varicose ulcer/protease

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Protease-modulating matrix treatments for healing venous leg ulcers.

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Venous leg ulcers (VLUs) are open skin wounds on the lower leg that occur because of poor blood flow in the veins of the leg; leg ulcers can last from weeks to years, and are both painful and costly. Prevalence in the UK is about 2.9 cases per 10,000 people. First-line treatment for VLUs is

Lower levels of PAI-2 may contribute to impaired healing in venous ulcers - a preliminary study.

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Plasminogen activators may potentially influence the wound healing processes of cell migration, matrix degradation and cellular adhesion in venous ulcers by their regulation of protease activity. The aim of this study was to assess the levels of plasminogen activators in venous ulcers and to gain

Venous ulcer fibroblasts compared with normal fibroblasts show differences in collagen but not fibronectin production under both normal and hypoxic conditions.

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Previous immunocytochemical analysis showed that the base of venous ulcers was deficient in fibronectin compared with surrounding "normal" dermis. Here, we investigate whether impaired synthetic ability of ulcer fibroblasts could underlie this observation. Ulcer fibroblasts, established in culture

Cytokine and protease levels in healing and non-healing chronic venous leg ulcers.

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Leg ulcers present a common and recurring problem in older people creating discomfort and distress for the patient and a great cost to the health care services. Cultured keratinocyte grafts have been used by many investigators to stimulate healing of chronic venous ulcers. It has been proposed that

Degradation of fibronectin and vitronectin in chronic wound fluid: analysis by cell blotting, immunoblotting, and cell adhesion assays.

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We used a combination of cell blotting, immunoblotting, and cell adhesion assays to analyze fibronectin and vitronectin in wound fluid from acute and chronic wounds. Acute wound fluid (e.g., suction blister fluid, mastectomy fluid) contained intact fibronectin and vitronectin as major cell adhesion

Which dressings reduce inflammation and improve venous leg ulcer healing.

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Chronic venous leg ulcers (VLU) affect around 1% of the adult population in the Western world. The impact of VLU is both social and economic, with significant expenditures on active venous ulcers to provide medical treatment and eventual healing. At the core of VLU is venous hypertension which

Matrix metalloproteinases and venous leg ulceration.

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Metalloproteinase-mediated proteolysis plays an important role during the phase of venous ulcer formation and wound repair. Venous ulcers manifest as a breakdown of the collagenous stromal tissue and are highly associated to chronic venous insufficiency. A major change in our understanding of the

[The non-healing wound].

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The most common chronic wounds are pressure ulcers, diabetic ulcers, arterial occlusive disease and venous ulcers. The therapeutic aim after appropriate diagnostic work-up is causal treatment. Pressure relief, revascularisation or compression head the list of potential measures. Apart from local

[Biotechnological production of acetylated thymosin beta4].

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Thymosin beta4 (43 aa) is a highly conserved acidic peptide which regulates actin polymerization in mammalian cells by sequestering globular actin. Thymosin beta4 is undergoing clinical trials as a drug for the treatment of venous stasis ulcers, corneal wounds and injuries, as well as acute

Up-regulation of elastase in acute wounds of healthy aged humans and chronic venous leg ulcers are associated with matrix degradation.

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Chronic wound healing states are often associated with aging, and despite the increased number of aged patients with nonhealing wounds, controversy still exists concerning the effects of age on wound repair. Our previous work showed that in both venous ulcers in humans and acute wounds in aged

Causes and effects of the chronic inflammation in venous leg ulcers.

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The pathogenesis of venous leg ulcers is multifactorial. In this review article new physiological, molecular and cellular abnormalities in venous ulcers related to the chronic inflammation are presented and discussed. Venous hypertension causes disturbed microcirculation and pathological changes of

Foam dressings for venous leg ulcers.

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BACKGROUND Venous leg ulcers are a common and recurring type of chronic or complex wound that are associated with considerable cost to patients and to healthcare providers. Primary wound contact dressings are usually applied beneath compression devices with the aim of aiding healing. Foam dressings

Multiplexed analysis of matrix metalloproteinases in leg ulcer tissue of patients with chronic venous insufficiency before and after compression therapy.

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Elevated matrix metalloproteinases (MMP) levels have been implicated in the pathogenesis of chronic venous insufficiency ulcers. Quantitative measurements of a broad range of MMP proteins in human tissue treated with compression bandaging have not been reported. The goal of this study was to

Heterologous fibrin sealant derived from snake venom: from bench to bedside - an overview.

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Hemostatic and adhesive agents date back to World War II, when homologous fibrin sealant came onto scene. Considering that infectious diseases can be transmitted via human blood, a new heterologous fibrin sealant was standardized in the 1990s. Its components were a serine protease (a thrombin-like

Effects of clinical isolates of Pseudomonas aeruginosa on Staphylococcus epidermidis biofilm formation.

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Pseudomonas aeruginosa is often found in chronic infections, including cystic fibrosis lung infections and those related to chronic wounds and venous ulcers. At the latter sites, P. aeruginosa can be isolated together with Staphylococcus epidermidis, and we have therefore explored the effect of

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