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  • Ovid Technologies (Wolters Kluwer Health)  (5)
  • 2010-2014  (5)
  • 1
    Online Resource
    Online Resource
    Helium Induces Preconditioning in Human Endothelium In Vivo  
    Ovid Technologies (Wolters Kluwer Health) ; 2013
    In:  Anesthesiology Vol. 118, No. 1 ( 2013-01-01), p. 95-104
    Details
    In: Anesthesiology, Ovid Technologies (Wolters Kluwer Health), Vol. 118, No. 1 ( 2013-01-01), p. 95-104
    Type of Medium: Online Resource
    ISSN: 0003-3022
    URL: Article
    DOI: 10.1097/ALN.0b013e3182751300
    RVK:
    XA 22600
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2013
    detail.hit.zdb_id: 2016092-6
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    Online Resource
  • 2
    Online Resource
    Online Resource
    Effects of an Antisense Oligonucleotide Inhibitor of C‐Reactive Protein Synthesis on the Endotoxin Challenge Response in Healthy Human Male Volunteers
    Ovid Technologies (Wolters Kluwer Health) ; 2014
    In:  Journal of the American Heart Association Vol. 3, No. 4 ( 2014-08-15)
    Details
    In: Journal of the American Heart Association, Ovid Technologies (Wolters Kluwer Health), Vol. 3, No. 4 ( 2014-08-15)
    Abstract: C‐reactive protein ( CRP ) binds to damaged cells, activates the classical complement pathway, is elevated in multiple inflammatory conditions, and provides prognostic information on risk of future atherosclerotic events. It is controversial, however, as to whether inhibiting CRP synthesis would have any direct anti‐inflammatory effects in humans. Methods and Results A placebo‐controlled study was used to evaluate the effects of ISIS 329993 ( ISIS ‐ CRP R x ) on the acute‐phase response after endotoxin challenge in 30 evaluable subjects. Healthy adult males were randomly allocated to receive 6 injections over a 22‐day period of placebo or active therapy with ISIS 329993 at 400‐ or 600‐mg doses. Eligible subjects were subsequently challenged with a bolus of endotoxin (2 ng/kg). Inflammatory and hematological biomarkers were measured before and serially after the challenge. ISIS ‐ CRP R x was well tolerated with no serious adverse events. Median CRP levels increased more than 50‐fold from baseline 24 hours after endotoxin challenge in the placebo group. In contrast, the median increase in CRP levels was attenuated by 37% (400 mg) and 69% (600 mg) in subjects pretreated with ISIS ‐ CRP R x ( P 〈 0.05 vs. placebo). All other aspects of the acute inflammatory response were similar between treatment groups. Conclusion Pretreatment of subjects with ISIS ‐ CRP R x selectively reduced the endotoxin‐induced increase in CRP levels in a dose‐dependent manner, without affecting other components of the acute‐phase response. These data demonstrate the specificity of antisense oligonucleotides and provide an investigative tool to further define the role of CRP in human pathological conditions.
    Type of Medium: Online Resource
    ISSN: 2047-9980
    URL: Article
    DOI: 10.1161/JAHA.114.001084
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2014
    detail.hit.zdb_id: 2653953-6
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  • 3
    Online Resource
    Online Resource
    Chemokine Ligand 2 Genetic Variants, Serum Monocyte Chemoattractant Protein-1 Levels, and the Risk of Coronary Artery Disease
    Ovid Technologies (Wolters Kluwer Health) ; 2010
    In:  Arteriosclerosis, Thrombosis, and Vascular Biology Vol. 30, No. 7 ( 2010-07), p. 1460-1466
    Details
    In: Arteriosclerosis, Thrombosis, and Vascular Biology, Ovid Technologies (Wolters Kluwer Health), Vol. 30, No. 7 ( 2010-07), p. 1460-1466
    Abstract: Objective— In humans, evidence about the association between levels of monocyte chemoattractant protein-1 (MCP-1), its coding gene chemokine (C-C motif) ligand 2 ( CCL2 ), and risk of coronary artery disease (CAD) is contradictory. Methods and Results— We performed a nested case-control study in the prospective EPIC-Norfolk cohort investigating the relationship between CCL2 single-nucleotide polymorphisms (SNPs), MCP-1 concentrations, and the risk of future CAD. Cases (n=1138) were apparently healthy men and women aged 45 to 79 years who developed fatal or nonfatal CAD during a mean follow-up of 6 years. Controls (n=2237) were matched by age, sex, and enrollment time. Using linear regression analysis no association between CCL2 SNPs and MCP-1 serum concentrations became apparent, nor did we find a significant association between MCP-1 serum levels and risk of future CAD. Finally, Cox regression analysis showed no significant association between CCL2 SNPs and the future CAD risk. In addition, we did not find any robust associations between the CCL2 haplotypes and MCP-1 serum concentration or future CAD risk. Conclusion— Our data do not support previous publications indicating that MCP-1 is involved in the pathogenesis of CAD.
