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  • Ovid Technologies (Wolters Kluwer Health)  (47)
  • 1
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    Online Resource
    Abstract 11802: Coronary Artery Calcification is the Strongest Predictor of Abnormal Duke Prognostic Coronary Artery Disease Index
    Ovid Technologies (Wolters Kluwer Health) ; 2014
    In:  Circulation Vol. 130, No. suppl_2 ( 2014-11-25)
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 130, No. suppl_2 ( 2014-11-25)
    Abstract: Background: Cardiac CT angiography (CCTA) is a useful non-invasive tool to assess coronary artery disease (CAD). The CCTA derived modified Duke prognostic CAD index (MDS) has been shown to predict coronary events in symptomatic patients. No prior study has investigated MDS in asymptomatic patients or the relationship of conventional biomarkers of CAD with MDS. Objective: We sought to determine the ability of clinical, serologic, and imaging biomarkers of CAD to predict abnormal MDS in asymptomatic patients. Methods: There were 374 asymptomatic patients in the High Risk Plaque Study who were evaluated by clinical, serologic, and imaging biomarkers of CAD that underwent CCTA. MDS was calculated from CCTA using a 16-segment convention for coronary tree (high MDS defined as ≥3). The association of MDS with clinical, serologic, and imaging biomarkers was assessed. Results: There were 58 patients identified with high MDS. These patients had lower HDL-C (44 v. 53, p 〈 0.001) and higher CACS (899 v. 26, p 〈 0.001), Framingham risk score (17.5 v. 11, p 〈 0.001), carotid intima-media thickness (0.82 v. 0.74, p=0.001), and triglycerides (150 v. 136, p = 0.011). In multivariate analysis, only CACS≥400 (OR = 15.3, 95% CI: 7.4-31.5, p 〈 0.001) and CACS overall (OR = 6.02, 95% CI: 3.58 - 10.09, p 〈 0.001) independently predicted MDS. Receiver operating characteristic curve analysis revealed improved prediction of MDS with addition of CACS: from AUC = 0.7531 to 0.8951. Conclusion: In asymptomatic patients, CACS is the strongest independent predictor of MDS when compared to conventional biomarkers of CAD.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/circ.130.suppl_2.11802
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2014
    detail.hit.zdb_id: 1466401-X
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  • 2
    Online Resource
    Online Resource
    Longitudinal Distribution of Mechanical Stresses in Carotid Plaques of Symptomatic Patients
    Ovid Technologies (Wolters Kluwer Health) ; 2010
    In:  Stroke Vol. 41, No. 5 ( 2010-05), p. 1041-1043
    Details
    In: Stroke, Ovid Technologies (Wolters Kluwer Health), Vol. 41, No. 5 ( 2010-05), p. 1041-1043
    Abstract: Background and Purpose— Mechanical stress may contribute to plaque rupture in patients with carotid atherosclerosis. We determined longitudinal mechanical stresses in carotid atherosclerotic plaques and compared them with known markers of plaque vulnerability. Methods— Nineteen symptomatic patients scheduled for carotid endarterectomy underwent carotid MRI with a multicontrast protocol to characterize plaque morphology and geometry. Longitudinal 2-dimensional computational models were generated from the MRI data, and the mechanical stresses were calculated. Results— Peak longitudinal mechanical stresses occurred predominantly in the shoulder regions of the carotid plaque and correlated inversely with fibrous cap thickness ( r s =−0.61; P =0.01), and increasing degrees of stenosis ( r s =0.71; P =0.003). Peak stress levels were asymmetrically distributed longitudinally, with 50% occurring proximal to the maximal stenosis, 25% at the point of maximal stenosis, and 25% distal to the maximal stenosis. Conclusion— The peak longitudinal mechanical stresses in the fibrous caps of symptomatic patients with carotid atherosclerotic stenosis were located at known predilection sites for plaque rupture, suggesting that mechanical stresses may play a role in plaque destabilization.
