht, Philipp. PY - 2016/6/14. Y1 - 2016/6/14. N2 - Objective: To develop consensus recommendations for reporting of quantitative optical coherence tomography (OCT) study results. Methods: A panel of experienced OCT researchers (including 11 neurologists, 2 ophthalmologists, and 2 neuroscientists) discussed requirements for performing and reporting quantitative analyses of retinal morphology and developed a list of initial recommendations based on experience and previous studies. The list of recommendations was subsequently revised during several ...

OCT data analysis was performed offline using proprietary software (LightLab Imaging Inc.). Analysis of angiographic images, quantitative coronary angiography (Medis, Leiden, the Netherlands), and OCT was performed by experienced investigators (P.B. and P.M.). Regarding blinding, the very different presentation of the 2 stent types (including, in particular, the hub of the devices and the angiographic appearances of the markers) made it impractical to blind the operators; however, for the angiographic and OCT analysis, investigators were blinded to the randomization arm. The analyst was blinded to all clinical and procedural variables and thus, did not have any knowledge of stent sizes or stent type. When a strut was felt to be malapposed, the distance from the strut to lumen surface was recorded. Only after completion of the analysis was the stent type used to then confirm the presence or absence of malapposition by incorporating the actual strut thickness for the 2 stents used. This is ...

The question of whether DES are safe, has become an area of considerable interest and controversy with the publication of a relatively small randomized trial (BASKET-LATE), an observational study and a meta-analysis reporting increased rates of ST, MI, and death with DES compared to BMS. The motivating factor was the presentation of a meta-analysis at the European Society of Cardiology meeting in Barcelona in September 2006, which suggested an increase in the risk of death and MI following implantation of sirolimus-eluting stents.. The major issue in these meta-analyses is that they were limited either by small sample sizes, duration of follow-ups, lack of access to source data, or by using landmark analyses that excluded events in first 6 months.. Moreover, the largest meta-analysis of DES vs. BMS and SES vs. PES published recently in The Lancet by Settler et al performed a network analyses with a mixed-treatment comparison of 38 randomized trials (18023 patients) with a follow-up of up to 4 ...

Our study demonstrated that vulnerable plaque characteristics, including thinner fibrous cap, greater lipid arc, longer lipid core length, and TCFA, were seen more frequently in UAP culprit lesions with NV when compared with those without NV, but not in the non-culprit lesions of UAP and in the lesions of SAP.. In this study, we observed NV in 35% of the culprit lesions in UAP patients. This finding is consistent with the previous report by Kitabata et al,9 where NV was found in 38% of the culprit lesions in UAP patients. NV was observed in 34% of non-culprit lesions and in 28% of the lesions in SAP patients. The difference was not significant between the three groups. Our findings, which associate NV with the presence of TCFA, thinner fibrous cap, and larger plaque burden, are also in good agreement with the previous report.9 The results obtained from the study by Fujii K et al13 have shown that ruptured plaques in culprit lesions of patients with acute coronary syndromes have greater plaque ...

The aim of the APOSTEL recommendations is to provide a consistent basis for assisting authors in composing conclusive reports of studies utilizing quantitative retinal OCT, allowing relevant comparisons across and between studies, and helping readers, reviewers, and editors to evaluate these findings. Furthermore, by emphasizing details that are of importance in such reports, we hope to generally improve the quality of future investigations in this area. Defining the relevant parameters for reporting may prompt researchers to thoroughly consider these criteria during the initial stages of study design. Such an approach could help facilitate OCT research in centers intending to incorporate OCT for clinical trials or other research purposes. Adherence to the recommendations can help avoid common pitfalls in the design and reporting of OCT studies. These recommendations are not intended to impose a rigid format on reports of OCT-based research, but rather to provide suggestions and guidance on ...

