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: pathophysiology of the hemolytic uremic syndrome using in vitro and in vivo models of Shiga toxin mediated renal damage
    sub title: a dissertation
  name:
    name part: Lentz, Erin K.
    role:
      role term: creator
  type of resource: text
  genre: bibliography
  origin info:
    place:
      place term: txu
    date issued: 2011
    issuance: monographic
  language:
    language term: eng
  physical description:
    form: print
    extent: x, 123 leaves : illustrations (some color) ; 28 cm.
  abstract: ABSTRACT: Shiga toxins (Stxs) are expressed by the enteric pathogens Shigella dysenteriae 1 and enterohemorrhagic Escherichia coli (EHEC). Stx-producing organisms cause bloody diarrhea with the potential to progress to acute renal failure. Stxs are potent protein synthesis inhibitors and are believed to be largely responsible for the renal damage seen in post diarrheal hemolytic uremic syndrome (D+HUS). Mice have been extensively employed as an animal model of renal damage caused by Shiga toxins. In this study, we examined the role of the proinflammatory cytokine tumor necrosis factor-[alpha] (TNF-[alpha]) in development of toxin-mediated renal disease in mice. Mice pre-treated with TNF-[alpha] adminstration and challenged with Shiga toxintype 1 (Stx1) showed increased survival compared to mice treated with Stx1 alone. Conversely, mice treated with Stx1 before TNF-[alpha] administration succumbed quicker than mice given Stx1 alone. Increased lethality in mice treated with Stx1 followed by TNF-[alpha] was associated with evidence of glomerular damage and loss of renal function. No differences in renal histopathology were noted between animals treated with Stx1 alone versus the TNF-[alpha] pre-treatment group, although we noted a sparing of renal function when TNF-[alpha] was administered before toxin. Compared to treatment with Stx1 alone, treatment with TNF-[alpha] after toxin altered the renal cytokine profile so that expression of proinflammatory cytokines TNF-[alpha] and Interluekin-1 beta (IL-1[beta]) increased, and expression of the anti-inflammatory cytokine Interleukin-10 (IL-10) decreased. Increased lethality in mice treated with Stx1 followed by TNF-[alpha] was associated with higher numbers of Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL)-positive renal tubule cells suggesting that increased lethality involved enhanced apoptosis. These data suggest that the early administration of TNF-[alpha] may be a candidate interventional strateg…
  note: by Erin K. Lentz.
  note: Vita.
  note: "Major Subject: Medical Sciences".
  note: "Submitted to the Office of Research and Graduate Studies at Texas A&M Health Science Center in partial fulfillment of the requirements for the degree of Doctor of Philosophy May 2011."
  note: Approved as to style and content by: Vernon L. Tesh, Alan Parrish, Jon Skare, Helene Andrews-Polymenis, James E. Samuel.
  note: Ph. D. Texas A&M University System Health Science Center 2011.
  note: Includes bibliographical references (leaves 102-121).
  subject:
    topic: Shiga Toxins
    topic: adverse effects
  subject:
    topic: Hemolytic-Uremic Syndrome
  subject:
    topic: Major Medical Sciences
  record info:
    record content source: TMV
    record creation date: 110502
    record change date: 20191204153908.0
    record identifier: in00004515372