rdf-syntax-grammar
mods:
  schema location: http://www.loc.gov/mods/v3 http://www.loc.gov/standards/mods/v3/mods-3-2.xsd
  title info:
    non sort: The
    title: hemostatic defect accompanying aflatoxin B₁ intoxication in rabbits
  name:
    name part: Baker, Dale Christopher.
    role:
      role term: creator
  name:
    name part: Corrier, D. E.
    role:
      role term: degree committee member.
  name:
    name part: Green, R. A.
    role:
      role term: degree supervisor.
  name:
    name part: Hightower, D.
    role:
      role term: degree committee member.
  name:
    name part: Pierce, K. R.
    role:
      role term: degree committee member.
  name:
    name part: Texas A & M University
    role:
      role term: degree granting institution.
  type of resource: text
  genre: bibliography
  genre: Academic theses
  origin info:
    place:
      place term: xx
    date issued: 1984
    issuance: monographic
  language:
    language term: eng
  physical description:
    form: print
    extent: x, 129 leaves : illustrations ; 29 cm
  abstract: The hemostatic defect accompanying chronic aflatoxin B(,1) (AFB(,1)) intoxication was evaluated in 3 groups of 6 New Zealand white rabbits. Group A rabbits served as controls, while group B and C rabbits received daily intraperitoneal injections of AFB(,1) at dose rates of 0.06 and 0.09 mg/kg respectively. Rabbits treated with AFB(,1) became progressively depressed and developed hepatotoxicity over the 14 day study period. Hemostatic defects became apparent in AFB(,1) treated rabbits shorty before death. Hemorrhage was evident in necropsy in 1 rabbit receiving AFB(,1), and thrombi were evident histologically in this rabbit and an additional AFB(,1) treated rabbit. The hemostatic defect was characterized by prolongation of activated partial thromboplastin time and prothrombin time with significant reduction in factor V, VII, and VIII activities and factor I concentration. Changes in fibrinogen degradation products, fibrin monomer or platelet count levels were not significant; however, platelet aggregation was impaired in AFB(,1) treated rabbits shortly before death. Significant correlation between albumin concentration and factor I, V, and VIII activities in AFB(,1) treated rabbits suggested that hepatic protein synthesis was impaired. In a similarly designed study, no significant differences between AFB(,1) treated and control rabbits were found with respect to specific incorporation of tritium-labeled amino acids into total serum proteins, fibrinogen, or platelet protein. Also, no significant alterations in fibrinogen half-life were found between groups. The pathogenesis of the hemostatic defect accompanying aflatoxicosis in rabbits was not clearly defined. Fibrinolysis was not evident nor was vitamin K antagonism important in the development of the hemostatic defect. Likewise, disseminated intravascular coagulation only occurred in 1 rabbit and was considered to be a result of acute hepatocellular necrosis. In the remaining AFB(,1) treated rabbits, DIC did not app…
  note: "Major subject: Veterinary Pathology."
  note: Typescript (photocopy).
  note: Vita.
  note: Ph. D. in Philosophy Texas A & M University 1984
  note: Includes bibliographical references (leaves 99-111).
  subject:
    topic: Aflatoxins
  subject:
    topic: Veterinary Pathology
  identifier: http://proxy.library.tamu.edu/login
  identifier: https://hdl.handle.net/1969.1/DISSERTATIONS-778300
  related item:
    location:
      url: http://proxy.library.tamu.edu/login
  related item:
    location:
      url: https://hdl.handle.net/1969.1/DISSERTATIONS-778300
  record info:
    record content source: TXA
    record creation date: 860816
    record change date: 20220104090510.0
    record identifier: in00000764203
    language of cataloging:
      language term: eng