Fibronectin-splice variant containing extra domain A (Fn-EDA) is associated with smooth muscle cells (SMCs) following vascular injury. The role of SMC-derived Fn-EDA in SMC phenotypic switching or its implication in neointimal hyperplasia remains unclear. Herein, using human coronary artery sections with a bare metal stent, we demonstrate the expression of Fn-EDA in the vicinity of SMC-rich neointima and peri-strut areas. In mice, Fn-EDA colocalizes with SMCs in the neointima of injured carotid arteries and promotes neointima formation in the comorbid condition of hyperlipidemia by potentiating SMC proliferation and migration. No sex-based differences were observed. Mechanistic studies suggested that Fn-EDA mediates integrin- and TLR4-dependent proliferation and migration through activation of FAK/Src and Akt1/mTOR signaling, respectively. Specific deletion of Fn-EDA in SMCs, but not in endothelial cells, reduced intimal hyperplasia and suppressed the SMC synthetic phenotype concomitant with ...

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Background: Reendothelialization following vascular injury after balloon angioplasty or stent implantation is clinically extremely relevant to promote vascular healing and prevent fatal events such as stent thrombosis and restenosis. We already identified the importance of Toll-like receptor (TLR) 2/6 for endothelial regeneration. We now investigated the therapeutic potential of the TLR2/6 agonist MALP-2 on reendothelialization in a murine model of vascular injury. Methods and Results: The left common carotid artery of C57BL/6N mice was experimentally injured and reendothelialization was quantified by Evans Blue staining after 3 days in en face prepared vessels. A single intravenous injection of MALP-2 (1 or 10 µg) following vascular injury dose-dependently accelerated reendothelialization up to 3.5-fold (n=12-18, P,0.001) which was abolished by administration of neutralizing antibodies against TLR2 and TLR6. Proliferation of endothelial cells at the wound margins determined by ...

Neurofibromin 2 (NF2), a potent tumor suppressor, is reported to inhibit proliferation in several cell types. The role of NF2 in neointima hyperplasia after vascular injury is unknown. We explored the role of NF2 in proliferation, migration of vascular smooth muscle cell (VSMC) and neointima hyperplasia after vascular injury. NF2 phosphorylation was elevated in VSMC subjected to platelet-derived growth factor (PDGF)-BB and in artery subjected to vascular injury. Mice deficient for Nf2 in VSMC showed enhanced neointima hyperplasia after injury, increased proliferation and migration of VSMC after PDGF-BB treatment. Mechanistically, we observed increased nuclear p-NF2, declined p-Yes-Associated Protein (YAP), nuclear translocation of YAP after PDGF-BB treatment or injury. NF2 knockdown or YAP overexpression showed similar phenotype in VSMC proliferation, migration and neointima hyperplasia. YAP inhibition abolished the above effects mediated by NF2 knockdown. Finally, NF2 knockdown further promoted

Results All endovascular procedures and OCT pullback runs were feasible. Stent apposition was satisfactory on the immediate post-stent OCT reconstructions. At 12-week controls, all stents and jailed branches were patent. Mean neointimal thickness was 0.11±0.04 mm on the free segments of the stent. The mean ostia surface at 12 weeks was 319 750±345 533 μm2 with 3D-OCT reconstructions and 351 198±396 355 μm2 with SEM image-derived calculations. Good correlation was found for ostia surface values between the two techniques; the values did not differ significantly in this preliminary study. ...

DESIGN:. Imaging and vasomotion Substudy:. 50 consecutive patients enrolled in the COMPARE II trial at the University of Fribourg Medical Center will undergo follow-up re-angiography 14 months after index procedure with assessment of Optical coherence tomography (OCT) and vasomotion testing.. ENDPOINT SUBSTUDY (all at 14 months):. Primary endpoint imaging: percentage of uncovered stent struts per lesion and mean neointimal thickness assessed by OCT.. vasomotion: coronary vasomotion assessed with quantitative coronary angiography at rest and during supine bicycle exercise. ...

Previous studies by Martínez-González et al7 using NOR1 silencing and our experiments in NOR1-deficient SMCs9 provided evidence that this receptor promotes SMC proliferation in vitro. Although these studies point to an important role for NOR1 in the regulation of SMC proliferation, the contribution of NOR1 to the proliferative response underlying neointima formation and the molecular mechanisms responsible for the mitogenic activity of NOR1 remain unknown. In the present study, we extend these earlier observations and demonstrate that NOR1 deficiency attenuates neointima formation, suggesting an important role of NOR1 signaling for proliferative vascular remodeling.. Consistent with the mitogenic activity of NOR1 in vitro,7,9 our data establish that NOR1 is required for cell cycle progression and cell survival. The main gatekeeper of G1→S phase progression is the Rb tumor suppressor protein,18 and we observed altered Rb phosphorylation in NOR1-deficient SMCs. Conversely, overexpression of ...

