Please use this identifier to cite or link to this item:
Type: Thesis
Title: The influence of insulin-like growth factor 1 and its analogues on fibroblasts and dermal wound healing
Author: Marshall, Nicholas John.
Issue Date: 1998
School/Discipline: Dept. of Surgery
Abstract: Examines the levels of insulin-like growth factor and the presence of IGF binding proteins in human wound fluid. Tests the potency of IGF-1 and 2 analogues in in vitro models of fibroblast activity and their effect on healing in normal and diabetic rodent wounds. Shows that IGF-1, IGF-2 and their binding proteins are present in fluid from a partial thickness cutaneous wound; that the binding proteins negatively modulate the activity of insulin-like growth factors in vitro, but that the IGFs do not necessarily show enhanced activity in vivo at the wound site if binding protein affinity is decreased. Discusses possible roles of these binding proteins in wound repair.
Dissertation Note: Thesis (M.D.) -- University of Adelaide, Dept. of Surgery, 2001?
Subject: Somatomedin.
Wound healing Physiology.
Wounds and injuries Microbiology.
Insulin-like growth factor-binding proteins.
Description: Includes bibliography (leaves 191-219).
x, 219 leaves
Provenance: This electronic version is made publicly available by the University of Adelaide in accordance with its open access policy for student theses. Copyright in this thesis remains with the author. This thesis may incorporate third party material which has been used by the author pursuant to Fair Dealing exception. If you are the author of this thesis and do not wish it to be made publicly available or If you are the owner of any included third party copyright material you wish to be removed from this electronic version, please complete the take down form located at:
Appears in Collections:Research Theses

Files in This Item:
File Description SizeFormat 
01front.pdf49.35 kBAdobe PDFView/Open
02whole.pdf9.71 MBAdobe PDFView/Open

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.