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Lorraine B Ware - One of the best experts on this subject based on the ideXlab platform.

Robert Rothlein - One of the best experts on this subject based on the ideXlab platform.

  • alterations in circulating Intercellular Adhesion Molecule 1 and l selectin further evidence for chronic inflammation in ischemic heart disease
    American Heart Journal, 1996
    Co-Authors: Robert Rothlein, Elizabeth Mainolfi, Herbert W Haught, Michael Mansour, Takashi Kei Kishimoto
    Abstract:

    Abstract Atherosclerosis is increasingly thought to be a chronic inflammatory disease. Inflammation requires transmigration of leukocytes from the circulation to the tissues. Adhesion of leukocytes to endothelial cells is the initial event in an inflammatory response and is mediated by expression of several Adhesion Molecules. In this study we characterize the contribution of Intercellular Adhesion Molecule-1 (ICAM-1) and L-selectin in patients with different coronary artery disease syndromes. Serum concentrations of cICAM-1 and sL-selectin were measured by enzyme-linked immunosorbent assay in 31 patients with stable angina, 30 patients with unstable angina, 18 patients with acute myocardial infarction and 20 healthy subjects in a control group. All patients underwent coronary angiography. Mean (±SE) cICAM-1 levels were higher ( p p

  • treatment of refractory rheumatoid arthritis with a monoclonal antibody to Intercellular Adhesion Molecule 1
    Arthritis & Rheumatism, 1994
    Co-Authors: Arthur F Kavanaugh, Robert Rothlein, Laurie S Davis, Lisa A Nichols, Stephen Norris, Linda Scharschmidt, Peter E Lipsky
    Abstract:

    Objective. To assess the safety and efficacy of a monoclonal antibody (MAb) to Intercellular Adhesion Molecule 1 (ICAM-1; CD54) in rheumatoid arthritis (RA). Methods. A phase I/II, open-label, dose-escalation study of 32 patients. Results. During treatment, a peripheral CD3+/CD4+ lymphocytosis was noted, and several patients demonstrated transient cutaneous anergy, which suggests that therapy modified T cell recirculation. Thirteen of the 23 patients who received 5 days of treatment demonstrated clinical improvement through day 29, and 9 of 23 through day 60. Adverse effects were minor and transient. Conclusion. Anti—ICAM-1 MAb therapy was well tolerated, resulted in a transient alteration in T lymphocyte recirculation, and effected clinical improvement in some RA patients.

  • circulating Intercellular Adhesion Molecule 1 in amniotic fluid maternal serum α fetoprotein levels and intrauterine growth retardation
    American Journal of Obstetrics and Gynecology, 1993
    Co-Authors: Carolyn Salafia, Greggory R Devore, Elizabeth Mainolfi, Joann C Kelly, John C Pezzullo, Robert Rothlein
    Abstract:

    Objective: Our purpose was to determine if circulating Intercellular Adhesion Molecule-1, a marker of chronic inflammation, is present in amniotic fluid in midtrimester, is increased in patients with elevated maternal serum α-fetoprotein level, and is associated with intrauterine growth retardation. Study Design: Amniotic fluid circulating Intercellular Adhesion Molecule-1 levels were assayed by enzyme-linked immunoassay in 273 samples obtained by midtrimester amniocentesis in gestations involving a single, structurally normal fetus. The control group consisted of 108 patients with normal maternal serum α-fetoprotein levels and 165 patients with elevated levels. Intrauterine growth retardation was diagnosed if birth weight was Results: Circulating Intercellular Adhesion Molecule-1 was detectable in amniotic fluid in 105 of 273 samples (38%). In the control group it was detectable in amniotic fluid in seven of 108 (6%). In patients with elevated maternal serum α-fetoprotein 97 of 164 (59%) had detectable levels ( p p p Conclusions: Midtrimester amniotic fluid from normal pregnancies does not generally contain detectable circulating Intercellular Adhesion Molecule-1. Detectable amniotic fluid levels are significantly related to a birth weight