Our study addressed the question of whether or not expression of vWF influenced neointimal formation in arteries with altered shear stress. We found that the absence of vWF did not alter the size of the neointimal lesions, the number of layers of cells in the neointima, or the expression of PCNA in the neointima or media. The exact mechanism of neointimal formation in arteries with altered shear stress is unknown but is likely to be multifactorial. It has been known for some time that many forms of vascular manipulation will induce neointimal formation, and there appear to be important species-dependent responses (reviewed in References 30 through 3230 31 32 ). First, simple surgical isolation of an artery induces neointima in rabbits, and thus, either the operative procedure alone or the disturbed flow that likely occurs during healing contributes to neointimal hyperplasia.33 Second, vascular injury applied either externally to a rabbit artery or endoluminally in rats, rabbits, and pigs induces ...

Three-dimensional morphological response of lipid-rich coronary plaques to statin therapy: a serial optical coherence tomography study

Core2 1-6-N-glucosaminyltransferase-I deficiency protects injured arteries from neointima formation in ApoE-deficient mice. - Huan Wang, Weiyu Zhang, Rong Tang, Robert P Hebbel, M Anna Kowalska, Chunxiang Zhang, Jamey D Marth, Minoru Fukuda, Chuhong Zhu, Yuqing Huo

Medical definition of neointima: a new or thickened layer of arterial intima formed especially on a prosthesis or in atherosclerosis by migration and proliferation of cells from the media.

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While not always apparent, as the vehicle's mileage climbs, its strut mounts often deteriorate. Therefore, when the struts are being replaced (especially on high mileage vehicles), it's also the perfect time to replace the strut mounts in order to help restore the vehicle's like-new...

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Neointimal hyperplasia refers to proliferation and migration of vascular smooth muscle cells primarily in the tunica intima, resulting in the thickening of arterial walls and decreased arterial lumen space. Neointimal hyperplasia is the major cause of restenosis after percutaneous coronary interventions such as stenting or angioplasty. The term neointima is used because the cells in the hyperplastic regions of the vascular wall have histological characteristics of both intima and normal artery cells. Neointimal hyperplasia first develops with damage to the arterial wall, followed by platelet aggregation at site of injury, recruitment of inflammatory cells, proliferation and migration of vascular smooth muscle cells, and collagen deposition. Mechanical injury of arterials due to stretching of arterial walls with a balloon catheter results in the recruitment of cells such as monocytes, macrophages, and neutrophils to the site of injury. Macrophages in particular express many growth factors, ...

Using a transgenic mouse model in which the human B-myb cDNA was driven by the basal CMV promoter, this study demonstrates for the first time that B-Myb leads to markedly reduced neointima formation after mechanical injury to the vasculature and to decreased α1(I) collagen mRNA expression in the aorta and femoral artery of adult animals. Three independent transgenic mouse lines were generated, all of which apparently developed and bred normally. An inverse relationship between levels of B-Myb protein and expression of α1(I) collagen mRNA in the adult aorta was demonstrated. A decrease was also seen in α2(V) collagen mRNA levels in the aorta and in cultured aortic SMCs isolated from adult transgenic B-myb mice (data not shown). Importantly, when a femoral artery model of endothelial denudation was used, a dramatic reduction in neointima formation was observed in arteries of transgenic versus WT mice 4 weeks after injury. After injury, the neointimal area and the ratio of the areas of the ...