    Type of Medium: Online Resource
    ISSN: 0039-2499 , 1524-4628
    URL: Article
    DOI: 10.1161/STROKEAHA.109.571588
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2010
    detail.hit.zdb_id: 1467823-8
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  • 3
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    Online Resource
    Remodelling of the left anterior descending artery in a porcine model of supravalvular aortic stenosis
    Ovid Technologies (Wolters Kluwer Health) ; 2002
    In:  Journal of Hypertension Vol. 20, No. 12 ( 2002-12), p. 2429-2437
    Details
    In: Journal of Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 20, No. 12 ( 2002-12), p. 2429-2437
    Type of Medium: Online Resource
    ISSN: 0263-6352
    URL: Article
    DOI: 10.1097/00004872-200212000-00023
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2002
    detail.hit.zdb_id: 2017684-3
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  • 4
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    Neointimal Cracks (Plaque Rupture?) and Thrombosis in Wrapped Arteries Without Flow
    Ovid Technologies (Wolters Kluwer Health) ; 2007
    In:  Arteriosclerosis, Thrombosis, and Vascular Biology Vol. 27, No. 1 ( 2007-01), p. 248-249
    Details
    In: Arteriosclerosis, Thrombosis, and Vascular Biology, Ovid Technologies (Wolters Kluwer Health), Vol. 27, No. 1 ( 2007-01), p. 248-249
    Type of Medium: Online Resource
    ISSN: 1079-5642 , 1524-4636
    URL: Article
    DOI: 10.1161/01.ATV.0000249644.86759.81
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2007
    detail.hit.zdb_id: 1494427-3
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  • 5
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    Plaque Rupture in Humans and Mice
    Ovid Technologies (Wolters Kluwer Health) ; 2007
    In:  Arteriosclerosis, Thrombosis, and Vascular Biology Vol. 27, No. 4 ( 2007-04), p. 705-713
    Details
    In: Arteriosclerosis, Thrombosis, and Vascular Biology, Ovid Technologies (Wolters Kluwer Health), Vol. 27, No. 4 ( 2007-04), p. 705-713
    Abstract: Despite the many studies of murine atherosclerosis, we do not yet know the relevance of the natural history of this model to the final events precipitated by plaque disruption of human atherosclerotic lesions. The literature has become particularly confused because of the common use of terms such as “instability”, “vulnerable”, “rupture”, or even “thrombosis” for features of plaques in murine model systems not yet shown to rupture spontaneously and in an animal surprisingly resistant to formation of thrombi at sites of atherosclerosis. We will argue that such terminology may mislead readers by implying knowledge that does not yet exist.
    Type of Medium: Online Resource
    ISSN: 1079-5642 , 1524-4636
    URL: Article
    DOI: 10.1161/01.ATV.0000261709.34878.20
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2007
    detail.hit.zdb_id: 1494427-3
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  • 6
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    Genetic Susceptibility of the Arterial Wall Is an Important Determinant of Atherosclerosis in C57BL/6 and FVB/N Mouse Strains
    Ovid Technologies (Wolters Kluwer Health) ; 2011
    In:  Arteriosclerosis, Thrombosis, and Vascular Biology Vol. 31, No. 8 ( 2011-08), p. 1814-1820
    Details
    In: Arteriosclerosis, Thrombosis, and Vascular Biology, Ovid Technologies (Wolters Kluwer Health), Vol. 31, No. 8 ( 2011-08), p. 1814-1820
    Abstract: How genetic variations among inbred mouse strains translate into differences in atherosclerosis susceptibility is of significant interest for the development of new therapeutic strategies. The objective of the present study was to examine whether genetically controlled arterial wall properties influence atherosclerosis susceptibility in FVB/N (FVB) and C57BL/6 (B6) apolipoprotein E knockout (apoE −/− ) mouse strains. Methods and Results— Common carotid artery segments from B6 apoE −/− , F1 apoE −/− , and FVB apoE −/− mice were transplanted to hybrid F1 apoE −/− mice, which can accept grafts from both parental strains without adaptive immune responses. The mice were fed a high-fat diet, and atherosclerosis was induced in the transplanted artery segments by placement of a perivascular constrictive collar. Artery segments from B6 apoE −/− mice developed much larger atherosclerotic lesions than artery segments from FVB or F1 apoE −/− mice. No differences in aortic arch atherosclerosis of the recipient mice were observed between groups. Conclusion— Genetically controlled factors acting at the level of the arterial wall are important determinants of atherosclerosis susceptibility in FVB apoE −/− and B6 apoE −/− mice.
    Type of Medium: Online Resource
    ISSN: 1079-5642 , 1524-4636
    URL: Article
    DOI: 10.1161/ATVBAHA.111.229674
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2011
    detail.hit.zdb_id: 1494427-3
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  • 7
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    Abstract 661: Targeting Sortilin in Immune Cells Reduces Atherosclerosis
    Ovid Technologies (Wolters Kluwer Health) ; 2014
    In:  Arteriosclerosis, Thrombosis, and Vascular Biology Vol. 34, No. suppl_1 ( 2014-05)
    Details
    In: Arteriosclerosis, Thrombosis, and Vascular Biology, Ovid Technologies (Wolters Kluwer Health), Vol. 34, No. suppl_1 ( 2014-05)
    Abstract: Targeting sortilin in immune cells reduces atherosclerosis. Background: SNPs at 1p13.3 have been strongly associated with myocardial infarction and plasma cholesterol levels in genome-wide association studies. This locus covers 3 genes; SORT1, CELSR2 and PSRC1. Previous studies on sortilin in cardiovascular disease have focused on sortilins role in hepatic lipoprotein metabolism. In the present study, we demonstrate that sortilin also modulates atherogenesis independent of its effect on lipoprotein metabolism. Methods and results: The effect of sortilin deficiency on atherosclerosis was studied in Apoe -/- mice. Absence of sortilin ( Sort1 -/- ) did not influence plasma cholesterol levels or the distribution between lipoprotein fractions, yet significantly reduced development of atherosclerosis after both 6 and 18 weeks of Western diet. To examine the possible mechanism we performed studies on murine bone marrow-derived macrophages (BMM) and th1-cells. Loss of sortilin did not impact foam-cell formation or cell activation, but specifically reduced the secretion of interleukin-6 (Il-6) and interferon-gamma (IFN-) from macrophages and th1 cells, respectively. Further, surface plasmon resonance analysis demonstrated that sortilin binds these two cytokines with high affinity. These results suggest that sortilin is involved in regulation of Il-6 and IFN- secretion and indicates that sortilin in immune cells may influence atherosclerosis. To test this hypothesis, 8 weeks old Apoe -/- were lethally irradiated and rescued with age- and sex-matched bone marrow from Sort1 +/+ Apoe -/- or Sort1 -/- Apoe -/- donor mice. Mice with a sortilin deficient bone marrow transplant had reduced development atherosclerosis compared to mice with a Sort1 +/+ transplant. Although these mice had normal numbers of circulating immune cells, they had reduced levels of circulating tumor necrosis factor-α and Il-6 in plasma, suggesting that absence of sortilin attenuates the inflammatory response. Conclusions: We conclude that targeting sortilin in immune cells reduces atherosclerosis by attenuation of the inflammatory response.