  • reduction of central nervous system ischemic injury by monoclonal antibody to Intercellular Adhesion Molecule
    Journal of Neurosurgery, 1991
    Co-Authors: Wayne M Clark, Robert Rothlein, Ken P Madden, Justin A Zivin
    Abstract:

    Activated leukocytes appear to be directly involved in potentiating ischemic central nervous system (CNS) injury. Adhesion of leukocytes to endothelium is essential for their migration and requires the binding of Adhesion receptors of the leukocyte (CD 18) to an Intercellular Adhesion Molecule (ICAM) on endothelium. Monoclonal antibodies to an ICAM can block leukocyte Adhesion and transendothelial migration. To determine the efficacy of anti-ICAM antibody treatment in preserving neurological function after CNS ischemia, two animal models were used. A 1-mg/kg dose of anti-ICAM was given to rabbits 30 minutes before induction of ischemia either in the spinal cord using temporary aortic occlusion or in the brain using intra-arterial microspheres. In this study, treatment with anti-ICAM produced a significant reduction in neurological deficits in the reversible spinal cord ischemia model but not in the irreversible brain ischemia model. This protective effect supports the active role of leukocytes in CNS reperfusion ischemic injury and offers potential for future therapy.

William R Wagner - One of the best experts on this subject based on the ideXlab platform.

  • ultrasound imaging of acute cardiac transplant rejection with microbubbles targeted to Intercellular Adhesion Molecule 1
    Circulation, 2003
    Co-Authors: Gregory E R Weller, William R Wagner, Melissa Csikari, Alexander L Klibanov, David Fischer, Flordeliza S Villanueva
    Abstract:

    Background— Noninvasive techniques for detecting acute cardiac transplant rejection are limited. We hypothesized that ultrasound contrast microbubbles targeted to the endothelial cell (EC) inflammatory marker Intercellular Adhesion Molecule-1 (ICAM-1) would selectively bind to rejecting versus nonrejecting myocardium and that myocardial contrast echocardiography can therefore detect acute rejection. Methods and Results— Lipid-based microbubbles were conjugated to anti-rat ICAM-1 (MBICAM) or isotype control antibody (MBControl). In vitro MBICAM Adhesion to cultured rat ECs, as assessed in a parallel plate flow apparatus, was greater to inflammatory versus normal ECs (11±3 versus 3±2 microbubbles/EC, P<0.005). In vivo abdominal heterotopic heart transplantation was performed in rats (rejection group: Brown Norway to Lewis strain; control group: Lewis to Lewis or Brown Norway to Brown Norway). Triggered myocardial contrast echocardiography was performed during intravenous MBICAM or MBControl (2.5×106) inject...

  • microbubbles targeted to Intercellular Adhesion Molecule 1 bind to activated coronary artery endothelial cells
    Circulation, 1998
    Co-Authors: Flordeliza S Villanueva, Ron J Jankowski, Sasha Klibanov, Maris L Pina, Sean Alber, Simon C Watkins, Gary H Brandenburger, William R Wagner
    Abstract:

    Background—Preclinical atherosclerosis is associated with increased endothelial cell (EC) expression of leukocyte Adhesion Molecules (LAMs), which mediate monocyte Adhesion during atherogenesis. Identification of cell-surface LAMs may uniquely allow assessment of endothelial function, but there are no in vivo methods for detecting LAMs. We tested a new microbubble designed to bind to and allow specific ultrasound detection of Intercellular Adhesion Molecule-1 (ICAM-1). Methods and Results—A perfluorobutane gas–filled lipid-derived microsphere with monoclonal antibody to ICAM-1 covalently bound to the bubble shell was synthesized. Bubbles with either nonspecific IgG or no protein on the shell were synthesized as controls. Coverslips of cultured human coronary artery ECs were placed in a parallel-plate perfusion chamber and exposed to 1 of the 3 microbubble species, followed by perfusion with culture medium. Experiments were performed with either normal or interleukin-1β–activated ECs overexpressing ICAM-1,...

