Zinc is an essential trace element in the human body and its importance in health and disease is appreciated. It serves as a cofactor in numerous transcription factors and enzyme systems including zinc-dependent matrix metalloproteinases that augment autodebridement and keratinocyte migration during wound repair. Zinc confers resistance to epithelial apoptosis through cytoprotection against reactive oxygen species and bacterial toxins possibly through antioxidant activity of the cysteine-rich metallothioneins. Zinc deficiency of hereditary or dietary cause can lead to pathological changes and delayed wound healing. Oral zinc supplementation may be beneficial in treating zinc-deficient leg ulcer patients, but its therapeutic place in surgical patients needs further clarification. Topical administration of zinc appears to be superior to oral therapy due to its action in reducing superinfections and necrotic material via enhanced local defense systems and collagenolytic activity, and the sustained release of zinc ions that stimulates epithelialization of wounds in normozincemic individuals. Zinc oxide in paste bandages (Unna boot) protects and soothes inflamed peri-ulcer skin. Zinc is transported through the skin from these formulations, although the systemic effects seem insignificant. We present here the first comprehensive account of zinc in wound management in relation to current concepts of wound bed preparation and the wound-healing cascade. This review article suggests that topical zinc therapy is underappreciated even though clinical evidence emphasizes its importance in autodebridement, anti-infective action, and promotion of epithelialization.

SF-12 and EQ-5D are suitable for exploring dimensions of health related quality of life in people with chronic venous leg ulceration. The responsiveness to healing of the Hyland questionnaire is unclear. We would recommend the use of generic instruments for the measurement of HRQoL in patients with venous leg ulcers.

The study compared the effect of a sustained silver-release foam dressing (Contreet Foam) with a foam dressing (Allevyn Hydrocellular) without added silver in critically colonised venous leg ulcers with delayed healing. The study was a multicentre, open, randomised, controlled study lasting for 4 weeks. Ulcer area and healing were assessed weekly. Odour, maceration, absorption capacity and leakage were evaluated at dressing changes. All adverse events were recorded. One hundred and twenty-nine patients were included (Contreet Foam: 65, Allevyn Hydrocellular: 64). The two groups were comparable in all respects. After 4 weeks, there was a significantly greater reduction in ulcer area in the Contreet Foam group (45%) than in the Allevyn Hydrocellular group (25%). After 1 and 4 weeks, odour was present in significantly less of the ulcers in the Contreet Foam group (17% and 19%, respectively) compared with the Allevyn Hydrocellular group (47% and 39%, respectively) and at the final visit there were significantly fewer leakages in the Contreet Foam group (19%) compared with the Allevyn Hydrocellular group (49%). Also, less maceration was observed after 1 and 4 weeks in the Contreet Foam group (34% and 37%, respectively) compared with the Allevyn Hydrocellular group (55% and 48%, respectively). The occurrence and cause of adverse events were equally distributed between the study groups. The present study provides evidence of the superior performance of the silver-releasing dressing, Contreet Foam, compared with a traditional moist foam wound healing dressing in the treatment of critically colonised, chronic venous leg ulcers. The results of this randomised, controlled study suggest an important role of sustained silver-releasing dressings in the treatment of critically colonised chronic wounds.

The aim of this analysis was to examine the cost-effectiveness of Contreet Foam (A) in comparison with three other commonly used venous leg ulcer treatment protocols: Aquacel Ag (B), Actisorb Silver (C) and Iodoflex (D). A health-economic analysis reflecting the UK treatment practice and cost structure was performed. The analysis was set up to assess the cost of relative wound area reduction over a 4-week treatment period. The model was validated by a UK expert panel consisting of four wound care specialists. To assure that the 4-week model had a realistic link to cost-effectiveness of complete wound healing, a Markov analysis was also performed. Sensitivity analyses were carried out to ensure validity. Protocol A and C proved to be the most effective treatments. The mean relative reduction in wound area after 4 weeks of treatment was 50.2% (protocol A), 23.9% (protocol B), 44.6% (protocol C) and 36.0% (protocol D). Cost-effectiveness ratios showed that protocol A proved to be the most cost-effective treatment, and protocol B the least. The cost per percentage reduction in wound area was 9.50 UK pounds for protocol A, compared to 16.50-17.60 UK pounds for the other treatment options. The cost-effectiveness of complete healing (Markov analysis) and sensitivity analyses confirmed these results. Using Contreet Foam instead of the other dressing alternatives may imply savings of 2.2-4.4 million UK pounds per year to the National Health Service.

The Escherichia coli ammonia channel protein, AmtB, is a homotrimeric polytopic inner membrane protein in which each subunit has 11 transmembrane helices. We have shown that the structural gene amtB encodes a preprotein with a signal peptide that is cleaved off to produce a topology with the N-terminus in the periplasm and the C-terminus in the cytoplasm. Deletion of the signal peptide coding region results in significantly lower levels of AmtB accumulation in the membrane but modification of the signal peptidase cleavage site, leading to aberrant cleavage, does not prevent trimer formation and does not inactivate the protein. The presence of a signal peptide is apparently not a conserved feature of all prokaryotic Amt proteins. Comparison of predicted AmtB sequences suggests that while Amt proteins in Gram-negative organisms utilize a signal peptide, the homologous proteins in Gram-positive organisms do not.