Fibronectin-splice variant containing extra domain A (Fn-EDA) is associated with smooth muscle cells (SMCs) following vascular injury. The role of SMC-derived Fn-EDA in SMC phenotypic switching or its implication in neointimal hyperplasia remains unclear. Herein, using human coronary artery sections with a bare metal stent, we demonstrate the expression of Fn-EDA in the vicinity of SMC-rich neointima and peri-strut areas. In mice, Fn-EDA colocalizes with SMCs in the neointima of injured carotid arteries and promotes neointima formation in the comorbid condition of hyperlipidemia by potentiating SMC proliferation and migration. No sex-based differences were observed. Mechanistic studies suggested that Fn-EDA mediates integrin- and TLR4-dependent proliferation and migration through activation of FAK/Src and Akt1/mTOR signaling, respectively. Specific deletion of Fn-EDA in SMCs, but not in endothelial cells, reduced intimal hyperplasia and suppressed the SMC synthetic phenotype concomitant with ...

Fibronectin-splice variant containing extra domain A (Fn-EDA) is associated with smooth muscle cells (SMCs) following vascular injury. The role of SMC-derived Fn-EDA in SMC phenotypic switching or its implication in neointimal hyperplasia remains unclear. Herein, using human coronary artery sections with a bare metal stent, we demonstrate the expression of Fn-EDA in the vicinity of SMC-rich neointima and peri-strut areas. In mice, Fn-EDA colocalizes with SMCs in the neointima of injured carotid arteries and promotes neointima formation in the comorbid condition of hyperlipidemia by potentiating SMC proliferation and migration. No sex-based differences were observed. Mechanistic studies suggested that Fn-EDA mediates integrin- and TLR4-dependent proliferation and migration through activation of FAK/Src and Akt1/mTOR signaling, respectively. Specific deletion of Fn-EDA in SMCs, but not in endothelial cells, reduced intimal hyperplasia and suppressed the SMC synthetic phenotype concomitant with ...

TY - JOUR. T1 - A proliferation analysis of arterial neointimal hyperplasia. T2 - Lessons for antiproliferative restenosis therapies. AU - Schwartz, Robert S.. AU - Chu, Aloysius. AU - Edwards, William D.. AU - Srivatsa, Sanjay S.. AU - Simari, Robert D.. AU - Isner, Jeffrey M.. AU - Holmes, David R.. PY - 1996/1. Y1 - 1996/1. N2 - Medial smooth muscle cell proliferation is frequently implicated as the major cause of coronary restenosis. Although antiproliferative agents have shown efficacy in animal studies, they are ineffective in human trials. To better understand these discrepancies, we performed a mathematical kinetic analysis of cellular proliferation in the neointimal hyperplasia of rats, pigs, and patients. A model was derived using a differential expression for proliferation, proportional to the number of cells present. Additional terms were included for inhibition of proliferation proportional to neointimal mass and time. The resulting equation was solved in closed form for the number ...

Lipoprotein (a) level is associated with plaque vulnerability in patients with coronary artery disease: An optical coherence tomography study

PhD Project - Exploring the similarities between neointimal formation after vascular injury and tumour growth at University of Bristol, listed on FindAPhD.com

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Bilirubin is a heme metabolite generated by the concerted action of the enzymes heme oxygenase and biliverdin reductase. Although long considered a toxic byproduct of heme catabolism, recent preclinical, and clinical studies indicate the bilirubin exerts beneficial effects in the circulation. In the present study, we determined whether local administration of bilirubin attenuates neointima formation following injury of rat carotid arteries. In addition, the ability of bilirubin to regulate the proliferation and migration of human arterial smooth muscle cells (SMCs) was investigated. Local perivascular administration of bilirubin immediately following balloon injury of rat carotid arteries significantly attenuated neointima formation. Bilirubin-mediated inhibition of neointimal thickening was associated with a significant decrease in ERK activity and cyclin D1 and A protein expression, and an increase in p21 and p53 protein expression in injured blood vessels. Treatment of human aortic SMCs with ...

