Effects of Plasma Tainted with CJD Still Under Scrutiny in U.K

Total Page:16

File Type:pdf, Size:1020Kb

Effects of Plasma Tainted with CJD Still Under Scrutiny in U.K Tuesday, July 14 BOSTON, MASSACHUSETTS ISTH 2009 DAILY XXII CONGRESS INTERNATIONAL SOCIETY ON THROMBOsis AND HAEMOSTAsis Dr. Hill cautioned against making INSIDE Effects of Plasma Tainted with too much of these findings. “There are many uncertainties about this data, and LATE-BREAKING RESULTS there are questions about the current Latest data released on five trials risk assessment. page 2 CJD Still Under Scrutiny in U.K. “We possibly don’t know the full ex- bout half of the 8,730 people in Among those 792 patients, 1,157 tent of contaminated batches. The pat- HISTORY FROM THE the United Kingdom who were have had treatment or exposure epi- terning incubation of time of variant BEGINNING Aexposed to plasma tainted with sodes with 12.7 million units of the im- CJD following exposure to plasma prod- variant Creutzfeldt-Jacob disease have plicated product. That is about half of uct may well be different even to expo- ISTH was founded 40 years ago not yet been treated. the 23 million that have been issued. sure through cellular product.” page 4 Physicians are trying to assess the risk Sixty-seven percent of this cohort had Finding answers to these questions to the patients who received the tainted received only one batch from an im- may involve better recruitment, post SNAKE BITE TREATMENT plasma from 1987 to 1999. Frank G. H. plicated donor, “but all have received mortem, results of longitudinal studies Research ongoing about when, if to Hill, MB, ChB, FRCPath, FRCPCH, other batches which may add to their involving these patients and the devel- administer fresh frozen plasma at Birmingham Children’s Hospital NHS cumulative risk.” opment of a blood test. page 6 Trust and the U.K. Haemophilia Centre Directors Organization, discussed the ex- Opening tent of exposure and risk stratification dur- YOUNG INVESTIGATORS ing a plenary session Monday morning. Ceremony Four Pier M. Mannucci Awards “Information on the National Haemo- announced Draws Large, page 8 philia Database shows us we have in ex- cess of 23,000 registered patients; 8,730 Festive Crowd of those have been treated,” said Hill. Hundreds of delegates “From annual return data, we can iden- gathered Sunday night tify 4,580 patients who have received to celebrate the opening U.K. plasma products and therefore are of the XXII ISTH at risk of variant CJD and require public Congress. TUESDAY health precautions with certain opera- AT A GLANCE tive procedures. Of those, 792 have been positively notified as having received an Ongoing implicated batch,” Dr. Hill said. Oral Communications, State- of-the-Art Lectures, Abstract Symposia, Nurses’ Sessions 9:45 a.m. – 10:30 a.m. PrPSC Detected in Spleen of Adult Hemophilic Patient in U.K. Plenary Lecture: Contribution nalyses of tissues from 17 Unit, said Monday products. All we can say we know for of Allosteric Disulfide Bonds patients exposed to variant that the patient “like- sure is that there was an infected donor to Regulation of Hemostasis Creutzfeldt-Jakob disease in ly” contracted the in this pool.” (Philip Hogg) A the United Kingdom showed that one disease from an un- Investigators performed prospective 3:00 p.m. – 3:15 p.m. patient with hemophilia had disease-as- identified source. and retrospective analyses on tissues ISTH General Membership sociated prion protein – PrPSC - in his “Because of the collected from biopsies or autopsies, Assembly spleen tissues. large volume of non- searching for the presence of disease-as- It is not yet known whether the pa- implicated products Dr. James W. sociated prion protein. All patients had 3:15 p.m. – 4:00 p.m. tient came in contact with the disease received, it is likely Ironside, FRCPath been treated with U.K.