  • microbubbles targeted to Intercellular Adhesion Molecule 1 bind to activated coronary artery endothelial cells
    Circulation, 1998
    Co-Authors: Flordeliza S Villanueva, Ron J Jankowski, Sasha Klibanov, Maris L Pina, Sean Alber, Simon C Watkins, Gary H Brandenburger, William R Wagner
    Abstract:

    BACKGROUND: Preclinical atherosclerosis is associated with increased endothelial cell (EC) expression of leukocyte Adhesion Molecules (LAMs), which mediate monocyte Adhesion during atherogenesis. Identification of cell-surface LAMs may uniquely allow assessment of endothelial function, but there are no in vivo methods for detecting LAMs. We tested a new microbubble designed to bind to and allow specific ultrasound detection of Intercellular Adhesion Molecule-1 (ICAM-1). METHODS AND RESULTS: A perfluorobutane gas-filled lipid-derived microsphere with monoclonal antibody to ICAM-1 covalently bound to the bubble shell was synthesized. Bubbles with either nonspecific IgG or no protein on the shell were synthesized as controls. Coverslips of cultured human coronary artery ECs were placed in a parallel-plate perfusion chamber and exposed to 1 of the 3 microbubble species, followed by perfusion with culture medium. Experiments were performed with either normal or interleukin-1beta-activated ECs overexpressing ICAM-1, and bubble adherence was quantified with epifluorescent videomicroscopy. There was limited adherence of control bubbles to normal or activated ECs, whereas a 40-fold increase in Adhesion occurred when anti-ICAM-1-conjugated bubbles were exposed to activated ECs compared with normal ECs (8.1+/-3.5 versus 0.21+/-0.09 bubbles per cell, respectively, P<0.001). Although diminished, this difference persisted even after perfusion at higher wall shear rates. CONCLUSIONS: A gas-filled microbubble with anti-ICAM-1 antibody on its shell specifically binds to activated ECs overexpressing ICAM-1. Diagnostic ultrasound in conjunction with targeted contrast agents has the unique potential to characterize cell phenotype in vivo.

Michael A Matthay - One of the best experts on this subject based on the ideXlab platform.

David R Jacobs - One of the best experts on this subject based on the ideXlab platform.

  • polymorphisms in the icam1 gene predict circulating soluble Intercellular Adhesion Molecule 1 sicam 1
    Atherosclerosis, 2011
    Co-Authors: Suzette J Bielinski, Alexander P Reiner, Deborah A Nickerson, Christopher S Carlson, Kent R Bailey, Bharat Thyagarajan, Leslie A Lange, Eric Boerwinkle, David R Jacobs
    Abstract:

    Abstract Objective Polymorphisms within the ICAM1 structural gene have been shown to influence circulating levels of soluble Intercellular Adhesion Molecule-1 (sICAM-1) but their relation to atherosclerosis has not been clearly established. We sought to determine whether ICAM1 SNPs are associated with circulating sICAM-1 concentration, coronary artery calcium (CAC), and common and internal carotid intima medial thickness (IMT). Methods and Results 3550 black and white Coronary Artery Risk Development in Young Adults (CARDIA) Study subjects who participated in the year 15 and/or 20 examinations and were part of the Young Adult Longitudinal Study of Antioxidants (YALTA) ancillary study were included in this analysis. In whites, rs5498 was significantly associated with sICAM-1 ( p ICAM1 SNPs. Conclusions In CARDIA, ICAM1 DNA segment variants were associated with sICAM-1 protein level including the novel finding that levels differ by the functional variant rs5491. However, ICAM1 SNPs were not strongly related to either IMT or CAC. Our findings in CARDIA suggest that ICAM1 variants are not major early contributors to subclinical atherosclerosis.