    Type of Medium: Online Resource
    ISSN: 1079-5642 , 1524-4636
    URL: Article
    DOI: 10.1161/atvb.34.suppl_1.661
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2014
    detail.hit.zdb_id: 1494427-3
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  • 8
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    Recommendation on Design, Execution, and Reporting of Animal Atherosclerosis Studies: A Scientific Statement From the American Heart Association
    Ovid Technologies (Wolters Kluwer Health) ; 2017
    In:  Circulation Research Vol. 121, No. 6 ( 2017-09)
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 121, No. 6 ( 2017-09)
    Abstract: Animal studies are a foundation for defining mechanisms of atherosclerosis and potential targets of drugs to prevent lesion development or reverse the disease. In the current literature, it is common to see contradictions of outcomes in animal studies from different research groups, leading to the paucity of extrapolations of experimental findings into understanding the human disease. The purpose of this statement is to provide guidelines for development and execution of experimental design and interpretation in animal studies. Recommendations include the following: (1) animal model selection, with commentary on the fidelity of mimicking facets of the human disease; (2) experimental design and its impact on the interpretation of data; and (3) standard methods to enhance accuracy of measurements and characterization of atherosclerotic lesions.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/RES.0000000000000169
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2017
    detail.hit.zdb_id: 1467838-X
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  • 9
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    Angina Pectoris and Disease Progression
    Ovid Technologies (Wolters Kluwer Health) ; 1995
    In:  Circulation Vol. 92, No. 8 ( 1995-10-15), p. 2033-2035
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 92, No. 8 ( 1995-10-15), p. 2033-2035
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/01.CIR.92.8.2033
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 1995
    detail.hit.zdb_id: 1466401-X
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  • 10
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    Smooth Muscle Cells Healing Atherosclerotic Plaque Disruptions Are of Local, Not Blood, Origin in Apolipoprotein E Knockout Mice
    Ovid Technologies (Wolters Kluwer Health) ; 2007
    In:  Circulation Vol. 116, No. 18 ( 2007-10-30), p. 2053-2061
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 116, No. 18 ( 2007-10-30), p. 2053-2061
    Abstract: Background— Signs of preceding episodes of plaque rupture and smooth muscle cell (SMC)–mediated healing are common in atherosclerotic plaques, but the source of the healing SMCs is unknown. Recent studies suggest that activated platelets adhering to sites of injury recruit neointimal SMCs from circulating bone marrow–derived progenitor cells. Here, we analyzed the contribution of this mechanism to plaque healing after spontaneous and mechanical plaque disruption in apolipoprotein E knockout (apoE −/− ) mice. Methods and Results— To determine the origin of SMCs after spontaneous plaque disruption, irradiated 18-month-old apoE −/− mice were reconstituted with bone marrow cells from enhanced green fluorescent protein (eGFP) transgenic apoE −/− mice and examined when they died up to 9 months later. Plaque hemorrhage, indicating previous plaque disruption, was widely present, but no bone marrow–derived eGFP + SMCs were detected. To examine the origin of healing SMCs in a model that recapitulates more features of human plaque rupture and healing, we developed a mechanical technique that produced consistent plaque disruption, superimposed thrombosis, and SMC-mediated plaque healing in apoE −/− mice. Mechanical plaque disruption was produced in irradiated apoE −/− mice reconstituted with eGFP + apoE −/− bone marrow cells and in carotid bifurcations cross-grafted between apoE −/− and eGFP + apoE −/− mice. Apart from few non–graft-derived SMCs near the anastomosis site in 1 transplanted carotid bifurcation, no SMCs originating from outside the local arterial segment were detected in healed plaques. Conclusions— Healing SMCs after atherosclerotic plaque disruption are derived entirely from the local arterial wall and not circulating progenitor cells in apoE −/− mice.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/CIRCULATIONAHA.107.722355
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2007
    detail.hit.zdb_id: 1466401-X
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