-sourced pooled Presidential Plenary through diet, blood transfusion or this could be the source of the infec- factor concentrates for bleeding disor- Abstracts pooled clotting factor concentrate. Dr. tion,” he said. “On the relative risk, it ders from 1980 and 2001. That pool is James W. Ironside, FRCPath, director is very difficult to discriminate between known to contain tainted plasma from 4:00 p.m. – 4:15 p.m. of the U.K.’s National CJD Surveillance the implicated and non-implicated (Ironside, continued on page 11) ISTH 2009 Congress Awards Presentation Tuesday, July 14, 6:30 PM – 7:30 PM 4:15 p.m. – 5:00 p.m. Industry Sponsored Technical Sessions TIPS OF THE DAY Presidential Plenary Abstracts Add future professional conferences to your calendar after • Network for Continuing • Rovi stopping by the Future Events Kiosk. 6:30 p.m. – 7:30 p.m. Medical Education (Novo Room 104 ABC Technical Sessions Nordisk) Stay connected at the Cyber Café & Message Center in the (Industry Sponsored) Room 107 ABC Exhibition Area. The ISTH 2009 Daily Congress news will also appear on the ISTH website at www.isth.org. TUESDAY • JULY 14, 2009 LATE BREAKING TRIAL ADVANCE-2: Favorable Risk-Benefit Profile With Apixaban pixaban for thromboprophy- lower major and paring efficacy and safety of 2.5 mg bleeding (major and clinically rel- laxis after total knee replace- clinically relevant apixaban twice daily for preventing evant nonmajor). A ment had better efficacy and non-major bleed- VTE vs. the current European stan- The primary outcome occurred safety compared to the current stan- ing rates in patients dard of care, 40 mg subcutaneous in 15.1% of patients in the apixaban dard of care enoxaparin, according to undergoing total enoxaparin once daily, said Michael group vs. 24.4% in the enoxaparin late-breaking results of ADVANCE-2 knee replacement. Lassen, MD, of the University of Co- group (P,.001). Major VTE oc- presented Monday. A D V A N C E - 1 penhagen, Hørsholm, Denmark. curred in 1.1% of apixaban patients ADVANCE-1 results, presented in compared apixa- Michael Primary efficacy outcome was the treated with apixaban vs. 2.2% of December 2008 at the 50th ASH An- ban with the North Lassen, MD composite of DVT by venography, patients treated with enoxaparin, Dr. nual Meeting, showed that apixaban American dosage symptomatic objectively confirmed Lassen said. failed to meet one of two prespeci- of enoxaparin 30 mg twice daily. DVT or pulmonary embolism, or Apixaban also conferred a better fied noninferiority criteria margins ADVANCE-2 was a randomized, death from any cause during treat- safety profile compared with apixaban in reducing rates of VTE but showed double blind, multicenter trial com- ment. Primary safety outcome was (3.5% vs.4.8%; respectively; P=.09). LATE BREAKING TRIAL dependent radiologists. The primary efficacy endpoint Four-Week Prophylaxis Better Than One Week was the combined incidence of to- tal documented symptomatic and After Abdominal, Pelvic Surgery asymptomatic DVT, nonfatal pul- monary embolism and deaths due to hen compared with a tients undergoing cancer abdominal patients; the efficacy analysis, 488. any cause. Primary safety endpoint one-week prophylaxis, or pelvic surgery. Prior to randomization, all patients was major hemorrhage, according to W four weeks with the low These results were part of the CAN- received 3,500 IU bemiparin starting six Dr. Kakkar. molecular weight heparin bemiparin BESURE trial presented Monday by hours postsurgery for eight days. They Patients assigned bemiparin had significantly reduced the rate of ma- Dr. Vijay V. Kakkar, MD, director were then randomly assigned 3,500 IU a 24.4% relative risk reduction for jor venous thromboembolism with- of the Thrombosis Research Institute, bemiparin once daily or placebo for 20 the primary endpoint and a 82.4% out increased complications in pa- London, as part of the late-breaking more