Journal of Dermatological Science RSS feed: Current Issue. The Journal of Dermatological Science accepts online submissions only. EES is a web-based submission and review system. Authors may submit manuscripts and track their progress through the system to publication. Reviewers can download manuscripts and submit their opinions to the editor. Editors can manage the whole submission/review/revise/publish process. Please register at http://ees.elsevier.com/desc to submit a paper. JSID members - click here to register for free access to Journal of Dermatological Science online. The Journal of Dermatological Science publishes high quality peer-reviewed manuscripts covering the entire scope of dermatology, from molecular studies to clinical investigations. Laboratory and clinical studies which provide new information will be reviewed expeditiously and published in a timely manner. The Editor and his Editorial Board especially encourage the publication of research based on a process of bilateral feedback between the clinic and the laboratory, in which incompletely understood clinical phenomena are examined in the laboratory and the knowledge thus acquired is directly reapplied in the clinic. This continuous feedback will refine and expand our understanding of both clinical and scientific domains. Although the Journal is the official organ of the Japanese Society for Investigative Dermatology, it serves as an international forum for the work of all dermatological scientists. With an internationally renowned Editorial Board, the Journal maintains high scientific standards in the evaluation and publication of manuscripts. The Journal also publishes invited reviews, commentaries, meeting announcements and book reviews. Letters to the Editor reporting new results or even negative scientific data, if they contribute to advances in dermatology are encouraged. Letters to the Editor should be less than 1000 words with up to 2 figures or tables. For more information, please check the homepage of the Japanese Society for Investigative Dermatology. For membership information please contact: Masayuki Amagai, Secretary General of JSID, Department of Dermatology, Keio University School of Medicine 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582 Tel/Fax: +81-3-5363-3596 E-mail: office@jsid.org http://www.jdsjournal.com/?rss=yesElsevier Inc.en © 2012 Published by Elsevier Inc. All rights reserved. Journal of Dermatological Science0923-1811662May 2012 © 2012 Published by Elsevier Inc. All rights reserved. healthpermissions@elsevier.comhttp://www.jdsjournal.com/article/PIIS0923181112001107/abstract?rss=yesEditorial Board10.1016/S0923-1811(12)00110-7Journal of Dermatological Science 66, 2 (2012)2012-05-01Journal of Dermatological Science2012-05-01662S0923-1811(12)X0005-7iihttp://www.jdsjournal.com/article/PIIS0923181112001168/abstract?rss=yesThe Editor's Choice10.1016/S0923-1811(12)00116-8Journal of Dermatological Science 66, 2 (2012)2012-05-01Journal of Dermatological Science2012-05-01662S0923-1811(12)X0005-78788http://www.jdsjournal.com/article/PIIS0923181112000898/abstract?rss=yesAbstract: Complex diseases are caused by both genetic and environmental factors. Over decades, scientists endeavored to uncover the genetic myth of complex diseases by linkage and association studies. Since 2005, the genome-wide association study (GWAS) has been proved to be the most powerful and efficient study design thus far in identifying genetic variants that are associated with complex diseases. More than 230 complex diseases and traits have been investigated by this approach. In dermatology, 10 skin complex diseases have been investigated, a wealth of common susceptibility variants conferring risk for skin complex diseases have been discovered. These findings point to genes and/or loci involved in biological systems worth further investigating by using other methodologies. Certainly, as our understanding of the genetic etiology of skin complex diseases continues to mature, important opportunities will emerge for developing more effective diagnostic and clinical management tools for these diseases.Genome-wide association study of skin complex diseasesXuejun Zhang10.1016/j.jdermsci.2012.02.017Journal of Dermatological Science 66, 2 (2012)2012-04-05Journal of Dermatological Science2012-04-05662S0923-1811(12)X0005-7Invited review article8997http://www.jdsjournal.com/article/PIIS0923181112000618/abstract?rss=yesAbstract: Background: Diverse growth factors secreted from