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Addition of Epidermal Growth Factor Improves the Rate of Sulfur Mustard Wound Healing in an In Vitro Model

, PhD, , LATg certified, , PhD, , PhD

Eplasty

Open Science Company, LLC

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      Abstract

      Objective: Sulfur mustard (SM) causes blisters on the human skin. These blisters delay healing of the skin and make the victims more susceptible to infection. In vitro models have been used for protection studies against SM injury, but study on wound healing after SM exposure has not been explored. The purpose of this study was to test whether the addition of exogenous growth factors could improve the rate of SM wound healing. Methods: The model consisted of normal human epidermal keratinocytes seeded into 6-well plates, exposed to SM, and wounded (disruption of the cell monolayer) with a sterile wounding instrument. Cells were then stained and images were captured to measure percentage wound fill. Epidermal growth factor (EGF) and keratinocyte growth factor (KGF) were tested in this model. Results: EGF (1 ng/mL) significantly increased wound fill on all of the days tested (days 6, 9, and 12). KGF did not significantly improve wound healing. Conclusions: EGF showed promise as a potential therapy for SM-induced wounds. This in vitro model was a valuable tool for screening therapeutics before animal testing. These results will be used to develop a dressing that can slowly release EGF on to a debrided wound bed to help speed the healing process.

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      Most cited references 66

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      Wound healing--aiming for perfect skin regeneration.

       Tamara Martin (1997)
      The healing of an adult skin wound is a complex process requiring the collaborative efforts of many different tissues and cell lineages. The behavior of each of the contributing cell types during the phases of proliferation, migration, matrix synthesis, and contraction, as well as the growth factor and matrix signals present at a wound site, are now roughly understood. Details of how these signals control wound cell activities are beginning to emerge, and studies of healing in embryos have begun to show how the normal adult repair process might be readjusted to make it less like patching up and more like regeneration.
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        Perspectives on cancer therapy-induced mucosal injury: pathogenesis, measurement, epidemiology, and consequences for patients.

        A frequent complication of anticancer treatment, oral and gastrointestinal (GI) mucositis, threatens the effectiveness of therapy because it leads to dose reductions, increases healthcare costs, and impairs patients' quality of life. The Multinational Association of Supportive Care in Cancer and the International Society for Oral Oncology assembled an international multidisciplinary panel of experts to create clinical practice guidelines for the prevention, evaluation, and treatment of mucositis. The panelists examined medical literature published from January 1966 through May 2002, presented their findings at two separate conferences, and then created a writing committee that produced two articles: the current study and another that codifies the clinical implications of the panel's findings in practice guidelines. New evidence supports the view that oral mucositis is a complex process involving all the tissues and cellular elements of the mucosa. Other findings suggest that some aspects of mucositis risk may be determined genetically. GI proapoptotic and antiapoptotic gene levels change along the GI tract, perhaps explaining differences in the frequency with which mucositis occurs at different sites. Studies of mucositis incidence in clinical trials by quality and using meta-analysis techniques produced estimates of incidence that are presented herein for what to our knowledge may be a broader range of cancers than ever presented before. Understanding the pathobiology of mucositis, its incidence, and scoring are essential for progress in research and care directed at this common side-effect of anticancer therapies. Copyright 2004 American Cancer Society.
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          Updated clinical practice guidelines for the prevention and treatment of mucositis.

          Considerable progress in research and clinical application has been made since the original guidelines for managing mucositis in cancer patients were published in 2004, and the first active drug for the prevention and treatment of this condition has been approved by the United States Food and Drug Administration and other regulatory agencies in Europe and Australia. These changes necessitate an updated review of the literature and guidelines. Panel members reviewed the biomedical literature on mucositis published in English between January 2002 and May 2005 and reached a consensus based on the criteria of the American Society of Clinical Oncology. Changes in the guidelines included recommendations for the use of palifermin for oral mucositis associated with stem cell transplantation, amifostine for radiation proctitis, and cryotherapy for mucositis associated with high-dose melphalan. Recommendations against specific practices were introduced: Systemic glutamine was not recommended for the prevention of gastrointestinal mucositis, and sucralfate and antimicrobial lozenges were not recommended for radiation-induced oral mucositis. Furthermore, new guidelines suggested that granulocyte-macrophage-colony stimulating factor mouthwashes not be used for oral mucositis prevention in the transplantation population. Advances in mucositis treatment and research have been complemented by an increased rate of publication on mucosal injury in cancer. However, additional and sustained efforts will be required to gain a fuller understanding of the pathobiology, impact on overall patient status, optimal therapeutic strategies, and improved educational programs for health professionals, patients, and caregivers. These efforts are likely to have significant clinical and economic impact on the treatment of cancer patients. Cancer 2007;109:820-31. (c) 2007 American Cancer Society.
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            Author and article information

            Affiliations
            Physiology and Immunology Branch, Research Division, US Army Medical Research Institute of Chemical Defense, Aberdeen Proving Ground, MD
            Department of Clinical Investigation, Dwight D. Eisenhower Army Medical Center, Fort Gordon, GA
            Medical Toxicology Branch, Analytical Toxicology Division, US Army Medical Research Institute of Chemical Defense, Aberdeen Proving Ground, MD
            Author notes
            Disclaimer: The opinions or assertions contained herein are the private views of the authors and are not to be construed as official or as reflecting the views of the US Army or the Department of Defense.
            Journal
            Eplasty
            ePlasty
            Eplasty
            Open Science Company, LLC
            1937-5719
            2008
            26 March 2008
            : 8
            2289780
            18438446
            16
            Copyright © 2008 The Author(s)

            This is an open-access article whereby the authors retain copyright of the work. The article is distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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            Surgery

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