Comparison of Wound Closure after Burn and Cold Injury in Human Skin Equivalents

Abstract

Stern RS (2001) The risk of melanoma in association with long-term exposure to PUVA. The PUVA Follow-Up Study. J Am Acad Dermatol 44:755-61 Stern RS, Nichols KT, Va ¨keva ¨LH, for the PUVA Follow-up Study (1997) Malignant melanoma in patients treated for psoriasis with methoxsalen (psoralen) and ultraviolet A radiation (PUVA). N Engl J Med 336: 1041-5 Uribe P, Wistuba II, Gonzalez S (2003) BRAF mutation: a frequent event in benign, atypical, and malignant melanocytic lesions of the skin. Am J Dermatopathol 25: 365-70 Wolf P, Kreimer-Erlacher H, Seidl H, Bck B, Soyer HP, Kerl H (2004) The ultraviolet fingerprint dominates the mutational spectrum of the p53 and Ha-ras genes in psoralen+ultraviolet A keratoses from psoriasis patients.

Determination of Microcirculatory Changes and Angiogenesis in a Model of Frostbite Injury In Vivo

“…Currently used in vivo frostbite models act via physical contact to the cold device, which makes it impossible to distinguish between contact trauma and thermal injury [8,9,12,[18][19][20][21][22][23][24]. This presents a major drawback for studies on frostbite injuries.…”

“…This presents a major drawback for studies on frostbite injuries. Besides, all previously established frostbite models produced significantly larger lesions than required for this study and do not allow for intravital microscopy during wound healing [8,9,23].…”

“…In addition, hostile working environments, for example cold-storage depots, accidental misuse of medical cold devices [4], and an increasing tendency to extreme outdoor activities further boost the frequency of severe frostbite [2,5,6]. To date, little is understood of the pathophysiologic process underlying the resulting tissue damage in cold injuries, consequently rendering it impossible to provide more than symptomatic treatment [2,[7][8][9][10][11][12]. Only a few authors mention allegedly successful experimental treatments of cold injuries in small studies or case-reports [2,13].…”

Differential Response of Human Adipose Tissue-Derived Mesenchymal Stem Cells, Dermal Fibroblasts, and Keratinocytes to Burn Wound Exudates: Potential Role of Skin-Specific Chemokine CCL27

“…For full-thickness burn injury, a metal device attached to a Weller Ò soldering station (WSD 81Cooper Tools, Besigheim, Germany), heated continuously at 128°C, was applied for 10 s to the epidermis as previously described. 25 Unwounded skin was used as a control. The (damaged) skin samples were placed dermis side down on a transwell (0.4 mm pore size; Costar Corning Incorporated, Corning, NY) and cultured at the air-liquid interface as described earlier.…”

Intravital Pathophysiologic Comparison of Frostbite and Burn Injury in a Murine Model

“…Currently, the exact pathophysiologic process underlying the resulting tissue damage in frostbite injuries is not well understood [3,5,[7][8][9][10][11]. The treatment includes a rewarming in 38 to 42 C warm water, antiphlogistics and painkillers, local disinfection, and dry dressings [5,12].…”