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Träfflista för sökning "WFRF:(Wells G) srt2:(1991-1994)"

Sökning: WFRF:(Wells G) > (1991-1994)

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1.
  • Tufveson, G, et al. (författare)
  • Hyaluronic acid accumulation; the mechanism behind graft rejection edema.
  • 1992
  • Ingår i: Transplant International. - 0934-0874 .- 1432-2277. ; 5 Suppl 1, s. S688-9
  • Tidskriftsartikel (refereegranskat)abstract
    • Hyaluronic acid (HA) is an important stabilizing consistuent of the loose connective tissue and regulates water homeostasis. Thus, excessive accumulation of HA in interstitial tissue immobilizes water and may thereby contribute to interstitial tissue edema. By the use of biotin labelled core protein and an avidin-enzyme system, we visualized HA in grafted rat kidney, rat heart, rat small bowel and also in human kidneys. By an extraction procedure the tissue amounts of HA were measured in the experimental grafts. Simple techniques for measuring water content were also employed. The extracellular amounts of HA increased between 100% and 350% in rejecting tissues as compared to syngeneic controls. The relative water content also increased and correlated well with the HA accumulation. The clinical value of these experimental observations was confirmed in human transplantation where rejecting kidney allografts demonstrated a highly significant increase in HA staining in the interstitium as compared to non-rejecting biopsy specimens. We therefore concluded that transplantation edema--a key features of graft rejection--is regulated by the accumulation of HA not only under experimental conditions but also in the clinical setting.
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2.
  • Wanders, A., et al. (författare)
  • Expression of an interferon-gamma-like substance in normal and transplanted rat heart tissue
  • 1992
  • Ingår i: J Heart Lung Transplant. ; 11:1 Pt 1, s. 142-6
  • Tidskriftsartikel (refereegranskat)abstract
    • The presence of interferon-gamma-like molecules has been reported not only in lymphocytes, but also in certain nerve cells and in normal skeletal muscle. We have studied the reactivity of the anti-interferon-gamma monoclonal antibody DB1 with frozen sections of normal and transplanted rat hearts. Cardiac grafts from PVG donor rats were transplanted to syngeneic PVG recipients or allogeneic Wistar/Kyoto recipient rats with the use of an accessory cervical heart transplantation technique. The allogeneic heart transplants were harvested 4 days and the syngeneic grafts 4 weeks after transplantation. In normal hearts there was a weak but distinct reactivity with the anti-interferon-gamma antibody in most muscle cells. In addition, some lymphocytes and the Purkinje fibers were positive. Hearts transplanted over an allogeneic barrier revealed that staining for interferon-gamma on muscle cells was substantially increased whereas no or only a moderate increase in the anti-interferon-gamma staining was seen in hearts transplanted to syngeneic recipients. These data indicate that interferon-gamma present in rat myocyte may be involved in the pathophysiology of graft rejection and also suggest that interferon-gamma may be of importance for the function of normal rat heart muscle cells.
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