days, Dr. Kakkar said. relative risk reduction for incidence abstracts session. Follow-up was three months. of major VTE (see chart). C A N B E S U R E Twenty-eight days after surgery, bi- Rates of major bleeding were simi- was a multicenter, lateral ascending venography was lar in both groups (0.6% vs. 0.3%, re- randomized, double performed and examined by five in- spectively; P=.572). blind parallel group trial. The study in- cluded 703 patients LATE BREAKING TRIAL aged 40 or older who were undergoing sur- gery on the gastroin- Better Anticoagulant Control testinal or genitouri- nary tract, or female With Warfarin reproductive organs. The safety analysis atients who switched from were randomly assigned to warfa- included data on 625 acenocoumarol to warfa- rin and 254 to phenprocoumon. P rin spent more time within An equal number of patients initiat- therapeutic ranges than those who ing and switching therapies were in switched to phenprocoumon, ac- both groups. LATE BREAKING TRIAL cording to late-breaking After six months’ follow- results presented Monday. up, the overall mean per- Enoxaparin Effective for VTE Prevention The trial compared warfa- centage of time spent within rin and phenprocoumon therapeutic ranges was in Advanced Pancreatic Cancer in patients who were ei- 74.6% for the warfarin group ther initiating anticoagulant and 65.3% for the phen- ONKO 004 trial results sug- CONKO 004 trial. treatment or switching from procoumon group (95% CI, gest that the low molecular In an intent-to-treat analysis, the vitamin K antagonist 5.8-12.8), she said. C weight heparin enoxaparin enoxaparin reduced the risk of VTE acenocoumarol to a new Yvonne van The difference in mean helped prevent symptomatic ve- by 65% with no increased safety com- therapy. Leeuwen, MSc percentage of time spent nous thromboembolism in patients plications, Dr. Reiss said. Yvonne van Leeuwen, within therapeutic ranges undergoing chemotherapy for ad- From April 2004 to January 2009, MSc, from the department of clini- was more substantial in patients vanced pancreatic cancer. 312 VTE- and chemotherapy-naive cal epidemiology at Leiden Univer- who switched therapies: 78.3% for H.B.
Recommended publications
  • Reflections a PAPER in a SERIES COMMISSIONED to CELEBRATE the CENTENARY of the JBC in 2005
    THE JOURNAL OF BIOLOGICAL CHEMISTRY Vol. 278, No. 51, Issue of December 19, pp. 50819–50832, 2003 © 2003 by The American Society for Biochemistry and Molecular Biology, Inc. Printed in U.S.A. Reflections A PAPER IN A SERIES COMMISSIONED TO CELEBRATE THE CENTENARY OF THE JBC IN 2005 JBC Centennial 1905–2005 100 Years of Biochemistry and Molecular Biology A Brief Historical Review of the Waterfall/Cascade of Blood Coagulation Published, JBC Papers in Press, October 21, 2003, DOI 10.1074/jbc.X300009200 Earl W. Davie From the Department of Biochemistry, University of Washington, Seattle, Washington 98195-7350 This article explores some of the events and people involved in unraveling the basic Downloaded from mechanisms leading to the clotting of blood. It also brings to focus the important role that my teachers and colleagues had on my career in research. When I entered college majoring in chemistry I had little idea that I would have an opportunity to become a professor of biochemistry at a major university. This was clearly the result of the excellent advice and encouragement that I received, particularly from my teachers early in my career. http://www.jbc.org/ As a senior at the University of Washington, I took a course in biochemistry to complete my credit requirements for a B.S. in chemistry. The biochemistry course was taught by Donald Hanahan, an excellent lipid biochemist who understood the importance of a quantitative measurement. I was fascinated by the biochemistry class that Hanahan taught, as well as by a course dealing with the chemistry of natural products.
