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  • Book
    Mushabbar A. Syed, Raad H. Mohiaddin, editors.
    Summary: This textbook is alone in focusing on the subject of cardiac magnetic resonance (CMR) imaging in pediatric and adult patients with congenital heart disease. The topic of congenital heart disease imaging is usually relegated to a single chapter in most general CMR texts. The expanding scope of CHD warrants a text dedicated to covering CHD and CMR imaging in detail. Our proposed book aims to be a comprehensive and authoritative text on this subject.

    Contents:
    General Principles of Cardiac Magnetic Resonance Imaging / Mark A. Fogel
    MRI Safety / Roger Luechinger
    Introduction to Congenital Heart Disease Anatomy / Pierangelo Renella, J. Paul Finn
    Venoatrial Abnormalities / Henryk Kafka
    Septal Defects / Sharon L. Roble
    Right Ventricular Anomalies / Frédérique Bailliard
    Tetralogy of Fallot / Michael A. Quail
    Ebstein's Anomaly and Other Tricuspid Valve Anomalies / Steve W. Leung
    Abnormalities of Left Ventricular Inflow and Outflow / Puja Banka, Tal Geva
    Single Ventricle and Fontan Procedures / Anna N. Seale
    Transposition of Great Arteries / Joel R. Wilson, Mushabbar A. Syed
    Aortic Anomalies / Sylvia S. M. Chen
    Inherited Cardiomyopathies / Rory O'Hanlon
    Coronary Artery Anomalies / Andrew M. Crean
    Pericardial Diseases / Edward T. Martin
    Cardiac Tumors / Mushabbar A. Syed
    Pediatric Cardiovascular Magnetic Resonance / Emanuela R. Valsangiacomo Bueche
    Interventional Cardiovascular Magnetic Resonance / Vivek Muthurangu
    Emerging Roles for Cardiovascular Magnetic Resonance in Adult Congenital Heart Disease Electrophysiology.
    Digital Access Springer 2012
  • Article
    Bick PH, Johnson AG.
    Scand J Immunol. 1977;6(11):1133-44.
    In vitro exposure of mouse thymocytes to complexes of polyadenylic:polyuridylic acid (poly A:U) effected, within 6 h, the release of soluble factor(s) capable of nonspecifically enhancing IgM and IgG plaque-forming cells (PFCs) in in vitro primary and secondary spleen cell responses to burro erythrocytes. Poly A:U stimulation was, most likely, polyclonal, since production of soluble factor(s) occurred in the absence of antigen and in serum-free culture media. Poly A:U-induced soluble factor(s) were not capable of substituting for T cells but were dependent on T cells for the expression of PFC enhancement. These data support the hypothesis that the mechanism of poly A:U's adjuvant action is polyclonal stimulation of T cells, causing early induction and release of nonspecific, soluble PFC-enhancing factor(s).
    Digital Access Access Options