This large-scale comparative real-life study shows that the silver foam dressing supports faster healing of delayed healing wounds.
Good nutritional status is essential for wound healing to take place. Ignoring nutritional status may compromise the patient's ability to heal and subsequently prolong the stages of wound healing. Glucose provides the body with its power source for wound healing and this give energy for angiogenesis and the deposition of new tissue. Therefore, it is vital that the body receives adequate amounts of glucose to provide additional energy for wound healing. Fatty acids are essential for cell structure and have an important role in the inflammatory process. Wound healing is dependent on good nutrition and the presence of suitable polyunsaturated fatty acids in the diet. Protein deficiency has been demonstrated to contribute to poor healing rates with reduced collagen formation and wound dehiscence. High exudate loss can result in a deficit of as much as 100g of protein in one day. This subsequently needs to be replaced with a high protein diet. Vitamins are also important in wound healing. Vitamin C deficiency contributes to fragile granulation tissue. There is a correlation between low serum albumin and body mass index (BMI) and the development of pressure ulcers. Also, low serum albumin and high Waterlow score have a positive association. The body automatically renews tissue while we are asleep but this does not mean that protein synthesis does not take place during our wakeful hours. Holistic assessment of nutrition and early detection of malnutrition are essential to promote effective wound healing.
1 GW274150 ([2-[(1-iminoethyl) amino]ethyl]-L-homocysteine) and GW273629 (3-[[2-[(1-iminoethyl) amino]ethyl]sulphonyl]-L-alanine) are potent, time-dependent, highly selective inhibitors of human inducible nitric oxide synthase (iNOS) vs endothelial NOS (eNOS) (4100-fold) or neuronal NOS (nNOS) (480-fold). GW274150 and GW273629 are arginine competitive, NADPH-dependent inhibitors of human iNOS with steady state K d values of o40 and o90 nM, respectively. 2 GW274150 and GW273629 inhibited intracellular iNOS in J774 cells in a time-dependent manner, reaching IC 50 values of 0.270.04 and 1.370.16 mM, respectively. They were also acutely selective in intact rat tissues: GW274150 was 4260-fold and 219-fold selective for iNOS against eNOS and nNOS, respectively, while GW273629 was 4150-fold and 365-fold selective for iNOS against eNOS and nNOS, respectively. 3 The pharmacokinetic profile of GW274150 was biphasic in healthy rats and mice with a terminal half-life of B6 h. That of GW273629 was also biphasic in rats, producing a terminal half-life of B3 h. In mice however, elimination of GW273629 appeared monophasic and more rapid (B10 min). Both compounds show a high oral bioavailability (490%) in rats and mice. 4 GW274150 was effective in inhibiting LPS-induced plasma NO x levels in mice with an ED 50 of 3.270.7 mg kg À1 after 14 h intraperitoneally (i.p.) and 3.871.5 mg kg À1 after 14 h when administered orally. GW273629 showed shorter-lived effects on plasma NO x and an ED 50 of 972 mg kg À1 after 2 h when administered i.p. 5 The effects of GW274150 and GW273629 in vivo were consistent with high selectivity for iNOS, as these inhibitors were of low potency against nNOS in the rat cerebellum and did not cause significant effects on blood pressure in instrumented mice.
Serum albumin may, in this patient group (in-patients over 64 years of age), be a useful predictor of pressure sore occurrence, though further work is needed to establish whether this is the case. Risk assessment of pressure sores can possibly be improved by adding serum albumin to one of the pre-existing tools such as the Waterlow score.
It has been proposed that lipoxygenases, specifically 15-lipoxygenase, may play an important role in promoting the oxidation of low-density lipoprotein (LDL) in the artery wall. It is well known that peroxides are unstable in the presence of transition metals, decomposing to form the alkoxy and peroxy radicals, and so initiating lipid peroxidation. To test whether lipoxygenase-derived peroxides may promote the oxidation of LDL in the presence of copper, the lipoprotein was enriched with lipid peroxides derived from the enzymic action of 5- and 15-lipoxygenases on either linoleic or arachidonic acid. All of these products were found to promote oxidation, whereas the related hydroxy fatty acids had no effect. This suggests that lipoxygenase-derived peroxides associated with the LDL particle may promote peroxidation in the presence of a suitable transition metal catalyst. This result has implications both for the mechanism of the potential pro-oxidant action of lipoxygenases in vivo and for the ex vivo assessment of the oxidizability of LDL samples isolated from different donors.
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