TY - JOUR. T1 - Protective Aptitude of Annexin A1 in Arterial Neointima Formation in Atherosclerosis-Prone Mice-Brief Report. AU - de Jong, Renske J.. AU - Paulin, Nicole. AU - Lemnitzer, Patricia. AU - Viola, Joana R.. AU - Winter, Carla. AU - Ferraro, Bartolo. AU - Grommes, Jochen. AU - Weber, Christian. AU - Reutelingsperger, Chris. AU - Drechsler, Maik. AU - Soehnlein, Oliver. PY - 2017/2. Y1 - 2017/2. KW - annexin A1. KW - macrophage. KW - neointima formation. KW - resolution of inflammation. KW - INFLAMMATION. KW - RECRUITMENT. U2 - 10.1161/ATVBAHA.116.308744. DO - 10.1161/ATVBAHA.116.308744. M3 - Article. VL - 37. SP - 312. EP - 315. JO - Arteriosclerosis Thrombosis and Vascular Biology. JF - Arteriosclerosis Thrombosis and Vascular Biology. SN - 1079-5642. IS - 2. ER - ...

Fingerprint Dive into the research topics of Comparisons of the effects of stent eccentricity on the neointimal hyperplasia between Sirolimus-eluting stent versus Paclitaxel-eluting stent. Together they form a unique fingerprint. ...

B,Accumulating evidence shows that inhibition of the vascular renin-angiotensin system results in suppression of injury-elicited neointima formation. We attempted to determine whether or not combined treatment with an angiotensin II type 1 receptor blocker (ARB) and angiotensin converting enzyme inhibitor (ACEI) has an additive inhibitory effect on balloon-injury-elicited neointima formation in the carotid artery. Male Sprague-Dawley rats were treated with an ARB (valsartan: 3 mg/kg/day) and/or an ACEI (benazepril: 0.3 mg/kg/day) from 1 week before until 2 weeks after balloon injury. Experiments were also conducted with one-third of the dose combination used in the original experiments. Both ARB and ACEI inhibited neointima formation without any blood pressure changes. The full-dose combination lowered blood pressure and suppressed neointima formation significantly compared with the levels in the groups treated with either ACEI or ARB alone. The low-dose combination without blood pressure ...

Sigma-Aldrich offers abstracts and full-text articles by [Nick D Tsihlis, Muneera R Kapadia, Ashley K Vavra, Walker D Flannery, Christopher S Oustwani, Qun Jiang, Melina R Kibbe].

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Thank you for taking the time to nominate a fellow for TCTMDs Featured Fellow section on the Fellows Forum. Nominees should be current general or interventional cardiology fellows who you have supervised or mentored and think should be recognized for a combination of their scholarship, skills, talent, and commitment to top-notch patient care. If your nominee is selected, you will be notified of our selection and alerted when the story appears on TCTMD. Please email [email protected] with any questions ...

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Purpose: To determine the choroidal thickness (CT) profile in keratoconus (KC) patients using swept-source optical coherence tomography (SS-OCT). Methods: This was a prospective, cross-sectional study. One hundred two eyes of 52 KC patients were studied using Pentacam and SS-OCT. The macular CT profile was created by manually measuring the distance between the retinal pigment epithelium and the choroid-sclera junction on horizontal b-scans at nine different macular locations. The results were compared to 93 eyes of 93 healthy controls. Results: Mean age of the KC group was 34.9 ± 13.5 years and mean axial length (AL) was 24.1 ± 1.3 mm. Mean topographic KC classification (TKC) was 2.0; 39 eyes were classified as early KC (TKC ,1-2), 34 eyes as moderate (TKC 2, 2-3), and 29 as advanced (TKC 3+). Mean subfoveal CT was 383.2 μm in KC patients and 280.5 μm in control group (P , 0.001). CT in KC patients was statistically thicker in all measure locations (P , 0.001). CT in KC eyes decreased with ...

title: Optical coherence tomographic observation of morphological features of neointimal tissue after drug-eluting stent implantation., doi: 10.3349/ymj.2014.55.4.944, category: Article

ObjectiveIn balloon-injured rat carotid arteries, angiotensin-converting enzyme inhibitors (ACEI) decrease neointima formation, and a kinin receptor antagonist partially reverses this inhibitory effect. We studied which of the events leading to neointima formation are involved in the effects of ACEI

Principal Investigator：SAKUMA Makoto, Project Period (FY)：1989 - 1990, Research Category：Grant-in-Aid for General Scientific Research (C), Research Field：General surgery

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