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  • Book
    Paolo Gresele, Gustav V. R Born, Carlo Patrono, Clive P. Page, editors.
    Contents:
    Part 1. Pathophysiology. Platelets: Production, Morphology and Ultrastructure / Jonathan N. Thon and Joseph E. Italiano
    Platelet Receptors / Alexandre Kauskot and Marc F. Hoylaerts
    Platelet Signaling / Timothy J. Stalker, Debra K. Newman, Peisong Ma, Kenneth M. Wannemacher and Lawrence F. Brass
    Platelet Interaction with the Vessel Wall / Philip G. de Groot, Rolf T. Urbanus and Mark Roest
    Platelets in Atherosclerosis and Thrombosis / Christian Schulz and Steffen Massberg
    Part 2. Pharmacology. Aspirin and Other COX-1 Inhibitors / Carlo Patrono and Bianca Rocca
    Thienopyridines and Other ADP-Receptor Antagonists / Isabell Bernlochner and Dirk Sibbing
    Glycoprotein IIb/IIIa Antagonists / Karen M. Hook and Joel S. Bennett
    Targeting Phosphodiesterases in Anti-platelet Therapy / Matthew T. Rondina and Andrew S. Weyrich
    PAR-1 Inhibitors: A Novel Class of Antiplatelet Agents for the Treatment of Patients with Atherothrombosis / Sergio Leonardi and Richard C. Becker
    Thromboxane Receptors Antagonists and/or Synthase Inhibitors / Giovanni Davì, Francesca Santilli and Natale Vazzana
    Inhibitors of the Interaction Between von Willebrand Factor and Platelet GPIb/IX/V / Paolo Gresele and Stefania Momi
    Inhibitors of the Interactions Between Collagen and Its Receptors on Platelets / Hans Deckmyn, Simon F. De Meyer, Katleen Broos and Karen Vanhoorelbeke
    Intracellular Signaling as a Potential Target for Antiplatelet Therapy / Patrick Andre
    Novel Targets for Platelet Inhibition / Kathleen Freson and Chris Van Geet
    Variability of Platelet Indices and Function: Acquired and Genetic Factors / Giovanni de Gaetano, Iolanda Santimone, Francesco Gianfagna, Licia Iacoviello and Chiara Cerletti
    Small RNAs as Potential Platelet Therapeutics / Leonard C. Edelstein and Paul F. Bray
    Pharmacological Modulation of the Inflammatory Actions of Platelets / Richard Amison, Clive Page and Simon Pitchford
    Part 3. Therapy. The Role of Laboratory Monitoring in Antiplatelet Therapy / Marco Cattaneo
    Antiplatelet Agents in Ischemic Heart Disease / Christopher H. May and A. Michael Lincoff
    Antiplatelet Therapy in Cerebrovascular Disorders / Ralph Weber, Johannes Brenck and Hans-Christoph Diener
    Antiplatelet Therapy in Peripheral Artery Disease / Francesco Violi, Stefania Basili, Jeffrey S. Berger and William R. Hiatt
    Primary Prevention of Ischaemic Cardiovascular Disorders with Antiplatelet Agents / Tom Mead.
    Digital Access Springer 2012
  • Article
    Somlyo AV, Shuman H, Somlyo AP.
    J Cell Biol. 1977 Sep;74(3):828-57.
    A method of rapid freezing in supercooled Freon 22 (monochlorodifluoromethane) followed by cryoultramicrotomy is described and shown to yield ultrathin sections in which both the cellular ultrastructure and the distribution of diffusible ions across the cell membrane are preserved and intracellular compartmentalization of diffusabler ions can be quantitated. Quantitative electron probe analysis (Shuman, H., A.V. Somlyo, and A.P. Somlyo. 1976. Ultramicros. 1:317-339.) of freeze-dried ultrathin cryto sections was found to provide a valid measure of the composition of cells and cellular organelles and was used to determine the ionic composition of the in situ terminal cisternae of the sarcoplasmic reticulum (SR), the distribution of CI in skeletal muscle, and the effects of hypertonic solutions on the subcellular composition if striated muscle. There was no evidence of sequestered CI in the terminal cisternae of resting muscles, although calcium (66mmol/kg dry wt +/- 4.6 SE) was detected. The values of [C1](i) determined with small (50-100 nm) diameter probes over cytoplasm excluding organelles over nuclei or terminal cisternae were not significantly different. Mitochondria partially excluded C1, with a cytoplasmic/ mitochondrial Ci ratio of 2.4 +/- 0.88 SD. The elemental concentrations (mmol/kg dry wt +/- SD) of muscle fibers measured with 0.5-9-mum diameter electron probes in normal frog striated muscle were: P, 302 +/- 4.3; S, 189 +/- 2.9;C1, 24 +/- 1.1;K, 404 +/- 4.3, and Mg, 39 +/- 2.1. It is concluded that: (a) in normal muscle the "excess CI" measured with previous bulk chemical analyses and flux studies is not compartmentalized in the SR or in other cellular organelles, and (b) the cytoplasmic C1 in low [K](0) solutions exceeds that predicted by a passive electrochemical distribution. Hypertonic 2.2 X NaCl, 2.5 X sucrose, or 2.2 X Na isethionate produced: (a) swollen vacuoles, frequently paired, adjacent to the Z lines and containing significantly higher than cytoplasmic concentrations of Na and Cl or S (isethionate), but no detectable Ca, and (b) granules of Ca, Mg, and P = approximately (6 Ca + 1 Mg)/6P in the longitudinal SR. It is concluded that hypertonicity produces compartmentalized domains of extracellular solutes within the muscle fibers and translocates Ca into the longitudinal tubules.
    Digital Access Access Options