human adipocyte-derived stem cells (hASCs) that support or manage adjacent cells have been studied for therapeutic potentials to a variety of pathological models. However, senescent growth arrest in hASCs during in vitro culture and subsequent defective differentiation potential, have been technical barriers to further genetic modification of hASCs for functional improvement.Objective: We investigated the feasibility of long-term hASC culture to enhance their therapeutic use.Methods: We used a MYC variant to generate hASCs expressing v-myc and determined their growth potential and growth factor secretion profile. We further introduced an AKT variant to generate constitutively active (CA)-Akt/v-myc hASCs. Finally, we tested the ability of promoting wound healing of medium conditioned with CA-Akt/v-myc hASCs.Results: The v-myc hASCs actively proliferated longer than control hASCs. Increased secretion of vascular endothelial growth factor (VEGF) by v-myc hASCs promoted the migration potential of hASCs and vasculogenesis in co-cultured endothelial cells. Additional genetic modification of v-myc hASCs using CA-Akt further increased VEGF secretion. In addition, injection of CA-Akt/v-myc hASCs-CM into wound-mice model promoted wound healing compared to normal hASCs-CM.Conclusion: Genetic modification of hASCs to stimulate secretion of growth factors is a novel strategy to maximize their paracrine effect and improve their therapeutic potential.Genetic modification of human adipose-derived stem cells for promoting wound healingSeung-Hyun Song, Mi-Ok Lee, Ji-Seon Lee, Ho-Chang Jeong, Hyung-Gi Kim, Won-Serk Kim, Mina Hur, Hyuk-Jin Cha10.1016/j.jdermsci.2012.02.010Journal of Dermatological Science 66, 2 (2012)2012-04-03Journal of Dermatological Science2012-04-03662S0923-1811(12)X0005-7Regular articles98107http://www.jdsjournal.com/article/PIIS0923181112000606/abstract?rss=yesAbstract: Background: Induction of α6β4 integrin in the differentiated epidermal cell layers in skin is a hallmark of human cutaneous squamous cell carcinoma (SCC) pathogenesis and stimulates chemically induced SCC formation in Invα6β4 transgenic mice, which exhibit persistent expression of α6β4 in the suprabasal epidermal layers. However, the molecular basis for the support of SCC development by suprabasal α6β4 is not fully understood.Objective: We examined the relevance for suprabasal α6β4 expression in the epidermis for the recruitment of immunosuppressive leukocytes during the early stages of tumor promotion.Methods: In this study, we made use of the Invα6β4 transgenic mouse model, which exhibits expression of α6β4 integrin in the suprabasal layers of the epidermis driven by the involucrin promoter. First, we examined protein lysates from Invα6β4 transgenic skin using a pro-inflammatory cytokine array panel. Next, we immunofluorescence labeling of murine skin sections was employed to immunophenotype tumor promoter-treated Invα6β4 transgenic skin. Finally, a macrophage colony stimulating factor (M-CSF) neutralizing antibody strategy was administered to resolve Invα6β4 transgenic skin inflammation.Results: Employing the Invα6β4 transgenic mouse model, we show that suprabasal α6β4 integrin expression selectively alters the profile of secreted pro-inflammatory molecules by epidermal cells, in particular CXCL5 and M-CSF, in response to acute tumor promoter treatment. The induction of CXCL5 and M-CSF in Invα6β4 transgenic epidermis was shortly followed by an exacerbated influx of CD200R+ myeloid-derived suppressor cells (MDSCs), which co-expressed the M-CSF receptor, and FoxP3+ Treg cells compared to wild-type mice. As a result, the levels of activated CD4+ T lymphocytes were dramatically diminished in Invα6β4 transgenic compared to wild-type skin, whereas similar levels of lymphocyte activation were observed in the peripheral blood. Finally, 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced CD200R+ infiltrative cells and epidermal proliferation were suppressed in Invα6β4 mice treated with M-CSF neutralizing antibodies.Conclusions: We conclude that aberrant expression of α6β4 integrin in post-mitotic epidermal keratinocytes stimulates a pro-tumorigenic skin microenvironment by augmenting the influx of immunosuppressive granular cells during tumor promotion.Epidermal α6β4 integrin stimulates the influx of immunosuppressive cells during skin tumor promotionSamar W. Maalouf, Surein Theivakumar, David M. Owens10.1016/j.jdermsci.2012.02.009Journal of Dermatological Science 66, 2 (2012)2012-04-05Journal of Dermatological Science2012-04-05662S0923-1811(12)X0005-7Regular articles108118http://www.jdsjournal.com/article/PIIS0923181112000862/abstract?rss=yesGraphical abstract: The steroids tested modulated the mRNA expression for distinct enzymes involved in the lipid metabolism in female hamsters’ flank organs.Abstract: Background: The initial step of steroidal action on target cells is gene activation; therefore, the quantification of mRNA is a direct method for comparing the role of different steroids in the skin.Objective: This study demonstrated the role of several steroids on the mRNA expression encoding for different enzymes involved in the lipid metabolism in hamsters’ flank organs, which are a pilosebaceous complex.Methods: To determine the effect of treatments with testosterone (T) progesterone (P), levonorgestrel (LNG), 17α-p-chlorobenzoyloxy-6-chloropregn-4,6-diene-3,20-dione (5) and 17α-p-chlorobenzoyloxy-4,6-pregnadiene-3,20-dione (6); T and/or LNG; T and 5 or 6; P and/or 5 or 6 on the expression of mRNA encoding for lipid enzymes, the steroids were applied to the glands; later, the mRNAs expression for the enzymes was determined by PCR. The binding of 5 and 6 to the progesterone receptor (PR) was also evaluated.Results: Treatments with T, LNG, T+LNG, P, T+P, 5, T+5, T+6, P, P+5 and P+6 increased the mRNA expression for glycerol 3-phosphate acyl transferase (GPAT), β-hydroxy-β-methylglutaryl-CoA synthase (HMG-CoA-S), β-hydroxy-β-methylglutaryl-CoA reductase (HMG-CoA-R), phosphatidylinositol synthase as compared to the controls. However, squalene synthase was increased with all treatments except with T+5 and 6; 6 did not significantly increase the expression for GPAT or HMG-CoA-S, however it increased the concentration of HMG-CoA-R enzyme.5 and 6 bind to the PR, thus indicating that the effect of these steroids on the mRNA expression could be the result of their binding.Conclusion: The lipid metabolism is regulated by several steroids thought different mechanism of action, in flank organs.Molecular interactions of natural and synthetic steroids in female hamsters’ flank organsMarisa Cabeza, Barak Naranjo, Yvonne Heuze, Araceli Sánchez, Mercedes Hernández, Teresita Sainz, Eugene Bratoeff10.1016/j.jdermsci.2012.02.014Journal of Dermatological Science 66, 2 (2012)2012-04-05Journal of Dermatological Science2012-04-05662S0923-1811(12)X0005-7Regular articles119126http://www.jdsjournal.com/article/PIIS0923181112000874/abstract?rss=yesAbstract: Background: Statins represent a class of drugs that effectively lowers cholesterol, however they also possess pleiotropic effects, like promotion of angiogenesis, prevention of bone loss, immunomodulatory and anti-inflammatory effects.Objectives: Thus, the aim of this study was to investigate the activity of simvastatin topically applied in mice in acute and chronic skin inflammation models.Methods: Skin inflammation was induced in mice ears by topical application of 12-O-tetradecanoylphorbol acetate (TPA). In the acute model, ear oedema was measured by the increase of ear thickness 6h after TPA (2.5μg/ear). The chronic inflammatory process was induced by multiple applications of TPA (2.0μg/ear) for nine alternate days, and the oedema was measured daily as the increase in ear thickness.Results: Topical treatment was applied immediately after TPA in acute model or started at 5th day of chronic experiment. For acute model treatment was simvastatin (0.24, 0.71 and 2.40μM), dexamethasone (0.13μM), both in acetone or vehicle alone (acetone). In chronic model simvastatin (1% and 3%) and dexamethasone (0.5%) were incorporated in ointment preparations, and a group received ointment alone (vehicle). Samples of ear tissue (6mm) were taken from acute and chronic models, weighted and prepared for histological analysis and myeloperoxidase (MPO) enzymatic activity evaluation. Application of simvastatin in acetone reduced the ear oedema after a single TPA application in a dose dependent manner [ID50 of 0.47 (0.22–1.13) μM], and the MPO enzymatic activity up to 61±10%. Also, both simvastatin ointment preparations 1% and 3% reduced acute TPA-induced ear oedema in 55±7% and 65±8%, respectively. In the chronic model, simvastatin ointment 1% was able to reduce ear oedema (25±3%) and ear weight (10±1%), though 3% formulation augmented both parameters. Histological analysis revealed a reduction of swelling and leukocyte migration in the acute model for both the formulations of simvastatin (1% and 