Abstract
For 20 years a significant research component has been integrated into the clinical services provided for patients with chronic leg wounds at Fremantle Hospital. The development of a team of clinicians, nurses and scientists has enabled a broad range of clinical and laboratory wound research to be undertaken on human subjects, which is only possible in a small number of centres worldwide. The key areas of research focus have been chronic wound epidemiology, clinical investigations, exercise and venous disease, pathophysiology of venous leg ulceration and clinical trials. Research on the pathophysiology of venous leg ulceration has been facilitated by the development of a human model of non-healing and healing venous ulcers. More recently, a genetic approach has been used to identify key molecules in venous ulcer pathogenesis through the investigation of gene polymorphisms as risk factors for the development of venous leg ulceration.
Genetic studies and randomised control trials for chronic wound therapies require large numbers of subjects to provide adequate statistical power. Additional funding and leadership is required to increase the number of centres across Australia with the capacity to participate in multi-centre chronic wound studies, and to facilitate effective collaborations between hospital- and community-based wound care providers, research institutions and industry.

Abstract
The prevalence of diabetes is increasing worldwide and has been forecasted to double in the next 20 years. The major increase in morbidity and mortality of diabetes is due to the development of complications, including failure of the wound healing process. Foot ulcers occur in 25% of all patients with diabetes and failure of healing eventually leads to deep-seated infection and amputation. Impaired wound healing is therefore the pivotal event responsible for most of the morbidity (and mortality) of diabetic foot disease. Consequently, a detailed understanding of the wound healing process in diabetes and how it can be improved is of great importance. However, efforts to develop new therapies are hampered by a lack of knowledge of the molecular mechanisms responsible for the poor wound healing.
Our laboratory is examining the role of matrix metalloproteinases (MMPs) in this regard. These proteolytic enzymes are important in normal wound repair and have been shown to be abnormally expressed in diabetic wounds. Our studies focus on evaluating MMPs as both markers and mediators of impaired wound healing in diabetes. Information will lead to a better understanding of poor wound healing in diabetes and ultimately more optimal therapeutic interventions.

Abstract
Skin plays a key role in protecting the body from the onslaught of pathogens and toxins we meet during our lifetime; thus, out of necessity, we have developed a rapid repair mechanism that quickly plugs any holes in this vital organ. Upon injury, a series of highly coordinated overlapping events, that include inflammatory, proliferation and maturation phases, result in the hasty closure of the wound and restoration of skin integrity. Over the past decade it has become clear that a number of immune cells that regulate the inflammatory phase, whilst important for removal of invading pathogens, are not necessary for repair and in fact may be responsible for the subsequent scar formation that seems to have resulted from having such a rapid repair process. The magnitude and length of inflammation in the wound not only appears to dictate the extent of scar formation but also in some cases may even prevent wound closure. In this review we will explore the two sides of inflammation in wound healing and review current and future drug therapies that target inflammation to modulate the healing outcome.

Abstract
Hypertrophic scar formation is a serious medical problem involving an excess fibro-proliferative response; it is particularly observed in burns patients and patients with a variety of diseases including keloids and scleroderma. Type I collagen is the major form of collagen produced in response to wounding and is involved in cutaneous fibrosis and scar formation. A recently discovered function of the well known c-myb proto-oncogene, previously reported to be involved in regulating cell growth and development, is its ability to regulate type I collagen protein production. Previously we have shown that c-myb plays an important role in wound repair, by regulating collagen synthesis and cellular proliferation and migration. Here we examine the involvement of c-myb in different human wound and scar tissues. Human tissue collected from hypertrophic scars, keloid scars, acute wounds and chronic venous leg ulcers were immunostained for c-myb and collagen I.
Our results reveal a significant increase in c-myb protein levels in hypertrophic scars but not acute wounds, keloids or chronic ulcers. Interestingly, this increase in c-myb expression corresponded to the increased expression of collagen I in hypertrophic scars. These findings suggest that c-myb may be an important modulator of collagen synthesis in hypertrophic scar formation and may be important in wound fibrosis and scarring. Manipulation of c-myb levels may be of value in promoting improved wound healing and reducing scar formation.

Abstract
Chronic wounds have a significant effect on patient morbidity and also result in high cost to both affected individuals and the healthcare system. Several engineering approaches have been devised to combat chronic cutaneous wounds; these can be broadly divided into chemical, biological and physical wound management. This review discusses the various approaches, with an emphasis on physical wound management, in particular the application of electric fields to accelerate wound healing.