    [Show full text]
  • Mukesh-Jain.Pdf
    CURRICULUM VITAE Date Prepared: 4/2019 I. General Information: Name: Mukesh K. Jain MD FAHA Ellery Sedgwick Chair & Distinguished Scientist Professor of Medicine Chief Academic Officer, University Hospitals Health System Chief Scientific Officer, Harrington Discovery Institute Vice Dean for Academic Affairs, Case Western Reserve University Visiting Professor, University of Oxford, United Kingdom Office Address: Iris & Bert L. Wolstein Research Building 2103 Cornell Road Cleveland, Ohio 44106 216-368-3607 E-mail: [email protected] Education: 1991 MD summa cum laude, University of Buffalo School of Medicine 1987 BS summa cum laude, University of Buffalo Postdoctoral Training: Internship and Residency 1994 Chief Resident, Brockton/West Roxbury, Veterans Administration Medical Center 1992 – 1994 Medical Resident, Beth Israel Hospital, Boston, MA 1991 – 1992 Medical Intern Beth Israel Hospital, Boston, MA Clinical and Research Fellowships 2000 - 2000 Research Fellow, Brigham & Women’s Hospital (Supervisor: Mu-En Lee MD PhD) 1997 – 2000 Clinical Fellow, Cardiovascular Division, Brigham & Women’s Hospital, Harvard Medical School (Supervisor: Peter Libby MD) 1994 – 1997 Research Fellow, Harvard School of Public Health (Supervisor: Edgar Haber MD) Mukesh K. Jain, MD, FAHA– 2 Licensure and Certifications: 2006 – Ohio Board of Registration in Medicine 2005 – Fellow, American Heart Association 2002 – Diplomate, American Board of Cardiovascular Disease 1994 – Diplomate, American Board of Internal Medicine 1994 – 2008 Massachusetts Board of Registration in Medicine Academic Appointments: 2019- Visiting Professor, University of Oxford, United Kingdom 2019- Co-Director, Oxford-Harrington Rare Disease Centre 2019 - Vice Dean of Academic Affairs, Case Western Reserve University 2006 – Professor of Medicine with tenure, Case Western Reserve University 2006 – Ellery Sedgwick Jr.
    [Show full text]
  • MAGELLAN Study
    Monday, July 25 KYOTO JAPAN XXIII Congress of The International Society on Thrombosis and Haemostasis Tuesday, July 26 KYOTO JAPAN XXIII Congress of The International Society on Thrombosis and Haemostasis INSIDE MAGELLAN Study MAGELLAN Study: page 1 Reducing the Risk of VTE in Acutely Ill Medical Patients Highlights from Opening Ceremony Rivaroxaban, one of a new class with rivaroxaban and the optimal diagnosed with acute heart failure, page 1 of anticoagulants, is not only duration of treatment. just under-third diagnosed with 57th Annual Meeting of effective in the treatment of deep In his presentation on Monday, acute infectious disease, and just the ISTH Scientific and vein thrombosis (DVT) but has also Alexander T. Cohen, MBBS, MSc, under one-quarter diagnosed with Standardization Committee been associated with a reduced MD, King’s College Hospital, London, acute respiratory failure. page 2 Wednesday, July 27 risk of venous thromboembolism UK, discussed results from the The two arms of the trial involved The ISTH XXIII General (VTE) in patients with acute medical multicenter, randomized, double- patients receiving either 10 mg Membership AssemblyKYOTOillness. JAPAN However, questions remain blind MAGELLAN study conducted once daily of oral rivaroxaban page 4 regarding increased bleeding risks to evaluate oral treatment with for 35 days or 40 mg once daily PreviewXXIII of Plenary Congress Lectures of The International Society on Thrombosis and Haemostasis Challenge to Novel Bioactive Peptides rivaroxaban compared with a of enoxaparin by subcutaneous - Kenji Kangawa standard 10-day treatment with injection for 10 days. Double- Recent Progress in Anticoagulant subcutaneous enoxaparin. blinding involved patients taking Therapy: Oral Direct Inhibitors of Thrombin and Factor Xa The study randomized 8,101 either 35 days of an oral placebo - Kenneth A.