3%), while in chronic model simvastatin 1% decreased ear swelling and epidermal thickness, but simvastatin 3% increased both parameters.Conclusion: The results confirm the anti-inflammatory activity of simvastatin when applied topically in both acute and chronic models of skin inflammation. Besides, the formulation of simvastatin ointment 1% shows to be a very effective formulation for a chronic usage.Simvastatin ointment, a new treatment for skin inflammatory conditionsMarina Adami, Arthur da Silveira Prudente, Daniel Augusto Gasparin Bueno Mendes, Cintia Delai da Silva Horinouchi, Daniela Almeida Cabrini, Michel Fleith Otuki10.1016/j.jdermsci.2012.02.015Journal of Dermatological Science 66, 2 (2012)2012-03-28Journal of Dermatological Science2012-03-28662S0923-1811(12)X0005-7Regular articles127135http://www.jdsjournal.com/article/PIIS0923181112000539/abstract?rss=yesAbstract: Background: Dry skin causes pruritus and discomfort in patients with xerosis and atopic dermatitis. General treatment for skin dryness involves the topical application of an emollient. However, more effective, simpler therapies are desired. Collagen tripeptide (CTP) is a highly purified, non-antigenic, low-allergenic collagen fraction that is known to have various biological effects.Objective: To clarify the therapeutic effects of CTP for dry skin using acetone-induced dry skin model mice.Methods: ICR mice were treated with acetone followed by oral administration of CTP (80 or 500mg/kg/day) for 3 days. Hyaluronic acid production induced by CTP was assessed using human dermal fibroblasts in vitro and in an acetone-induced dry skin model mice in vivo. Transepidermal water loss (TEWL) and scratching behavior were evaluated. Furthermore, the effects of CTP on intraepidermal nerve fibers and expression of semaphorin 3A (Sema3A) and nerve growth factor (NGF) were examined by immunohistochemistry and quantitative RT-PCR.Results: CTP enhanced hyaluronic acid production in human dermal fibroblasts in vitro and in murine skin in vivo. Oral administration of CTP in acetone-induced dry skin model mice significantly decreased TEWL and suppressed scratching behavior. Intraepidermal nerve growth was dramatically inhibited in CTP-treated mice. Quantitative PCR analysis and immunohistochemical study revealed that CTP abolished the increased NGF and decreased Sema3A levels induced by acetone treatment.Conclusion: Oral administration of CTP improves dry skin and normalizes axon-guidance factors in the epidermis in addition to reducing pruritus. CTP may be used in a new therapeutic strategy against dry skin and pruritus.Oral administration of collagen tripeptide improves dryness and pruritus in the acetone-induced dry skin modelTomoko Okawa, Yukie Yamaguchi, Shinnosuke Takada, Yasuo Sakai, Noriaki Numata, Fumio Nakamura, Yoji Nagashima, Zenro Ikezawa, Michiko Aihara10.1016/j.jdermsci.2012.02.004Journal of Dermatological Science 66, 2 (2012)2012-03-14Journal of Dermatological Science2012-03-14662S0923-1811(12)X0005-7Regular articles136143http://www.jdsjournal.com/article/PIIS092318111200059X/abstract?rss=yesAbstract: Background: Trichophyton-induced superficial skin mycosis is a common infectious human disease, but the immunological mechanism against Trichophyton infection is unclear with regard to many points. Since Trichophyton cannot colonize mice, guinea pigs were used in previous experiments on Trichophyton infection. However, it is difficult to perform immunological and genetic analyses in guinea pigs.Objective: The objective of this study was to establish a mouse Trichophytin-associated inflammation model of superficial skin mycosis in which immunological and genetic analyses can be performed.Methods: We established a mouse Trichophyton-induced contact hypersensitivity model by applying Trichophytin, the Trichophyton antigen, extracted from Trichophyton mentagrophytes, to mice. Using a Th1-dominant strain, C57BL/6, and a Th2-dominant strain, BALB/c, we investigated the expression of inflammatory cytokines and receptors of the innate immune system for fungi, TLR4, TLR2, and dectin-1, and their influences on responses of the acquired immune system.Results: In C57BL/6 mice, expressions of IFN-γ and IL-17 A in regional lymph nodes and IL-1β, IFN-γ, IL-6, and IL-23 in the inflammatory auricular skin were enhanced by Trichophytin challenge, suggesting that not only Th1 cells but also Th17 cells were induced. In BALB/c mice, expressions of IL-4 in regional lymph nodes, and TSLP and