No abstract

Chronic wound pain is not well understood and the literature is limited. Six of 10 patients venous leg ulcer experience pain with their ulcer, and similar trends are observed for other chronic wounds. Chronic wound pain can lead to depression and the feeling of constant tiredness. Pain related to the wound should be handled as one of the main priorities in chronic wound management together with addressing the cause. Management of pain in chronic wounds depends on proper assessment, reporting and documenting patient experiences of pain. Assessment should be based on six critical dimensions of the pain experience: location, duration, intensity, quality, onset and impact on activities of daily living. Holistic management must be based on a safe and effective mix of psychosocial approaches together with local and systemic pain management. It is no longer acceptable to ignore or inadequately document persistent wound pain and not to develop a treatment and monitoring strategy to improve the lives of persons with chronic wounds. Unless wound pain is optimally managed, patient suffering and costs to health care systems will increase.

Persistent (chronic) wound-related pain is a common experience that requires appropriate assessment and treatment. It is no longer adequate for health care professionals to concentrate on the acute (temporary) pain during dressing change alone. The study provides useful recommendations and statements for assessing and managing total wound-related pain for patients, health care professionals and other policymakers. The recommendations have been developed with the involvement of an interprofessional panel of health care professionals from around the world.

No abstract

Human cellular retinoic acid-binding protein (CRABP) type I and type II were expressed in Escherichia coli from cloned cDNAs. Expressed proteins were purified by gel filtration and ion-exchange chromatography, resulting in highly pure proteins. The yield after gel filtration was approximately 50 mg/liter bacterial culture. In binding studies the equilibrium dissociation constant, Kd, of retinoic acid (RA) for E. coli-derived CRABP-I and CRABP-II was 6.8 and 39 nM, respectively. The Kd of the synthetic retinoid analog CD 367 was 2.2 nM for CRABP-I and 3.0 nM for CRABP-II. RA competed with the binding of CD 367 to CRABP-I and CRABP-II with IC50 values of 20.0 and 90.0 nM, respectively. Retinoid analogs competed with the binding of CD 367 to CRABP-I and CRABP-II in the following order: (p-[(E)-2-(5,6,7,8-tetrahydro-5,5,8,8- tetramethyl-2-naphtyl)-1-propenyl]-benzoic acid (TTNPB) > 4-oxo-RA > 4-OH-RA > 13-cis-RA = 9-cis-RA. m-carboxy-TTNPB and CD 271 were found not to compete with the binding of CD 367 to CRABP-I or CRABP-II even at 500-fold molar excess. These data demonstrate that E. coli-derived CRABP-I has a higher affinity for RA than CRABP-II and that retinoic acid metabolites have a lower affinity for these proteins. The observed difference in affinity for RA supports the idea that CRABP-I, which is constitutively expressed, and CRABP-II, which is induced by RA, have different functions in the cell. In addition, 9-cis-RA, a natural ligand for the retinoid X receptors, is not a physiological ligand for either CRABP-I or CRABP-II.