    [Show full text]
  • Clotting Factor XII (Hageman) Deficiency Predisposing Acute Non-Hemorrhagic Stroke
    World Journal of Research and Review (WJRR) ISSN:2455-3956, Volume-6, Issue-6, June 2018 Pages 12-15 Case Report: Clotting Factor XII (Hageman) Deficiency Predisposing Acute non-hemorrhagic Stroke Dr. Riyadh Ali Hammamy, Dr. Mohamed Kamal Hassan Sabra related people which had the deficiency. Abstract— Prolonged Activated Partial ThromboplastinTime Paradoxically,pulmonary embolism or myocardial infarction (APTT) on routine coagulation screening would usually attract contributed to Hageman’s death after an occupational clinician’s attention toward bleeding tendency specially when accident[3,4].Since then, case series clinical studies have done as preoperative preparation. Factor XII (Hageman factor) identified an association of thrombosis and factor XII is one of the factors involved in the intrinsic coagulation cascade and deficiency of these factors eventually prolong APTT with deficiency, though the pathophysiologyof the relationship is bleeding tendency. However, factor XII deficiency are more unclear. It has been described that Hegman factor deficiency liable for thromboembolism through defective fibrinolytic would cause pregnancy losses and venous thromboembolism pathway rather than bleeding tendency. and reported cases of myocardial infarctions. A case of 27 years old male patient without past medical Factor XII (Hageman Factor) deficiency is a rare detection, illnesses or significant risk factors presented with acute middle usually persistent prolongations of APTT either suggests of cerebral artery non-hemorrhagic stroke, screening to almost all etiological and predisposing factors were negative apart from Hemophilia or presence of antiphospholipid antibodies which prolonged APTT which was due to Factor XII (Hageman we have ruled out in this patient. Patient had no history factor) deficiency. warfarin intake or other anticoagulation drugs, so the diagnosis was challenging.Our case is an example of the Index Terms— Factor XII deficiency, Hageman factor, thrombophilia tendency to those who have factor XII Prolonged APTT, Stroke.
    [Show full text]
  • (Hageman Factor) Deficiency: a Very Rare Coagulation Disorder
    Open Journal of Blood Diseases, 2015, 5, 39-42 Published Online December 2015 in SciRes. http://www.scirp.org/journal/ojbd http://dx.doi.org/10.4236/ojbd.2015.54006 Factor XII (Hageman Factor) Deficiency: A Very Rare Coagulation Disorder Mohammad Arphan Azaad, Qiurong Zhang*, Yongping Li Department of Clinical Medical College, Dali University, Dali, Yunnan, China Email: *[email protected], [email protected] Received 14 September 2015; accepted 20 October 2015; published 23 October 2015 Copyright © 2015 by authors and Scientific Research Publishing Inc. This work is licensed under the Creative Commons Attribution International License (CC BY). http://creativecommons.org/licenses/by/4.0/ Abstract Background: Factor XII (Hageman Factor) is the initiating factor for the Intrinsic Pathway of Coa- gulation. Very low levels of Factor XII have been associated with increased levels of activated Par- tial Thromboplastin Time (aPTT). Association of Factor XII deficiency is more with thromboem- bolic disorders rather than bleeding tendencies. Aim: To learn more about the relationship of fac- tor XII (Hageman Factor) deficiency and high levels of activated Partial Thromboplastin Time. Case Presentation: The Patient was admitted with complains of recurrent headaches and loin pain. Patient was incidentally found to have prolonged activated Partial Thromboplastin Time. This led to investigations which ultimately provided the evidence of severely low levels of Hageman Factor. Conclusion: Hageman Factor deficiency causes prolonged activated Partial Thromboplastin Time. However, most of the patients are asymptomatic for many years despite Hageman Factor defi- ciency. Keywords Factor XII Deficiency, Prolonged aPTT (Activated Partial Thromboplastin Time) 1. Introduction Factor XII, also called Hageman factor, is an enzyme initiating the coagulation cascade.