IL-4 in the auricular skin were enhanced by Trichophytin challenge. Interestingly, dectin-1-neutralizing antibody inhibited the promotion of IFN-γ production in C57BL/6 mice, and dectin-1-expressing immune cells had crucial actions in Trichophyton-induced IFN-γ production.Conclusion: These results suggest that inflammatory mediators differently regulate Trichophytin-induced contact hypersensitivity on the basis of the status of host immunity.Analysis of Trichophyton antigen-induced contact hypersensitivity in mouseTomoya Nakamura, Akiko Nishibu, Mitsue Yasoshima, Chiaki Tanoue, Naoki Yoshida, Junko Hatta, Takayuki Miyamoto, Masahiro Nishii, Tsutomu Yanagibashi, Yoshinori Nagai, Kiyoshi Takatsu, Takashi Mochizuki, Kazuo Ogawa10.1016/j.jdermsci.2012.02.008Journal of Dermatological Science 66, 2 (2012)2012-03-29Journal of Dermatological Science2012-03-29662S0923-1811(12)X0005-7Regular articles144153http://www.jdsjournal.com/article/PIIS092318111200062X/abstract?rss=yesAbstract: Background: Atopic dermatitis (AD) shows dry skin. Water-soluble, low molecular weight components, collectively known as natural moisturizing factor (NMF), play an important role in maintaining the stratum corneum (SC) hydration. Previous studies focused on reduced levels of free amino acids (FAAs) in NMF from AD skin. It remains unknown, however, whether other NMF components are also altered in AD.Objective: To characterize the levels of various NMF components in the SC of healthy subjects and in mild AD adult patients.Methods: NMF components were extracted from three sequential tape-stripped SC samples obtained from the volar forearm. NMF components which were decreased in AD skin were topically applied to examine their contribution to SC moisturization in AD skin.Results: We found that although FAAs levels were not remarkably reduced, levels of pyrrolidone carboxylic acid (PCA), lactate, urea, sodium and potassium were significantly decreased in NMF from mild AD skin. Among those components, only the topical application of potassium lactate effectively increased skin surface hydration indicating that reductions of lactate and potassium influence dry skin in mild AD patients. Unlike the distribution of filaggrin-derived FAAs and PCA, lactate, urea, potassium and sodium were abundant in the surface layer of the SC compared with the inner layer of the SC. Such findings strongly suggest that those components are supplied from outside the SC, i.e. they originate from sweat.Conclusion: The reduced levels of sweat-derived NMF components in mild AD patients suggests that impaired sweat function might in part result in the SC dryness.Decreased lactate and potassium levels in natural moisturizing factor from the stratum corneum of mild atopic dermatitis patients are involved with the reduced hydration stateTomoko Sugawara, Katsuko Kikuchi, Hachiro Tagami, Sestuya Aiba, Shingo Sakai10.1016/j.jdermsci.2012.02.011Journal of Dermatological Science 66, 2 (2012)2012-04-05Journal of Dermatological Science2012-04-05662S0923-1811(12)X0005-7Regular articles154159http://www.jdsjournal.com/article/PIIS0923181112000060/abstract?rss=yesThe repigmentation of adult skin after wound healing, or loss of melanocytes (e.g. vitiligo), poses a particular and unique challenge to the invading population of melanocytes. The melanocytes, or their precursors, resident in adjacent skin or in nearby niches, must be activated to proliferate, and then negotiate their way through a tightly held epidermal barrier. The mechanisms whereby melanocytes negotiate their way through the epidermis to achieve this repigmentation have not been described in any detail and may occur trans-epidermally, and/or along the basement membrane and/or in the dermis. While there have been many studies on migratory cells during embryonic development and in particular physiological processes , these situations differ from the adult skin epidermal environment. To migrate through the tight spaces between keratinocytes, either junctions must be broken and spaces thus created, or alternatively, quite extreme cellular contortions would need to occur to allow the cell to move through the narrow paracellular spaces. Further knowledge of these processes will certainly contribute towards elucidating the mechanisms of repigmentation in pigmentary disorders.Migration of human melanocytes into keratinocyte monolayers in vitroDheshnie Keswell, Lester M. Davids, Susan H. Kidson10.1016/j.jdermsci.2012.01.005Journal of Dermatological Science 