    Type of Medium: Online Resource
    ISSN: 1079-5642 , 1524-4636
    URL: Article
    DOI: 10.1161/ATVBAHA.110.205526
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2010
    detail.hit.zdb_id: 1494427-3
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  • 4
    Online Resource
    Online Resource
    C-Reactive Protein, Fatal and Nonfatal Coronary Artery Disease, Stroke, and Peripheral Artery Disease in the Prospective EPIC-Norfolk Cohort Study
    Ovid Technologies (Wolters Kluwer Health) ; 2013
    In:  Arteriosclerosis, Thrombosis, and Vascular Biology Vol. 33, No. 12 ( 2013-12), p. 2888-2894
    Details
    In: Arteriosclerosis, Thrombosis, and Vascular Biology, Ovid Technologies (Wolters Kluwer Health), Vol. 33, No. 12 ( 2013-12), p. 2888-2894
    Abstract: Circulating levels of C-reactive protein (CRP) are associated with an increased risk of coronary artery disease (CAD), stroke, and peripheral artery disease (PAD). Observational and experimental evidence suggest that CRP might differentially predict fatal and nonfatal cardiovascular events. Here, we sought to determine the predictive value of CRP for fatal and nonfatal CAD, stroke, or PAD. Approach and Results— CRP levels were measured in 18 450 apparently healthy participants in the European Prospective Investigation into Cancer and Nutrition (EPIC)-Norfolk cohort. Cox proportional hazards models were used to quantify the association between CRP levels and fatal and nonfatal CAD events, strokes, and PAD events. Bootstrapping was applied to test for significant differences between the risk of fatal and nonfatal events. During 208 485 person-years at risk, 2915 CAD events, 361 strokes, and 657 PAD events occurred. CRP was associated with fatal and nonfatal CAD events and nonfatal PAD events. When adding CRP to predictive risk models for fatal and nonfatal events corrected for known cardiovascular risk factors, the net reclassification index was 2.1% for fatal and 1.9% for nonfatal events. Multivariate adjusted hazard ratios for fatal CAD events (hazard ratio, 1.36; 95% confidence interval, 1.27–1.46) differed significantly (mean difference, 13%; 95% confidence interval, 5.1%–21.9%; P 〈 0.001) from the multivariate adjusted hazard ratio for nonfatal CAD events (hazard ratio, 1.21; 95% confidence interval, 1.15–1.26). Conclusions— In the EPIC-Norfolk cohort, CRP was associated with fatal and nonfatal CAD events, as well as nonfatal PAD events. Adding CRP to risk stratification models resulted in a small improvement in classification for both fatal and nonfatal events. Importantly, CRP was significantly more strongly associated with fatal CAD events than with nonfatal CAD events.
    Type of Medium: Online Resource
    ISSN: 1079-5642 , 1524-4636
    URL: Article
    DOI: 10.1161/ATVBAHA.113.301736
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2013
    detail.hit.zdb_id: 1494427-3
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  • 5
    Online Resource
    Online Resource
    Endothelial Shear Stress : A Critical Determinant of Arterial Remodeling and Arterial Stiffness in Humans—A Carotid 3.0-T MRI Study
    Ovid Technologies (Wolters Kluwer Health) ; 2010
    In:  Circulation: Cardiovascular Imaging Vol. 3, No. 5 ( 2010-09), p. 578-585
    Details
    In: Circulation: Cardiovascular Imaging, Ovid Technologies (Wolters Kluwer Health), Vol. 3, No. 5 ( 2010-09), p. 578-585
    Abstract: Low endothelial shear stress (ESS) elicits endothelial dysfunction. However, the relationship between ESS and arterial remodeling and arterial stiffness is unknown in humans. We developed a 3.0-T MRI protocol to evaluate the contribution of ESS to arterial remodeling and stiffness. Methods and Results— Fifteen young (aged 26±3 years) and 15 older (aged 57±3 years) healthy volunteers as well as 15 patients with cardiovascular disease (aged 63±10 years) were enrolled. Phase-contrast MRI of the common carotid arteries was used to derive ESS data from the spatial velocity gradients close to the arterial wall. ESS measurements were performed on 3 occasions and showed excellent reproducibility (intraclass correlation coefficient, 0.79). Multiple linear regression analysis accounting for age and blood pressure revealed that ESS was an independent predictor of the following response variables: carotid wall thickness (regression coefficient [b], −0.19 mm 2 per N/m 2 ; P =0.02), lumen area (b, −15.5 mm 2 per N/m 2 ; P 〈 0.001), and vessel size (b, −24.0 mm 2 per N/m 2 ; P 〈 0.001). Segments of the artery wall exposed to lower ESS were significantly thicker than segments exposed to higher ESS within the same artery ( P =0.009). Furthermore, ESS was associated with arterial compliance, accounting for age, blood pressure, and wall thickness (b, −0.003 mm 2 /mm Hg per N/m 2 ; P =0.04). Conclusions— Our carotid MRI data show that ESS is an important determinant of arterial remodeling and arterial stiffness in humans. The data warrant further studies to evaluate use of carotid ESS as a noninvasive tool to improve the understanding of individual cardiovascular disease risk and to assess novel drug therapies in cardiovascular disease prevention.
    Type of Medium: Online Resource
    ISSN: 1941-9651 , 1942-0080
    URL: Article
    DOI: 10.1161/CIRCIMAGING.109.916304
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2010
    detail.hit.zdb_id: 2440475-5
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