    [Show full text]
  • Anticoagulant Drugs
    California CATHOLIC MEDICAL CENjTS* ENTRAL MEDICAL LIBRARY Medicine 88-2I5153rd STREET N~WYORK .11I432q Blood Coagulation and the Coumarin Anticoagulant Drugs PAUL M. AGGELER, M.D., San Francisco DR. LESLIE L. BENNETT*: Ladies and gentlemen, ing with clotting mechanisms, which appeared in it gives me unusual pleasure to introduce Dr. Paul 1938. Early recognizing the importance of the M. Aggeler as Faculty Research Lecturer from the work of Dam and Almquist on the bleeding dia- San Francisco Division of the Academic Senate thesis of vitamin K-deficient chicks and the prob- for 1966. There is no higher honor that the fac- able significance for human disease of the observa- ulty can bestow upon one of its colleagues than to tion of Greaves and Schmidt of the effectiveness select him to represent publicly the faculty's com- of vitamin K in controlling the bleeding of rats with mon urge toward creativity which primarily mani- biliary fistulas, he began in the late 1930's his in- fests itself in our scientific setting as research. vestigation of the role of vitamin K in controlling Dr. Aggeler is uniquely a Californian. He is one prothrombin levels in patients with jaundice and of those rare individuals, a native son. His birth hepatic disease. This is the first of his classic works occurred in Ferndale among the redwoods of Hum- referred to in the citation of the Research Com- boldt County. After attending St. Ignatius High mittee. School in San Francisco, he enrolled as a pre- In this year, 1966, when there is increased medical student at the University of California awareness of the ethical responsibilities of physi- in Berkeley in 1929 and received the M.D.
    [Show full text]
  • Thrombosis and Haemostasis Research
    ©2007 Schattauer GmbH,Stuttgart AnniversaryIssueContribution Thrombosis and haemostasis research: 1957–2007) Stimulating, hardwork andfun y( Margareta Blombäck Department of Molecular Medicine and Surgery, Karolinska Institutet, Karolinska University Hospital,Stockholm, Sweden Anniversar odoresearch is to be inquisitive,tobeprepared to setout The first attemptatclinical useoffraction I-0 prepared from th in unexpected directions in response to newfindings –be humanplasma wasmade on apatient with acquired fibrinogen 50 T theynegativeorpositive. Research is likeanincurable in- deficiency; however, the patient went into averysevere fibrino- fectious disease –once you’ve got it, you’ve got it for life. A lytic state.Welater understood thatpyrogens cangiverise to fi- negative result or aresultthat contradicts what youpreviously brinolysis (wehad,for the preparation, used waterwhich wasnot believedoften leads to newideasand inventions.Research also pyrogen free).Weknew, however, thatCohn’sfraction Icon- givesyou friends all over the world, both collaboratorsand com- tained an antihaemophilic component, so working with Inga petitors. BelowImention just some colleagues with whom we Marie Nilsson from Malmö, we testedfraction I-0 for the pres- performed the basic and clinicalresearch,but rest assured: Ihave ence of factor VIII (FVIII). Thefirst sample testedgaveavery not forgotten anyone. high yield. Later it wasfound out that we had used haemophilia Bplasma in testing the activity of this sample.Wehad notyet characterized Stockholm’shaemophiliacs in termsofhaemophi- 1950s: Fibrinogen, factorVIII, vonWillebrand lia Aand B. However, it did indeed have 100% yield of the FVIII factor(VWF) activity of the original plasma when testedproperly. Dr.IkuoYamashina (3),watching me and Inga Marie sitting After afew years studying literatureand socialwork, respect- on eitherside of awaterbathtilting tubestostudy clot formation, ively, BirgerBlombäck and I, then24years old, started studying said “Maybe or maybe not”.
    [Show full text]
  • Scott Hamilton Goodnight, Jr., M.D
    OREGON HEALTH & SCIENCE UNIVERSITY ORAL HISTORY PROGRAM INTERVIEW WITH Scott Hamilton Goodnight, Jr., M.D. Interview conducted October 9, 2015 by Grover C. Bagby, M.D. 2016 Oregon Health & Science University Narrator: Dr. Scott Goodnight Interviewer: Dr. Grover Bagby Date: October 9, 2015 Transcribed by: Teresa Bergen [Begin Track One.] Grover Bagby: My name’s Grover Bagby and I’m interviewing Dr. Scott Goodnight for the OHSU Oral History Program. It’s October the ninth, 2015, and we are in the Biomedical Information and Communications Center Building at OHSU. Thanks for coming in from Hood River to tell us about the history of OHSU. Scott Goodnight: Looking forward to it, Grover. Bagby: You are one of the faculty members that I knew that actually was raised in this town. Can you tell us a little bit about your early childhood and how it all started? Goodnight: Yeah, well, I guess it started with my father moving here from Wisconsin. He went to medical school at the University of Wisconsin, where his father was the dean of men. And after two years of medical school here with his father sort of the spreading tree, he was a very powerful guy, and he [my dad] decided to escape and to come to Portland to the University of Oregon Medical School for his two clinical years. So he arrived here in about 1930 with my mother. And went into, first, he had several fellowships in pediatrics. And he ended up joining up with Bill Bilderback who was the first chair of pediatrics here, I believe, at the medical school.
