The medical literature describes numerous in vitro and in vivo wound-healing models. The selection of an animal model depends on a number of factors including availability, cost, ease of handling, investigator familiarity, and anatomical/functional similarity to humans. Small mammals are frequently used for wound healing studies, however, these mammals differ from humans in a number of anatomical and physiological ways. Anatomically and physiologically, pig skin is more similar to human skin. The many similarities between man and pig would lead one to believe that the pig should make an excellent animal model for human wound healing. The purpose of this paper is to review the existing literature for evidence of this supposition and determine how well the various models correlate to human wound healing. Studies of wound dressings, topical antimicrobials, and growth factors are examined. Over 180 articles were utilized for this comparative review. Our conclusion is that the porcine model is an excellent tool for the evaluation of therapeutic agents destined for use in human wounds.

Infliximab is a promising agent for the treatment of HS. These initial results suggest that infliximab is associated with objective and subjective improvement in HS. Further controlled studies of the efficacy of infliximab and its effect on the course of the disease are warranted.

Treatment with imiquimod 5% cream, capable of inducing interferon (IFN)-alpha, effectively cures basal cell carcinoma (BCC), both clinically and histologically. IFN-alpha induces expression of CD95-receptor (FasR) on BCC cells, which normally fail to express Fas receptor (FasR). Expression of the FasR is postulated to lead to apoptosis via CD95 receptor-CD95 ligand (FasL) interaction. Absence of this receptor may be responsible for the longevity of the cells of BCCs by preventing them undergoing 'suicidal' apoptosis, as well as apoptosis induced by neighbouring BCC cells and/or by infiltrating T-lymphocytes. We examined the expression of FasR on BCC after very short-term exposure to imiquimod 5% cream or vehicle. In a double-blind study, 10 patients with BCC applied either imiquimod (n = 5) or vehicle (n = 5) five times per week for up to 2 weeks. At the end of treatment, the treated area was excised and examined for the presence or absence of FasR by immunoperoxidase staining of rat antihuman FasR with haematoxylin and eosin counterstaining. Histologically, BCC cells were present in all (5/5) of the vehicle-treated BCCs and in 4/5 of the imiquimod-treated BCCs. BCC cells expressed FasR in 3/4 imiquimod-treated BCCs but in none (0/5) of the vehicle-treated tumours. T-lymphocytes apposed to BCC cells were evident in all three imiquimod-treated BCCs expressing FasR and in none of the FasR-negative, vehicle-treated BCCs. Imiquimod-induced FasR-mediated apoptosis may contribute to the effectiveness of imiquimod 5% cream for the treatment of BCC.

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Infliximab was well tolerated in most patients and the majority benefited from the use of infliximab.