66, 2 (2012)2012-02-06Journal of Dermatological Science2012-02-06662S0923-1811(12)X0005-7Letters to the Editor160163http://www.jdsjournal.com/article/PIIS0923181112000308/abstract?rss=yesDickkopf1 (DKK1), which is secreted by fibroblasts is an inhibitor of the Wnt signaling . Recently, it has been reported that DKK1 is highly expressed in palmoplantar fibroblasts at the mRNA and protein levels and is responsible for thickened and hypopigmented palmoplantar epidermis . DKK1 inhibits the function and proliferation of melanocytes by suppressing the Wnt/beta-catenin/Microphthalmia-associated transcription factor (MITF)-signaling pathway . In this study, to confirm our hypothesis which DKK1 could be involved in the pathogenesis of vitiligo as one of dermal factor, immunohistochemistry and real-time RT-PCR for DKK1, beta-catenin and PAR-2 were performed using vitiligo lesional and non-lesional skin specimens.DKK1 is highly expressed in the dermis of vitiligo lesion: Is there association between DKK1 and vitiligo?Sang Ho Oh, Ji Young Kim, Mi Ri Kim, Jeong Eun Do, Jae Yong Shin, Seung-Kyung Hann10.1016/j.jdermsci.2012.01.010Journal of Dermatological Science 66, 2 (2012)2012-03-05Journal of Dermatological Science2012-03-05662S0923-1811(12)X0005-7Letters to the Editor163165http://www.jdsjournal.com/article/PIIS0923181112000849/abstract?rss=yesThe epidermal growth factor receptor (EGFR) plays pivotal roles not only in the maintenance of epithelial homeostasis but also in the progression of cancer cells. Therefore, EGFR inhibitors (EGFR-Is) have been effective in treating various types of cancers, including lung and colon carcinomas. In addition, EGFR-Is have less frequent systemic side effects compared with conventional chemotherapies . However, since EGFR is expressed in many normal epithelial cells, treatment with EGFR-Is is associated with a high prevalence of dermatologic side effects. Papulopustular eruption (PPE) is the most frequent adverse side effect, occurring in the majority (45–100%) of patients treated with EGFR-Is . PPE was formerly called acne-like eruption, but is distinct from folliculitis or acne by its clinical manifestations, including the absence of comedones, frequent pruritus and effectiveness of topical corticosteroids. However, the underlying pathomechanism of PPE due to treatment with EGFR-Is remains undefined. Epidermal keratinocytes have been thought to be the primary target of EGFR-Is which results in the development of PPE. In vitro treatment of normal human epidermal keratinocytes (NHEK) with EGFR-Is attenuates DNA synthesis, but initiates cell differentiation and induces apoptosis . However, since PPE develops around the pilosebaceous apparatus, we assumed that EGFR-Is directly affects sebaceous glands. A recent study showed that treatment of SCID mice with EGFR-Is significantly increases the size of sebaceous glands, even prior to the onset of inflammation . They hypothesized that EGFR-Is facilitate the maturation of sebocytes, eventually resulting in sebaceous hypertrophy, follicular distention and concomitant increase in tumor necrosis factor-alpha (TNF-α) levels, which could contribute to skin inflammation. Therefore, we investigated the potential roles of sebaceous glands in the development of EGFR-Is-induced PPE.Sebaceous glands as the primary target of EGFR-inhibitors in the development of papulopustular eruptionTomoya Takata, Masahito Tarutani, Shigetoshi Sano10.1016/j.jdermsci.2012.02.012Journal of Dermatological Science 66, 2 (2012)2012-03-23Journal of Dermatological Science2012-03-23662S0923-1811(12)X0005-7Letters to the Editor165168http://www.jdsjournal.com/article/PIIS0923181112001247/abstract?rss=yesThe authors regret that when this paper was first published, The captions for were transposed. The correct figures and their captions are shown below: Corrigendum to “Mesenchymal stem cells delivered in a microsphere-based engineered skin contribute to cutaneous wound healing and sweat gland repair” [J. Dermatol. Sci. 66 (2012) 29–36]Sha Huang, Gang Lu, Yan Wu, Enhe Jirigala, Yongan Xu, Kui Ma, Xiaobing Fu10.1016/S0923-1811(12)00124-7Journal of Dermatological Science 66, 2 (2012)2012-05-01Journal of Dermatological Science2012-05-01662S0923-1811(12)X0005-7Corrigendum169170http://www.jdsjournal.com/article/PIIS0923181112001296/abstract?rss=yesAnnouncements10.1016/S0923-1811(12)00129-6Journal of Dermatological Science 66, 2 (2012)2012-05-01Journal of Dermatological Science2012-05-01662S0923-1811(12)X0005-7171171