Clot Retraction
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Factor XIII Activity Mediates Red Blood Cell Retention in Venous Thrombi
RESEARCH ARTICLE The Journal of Clinical Investigation Factor XIII activity mediates red blood cell retention in venous thrombi Maria M. Aleman,1 James R. Byrnes,1 Jian-Guo Wang,1 Reginald Tran,2 Wilbur A. Lam,2 Jorge Di Paola,3 Nigel Mackman,4,5 Jay L. Degen,6 Matthew J. Flick,6 and Alisa S. Wolberg1,4 1Department of Pathology and Laboratory Medicine, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA. 2Wallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology and Emory University, Atlanta, Georgia, USA. 3Department of Pediatrics and Human Medical Genetics and Genomics Program, University of Colorado, Denver, Colorado, USA. 4McAllister Heart Institute and 5Department of Medicine, Division of Hematology/Oncology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA. 6Department of Pediatrics, Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio, USA. Venous thrombi, fibrin- and rbc-rich clots triggered by inflammation and blood stasis, underlie devastating, and sometimes fatal, occlusive events. During intravascular fibrin deposition, rbc are thought to become passively trapped in thrombi and therefore have not been considered a modifiable thrombus component. In the present study, we determined that activity of the transglutaminase factor XIII (FXIII) is critical for rbc retention within clots and directly affects thrombus size. Compared with WT mice, mice carrying a homozygous mutation in the fibrinogenγ chain (Fibγ390–396A) had a striking 50% reduction in thrombus weight due to reduced rbc content. Fibrinogen from mice harboring the Fibγ390–396A mutation exhibited reduced binding to FXIII, and plasma from these mice exhibited delayed FXIII activation and fibrin crosslinking, indicating these residues mediate FXIII binding and activation. -
Thromboprophylaxis in Cancer Patients with Central Venous Catheters
Thromboprophylaxis in Cancer Patients with Central Venous Catheters by Annie Young A thesis submitted to The University of Birmingham for the degree of DOCTOR OF PHILOSOPHY College of Medical and Dental Sciences Birmingham, November 2010 Acknowledgments I would like to acknowledge my supervisors, Professors Collette Clifford and Keith Wheatley who have inspired me to participate in and lead research for the past 15 years and who have encouraged and supported me to complete this thesis. I would like to thank many of the Clinical Trials Team in Birmingham, in particular Gulnaz Begum, Laura Buckley and Cindy Billingham who steered me through some of the statistical analysis. I must also acknowledge the excellent clinical teams in the 68 UK centres who participated in the WARP trial, many of whom I have now met. Lastly and most importantly, I would like to express appreciation to all the patients, willing to be randomised into the trial. After all these years, even though I have never met them, I feel I know or knew them well. Thank you. Dedicated to my family: David, my remarkable husband who put up with me hiding in the study night after night and my three wonderful and patient children, Stewart, Sarah and Fiona; my dad, two sisters, who care for me always and in memory of my mum who died in November 2008 and when well, constantly encouraged me to „go for it‟. 2 CONTENTS 1. Glossary 18 2. Abstract 20 3. Introduction and Background 21 3.1 Introduction 21 3.2 Aims and Objectives of Thesis 23 3.3 Background 24 3.3.1 Venous Thromboembolism -
Rationale for IV Tpa Inclusion/Exclusion
AHA/ASA Scientific Statement Scientific Rationale for the Inclusion and Exclusion Criteria for Intravenous Alteplase in Acute Ischemic Stroke A Statement for Healthcare Professionals From the American Heart Association/American Stroke Association The American Academy of Neurology affirms the value of this statement as an educational tool for neurologists. Endorsed by the American Association of Neurological Surgeons and Congress of Neurological Surgeons Bart M. Demaerschalk, MD, MSc, FRCPC, FAHA, Chair; Dawn O. Kleindorfer, MD, FAHA, Vice-Chair; Opeolu M. Adeoye, MD, MS, FAHA; Andrew M. Demchuk, MD; Jennifer E. Fugate, DO; James C. Grotta, MD; Alexander A. Khalessi, MD, MS, FAHA; Elad I. Levy, MD, MBA, FAHA; Yuko Y. Palesch, PhD; Shyam Prabhakaran, MD, MS, FAHA; Gustavo Saposnik, MD, MSc, FAHA; Jeffrey L. Saver, MD, FAHA; Eric E. Smith, MD, MPH, FAHA; on behalf of the American Heart Association Stroke Council and Council on Epidemiology and Prevention Purpose—To critically review and evaluate the science behind individual eligibility criteria (indication/inclusion and contraindications/exclusion criteria) for intravenous recombinant tissue-type plasminogen activator (alteplase) treatment in acute ischemic stroke. This will allow us to better inform stroke providers of quantitative and qualitative risks associated with alteplase administration under selected commonly and uncommonly encountered clinical circumstances and to identify future research priorities concerning these eligibility criteria, which could potentially expand the safe and judicious use of alteplase and improve outcomes after stroke. Methods—Writing group members were nominated by the committee chair on the basis of their previous work in relevant topic areas and were approved by the American Heart Association Stroke Council’s Scientific Statement Oversight Committee and the American Heart Association’s Manuscript Oversight Committee. -
Clot Retraction: Cellular Mechanisms and Inhibitors, Measuring Methods, and Clinical Implications
biomedicines Review Clot Retraction: Cellular Mechanisms and Inhibitors, Measuring Methods, and Clinical Implications Ellen E. Jansen 1 and Matthias Hartmann 2,* 1 Clinic for Operative Dentistry, Periodontology and Preventive Dentistry, RWTH Aachen University, 52074 Aachen, Germany; [email protected] 2 Klinik für Anästhesiologie und Intensivmedizin, Universitätsklinikum Essen, Universität Duisburg-Essen, 45122 Essen, Germany * Correspondence: [email protected] Abstract: Platelets have important functions in hemostasis. Best investigated is the aggregation of platelets for primary hemostasis and their role as the surface for coagulation leading to fibrin- and clot- formation. Importantly, the function of platelets does not end with clot formation. Instead, platelets are responsible for clot retraction through the concerted action of the activated αIIbβ3 receptors on the surface of filopodia and the platelet’s contractile apparatus binding and pulling at the fibrin strands. Meanwhile, the signal transduction events leading to clot retraction have been investigated thoroughly, and several targets to inhibit clot retraction have been demonstrated. Clot retraction is a physiologically important mechanism allowing: (1) the close contact of platelets in primary hemostasis, easing platelet aggregation and intercellular communication, (2) the reduction of wound size, (3) the compaction of red blood cells to a polyhedrocyte infection-barrier, and (4) reperfusion in case of thrombosis. Several methods have been developed to measure clot