    [Show full text]
  • 1 Tuesday, 3 May 2011
    1 Tuesday, 3 May 2011 2 (9.30 am) 3 THE CHAIRMAN: Professor, we are treating your affirmation 4 of the last time as simply continuing. So we won't 5 repeat that. Forgive me just a second, Ms Dunlop. 6 Right. 7 PROFESSOR CHRISTOPHER LUDLAM (continued) 8 Questions by MS DUNLOP (continued) 9 MS DUNLOP: This morning Professor Christopher Ludlam has 10 rejoined us to give his evidence on topic B2 and, 11 professor, we need to start by looking at your CV and 12 your publications because, as I said last time, you were 13 just here to talk about some statistics and we would 14 defer looking at your professional background until May. 15 So that's why we need to do that today. 16 Firstly, your CV, which is PEN0020650. From that, 17 Professor Ludlam, if we go to the first page in, we can 18 see you have been professor of haematology and 19 coagulation medicine at Edinburgh University from 1999 20 and other appointments in haematology, including that 21 you have been the director of the haemophilia centre in 22 Edinburgh since 1980 and you are also an honorary 23 consultant to the Blood Transfusion Service, and that's 24 since 1987. 25 You are a graduate of Edinburgh University, having 1 1 done your medical degree there between 1965 and 1971. 2 We see you won a number of awards as a student. 3 Then if we move to the next page, you also did a BSc 4 in biochemistry. Is that one of those arrangements 5 where you can do a BSc as you move through your medical 6 degree by taking a year out? 7 A.
    [Show full text]
  • Fathers of Modern Coagulation
    ©2007 Schattauer GmbH,Stuttgart AnniversaryIssueContribution Fathersofmoderncoagulation Dougald M. Monroe,MaureaneHoffman, Harold R. Roberts 1957–2007) Division of Hematology/Oncology,Department Medicine,University of North Carolina, Chapel Hill, North Carolinaand DurhamVA Medical y( Center and Duke University,Durham, North Carolina, USA he best contribution we could make for the 50th anniver- The legend of Figure 2gives the namesofthose whowere pres- sary of Thrombosis and Haemostasis,the former official ent at the meeting. Some members, namely, GwynneMacfarl- Anniversar T journalofthe InternationalSociety on Thrombosis and ane, RosemaryBiggs,Oscar Ratnoff,and Paul Aggeler were ap- th Haemostasis (ISTH), wastorecount the history of some of the parently absent fromthe meeting, buttheir influencewas felt. 50 people whoopenedthe door to major advances in coagulation re- While allofthe membersofthe Committee in Figure 2are shown search.Manyofthese people were among the first to contribute withsmilesontheir faces,the discussions leading to decisions articlestothe Journal whichwas initiallynamed Thrombosiset on nomenclature were often heated and forceful (4). DiathesisHaemorrhagica. Most of the menshown in Figure 2are legendary for their The storybegins in the early1950s shortlyafter the end of the contributionstothe fieldofcoagulation. H. Jensen(#1), who secondWorld War. In the late 1940s throughthe 1950s, scientists worked at the US Army Research Labs, studiedthe proteasesin from several nations made major breakthroughsinour under- coagulation looking at the balancebetween proteolytic action standing of the mechanism of coagulation. This waslargelydue (thrombin generation and fibrinolysis) and anti-proteolytic ac- to the discovery of several newclotting factors. In 1945 the tion. WalterSeegers(#2) had isolatedprothrombin and had dis- major clotting theoryrestedonthat of Morawitz as shown in Fig- covered several other vitamin-K-dependent factorsinhis pro- ure 1(1).
    [Show full text]