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. Chief Editor's Report 2008 Editorial Report 2008 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: Hiroshi Shimizu, Secretary General of JSID, Department of Dermatology, Hokkaido University Graduate School of Medicine, N15 W7 Sapporo 060-8638, Japan Tel: +81-11-706-7387 Fax: +81-11-706-7820 E-mail: jsid@pop.med.hokudai.ac.jp (Hiroshi Shimizu, Secretary General/ Machika Osanai, Secretary)http://www.jdsjournal.com/?rss=yesElsevier Inc.en © 2010 Published by Elsevier Inc. All rights reserved. Journal of Dermatological Science0923-1811572February 2010 © 2010 Published by Elsevier Inc. All rights reserved. healthpermissions@elsevier.comhttp://www.jdsjournal.com/article/PIIS0923181110000071/abstract?rss=yesEditorial Board10.1016/S0923-1811(10)00007-1Journal of Dermatological Science 57, 2 (2010)2010-02-01Journal of Dermatological Science2010-02-01572S0923-1811(10)X0002-0iihttp://www.jdsjournal.com/article/PIIS0923181109003077/abstract?rss=yesAbstract: Herpes simplex virus type 1 (HSV-1) and type 2 (HSV-2) are important human pathogens that cause a variety of diseases from mild skin diseases such as herpes labialis and herpes genitalis to life-threatening diseases such as herpes encephalitis and neonatal herpes. A number of studies have elucidated the roles of this virus in viral replication and pathogenicity, the regulation of gene expression, interaction with the host cell and immune evasion from the host system. This research has allowed the development of potential therapeutic agents and vectors for human diseases. This review focuses on the basic functions and roles of HSV gene products and reviews the current knowledge of medical applications of genetically engineered HSV mutants using different strategies. These major HSV-derived vectors include: (i) amplicons for gene delivery vectors; (ii) replication-defective HSV recombinants for vaccine vectors; (iii) replication-attenuated HSV recombinants for oncolytic virotherapy.Medical application of herpes simplex virusDaisuke Watanabe10.1016/j.jdermsci.2009.10.014Journal of Dermatological Science 57, 2 (2010)2010-02-01Journal of Dermatological Science2010-02-01572S0923-1811(10)X0002-0Invited review article7582http://www.jdsjournal.com/article/PIIS0923181109003673/abstract?rss=yesAbstract: The pilosebaceous unit is a complex structure that undergoes a specific growth cycle and comprises a few important drug targeting sites. For example, drugs can be targeted to the bulge region with stem cells or to the sebaceous glands. Interest in pilosebaceous units is directed towards their utilization as reservoirs for localized therapy and also as a transport pathway for systemic drug delivery. Improved investigative methods, such as differential stripping, are being developed in order to determine follicular penetration. This article reviews relevant aspects of effective follicle-targeting formulations and delivery systems as well as the activity status of hair follicles, and variations in follicle size and distribution throughout various body regions. Each of these factors strongly affects follicular permeation. We provide examples of improved penetration of particle-based formulations and of a size-dependent manner of follicular penetration. Contradictions are also discussed, indicating the need for detailed future investigations.Targeting to the hair follicles: Current status and potentialHanna Wosicka, Krzysztof Cal10.1016/j.jdermsci.2009.12.005Journal of Dermatological Science 57, 2 (2010)2010-02-01Journal of Dermatological Science2010-02-01572S0923-1811(10)X0002-0Review article8389http://www.jdsjournal.com/article/PIIS0923181109003600/abstract?rss=yesAbstract: Backgrounds: Epidermolysis bullosa simplex (EBS) is a group of hereditary bullous disorders caused by mutations in the keratin genes KRT5 and KRT14. A significant genotype–phenotype correlation has been noted in previous studies of EBS.Objective: In order to identify additional EBS mutations and elucidate the genotype–phenotype correlations in Korean EBS patients, we performed the first large scale mutational analysis of EBS patients of Korean origin.Methods: We investigated fifteen Korean EBS patients by performing a sequence analysis of the entire coding sequences of KRT5 and KRT14.Results: We identified six novel mutations, four within KRT5 (p.V143F, p.R265P, p.C479X and p.Asn177del), and two within KRT14 (p.R125L and p.L401P). In all, 13 missense, 1 nonsense, and 1 small deletion mutation were found. Five mutations in Dowling–Meara type (K14-p.R125H, K14-p.R125L, K5-E477K, K5-p.C479X and K5-p.Asn177del) were located in the highly conserved ends of the alpha-helical rod domain, the helix initiation (HIP), or helix termination (HTP) peptides of KRT5 and KRT14. Further, seven and three mutations were identified in EBS-generalized type and EBS-localized type, respectively. The positions of the mutations in both subtypes were more widely distributed within the rod domains and in the L12 linker domains of both keratin genes.Conclusions: This study should provide useful data and enhance our understanding of the EBS genotype–phenotype relationship. The genotype–phenotype correlation in Korean EBS patients was similar to previous studies performed in other ethnic groups. Lastly, our results confirmed that the mutational location in KRT5 or KRT14 is the most important factor in determining the phenotype severity.Novel and recurrent mutations in Keratin 5 and 14 in Korean patients with Epidermolysis bullosa simplexTae-Won Kang, Jeong Seon Lee, Song-Ee Kim, Se-Woong Oh, Soo-Chan Kim10.1016/j.jdermsci.2009.12.002Journal of Dermatological Science 57, 2 (2010)2010-02-01Journal of Dermatological Science2010-02-01572S0923-1811(10)X0002-0Regular articles9094http://www.jdsjournal.com/article/PIIS0923181109002862/abstract?rss=yesAbstract: Background: Parakeratosis, the persistent presence of nuclei in the stratum corneum (SC) is associated with serious disruption of skin barrier function. Squamous cell carcinoma antigen 1 (SCCA1) is strongly up-regulated in inflamed and parakeratotic skin.Objective: To find a biochemical marker for the SC barrier disruption, especially the disruption associated with parakeratosis.Methods: An ELISA assay system was established to quantify SCCA1 in the extract of tape-stripped cornified cells. Transepidermal water loss (TEWL) and other skin parameters were measured and compared with the amount of SCCA1. Localization of SCCA1 was investigated immunohistochemically in various skin diseases with parakeratosis. Nuclei and SCCA1 on the skin surface were detected by staining of corniocytes collected on an adhesive-coated slide glass.Results: SCCA1 showed strong up-regulation in lesional skin with psoriasis (466-fold), hayfever skin caused by Japanese ceder pollen (232-fold) and sun-exposed skin of healthy individuals (90-fold) compared to their normal sun-protected skin. The increased levels of SCCA1 were well correlated with increased values of TEWL and the number of parakeratotic cells in the SC. Furthermore, subjects with high levels of SCCA1 in the epidermis were more susceptible to barrier disruption by external stimuli, and this was accompanied with a further increase of SCCA1. We confirmed that localization of SCCA1 was limited to parakeratotic areas by using the skin surface staining technique. Immunohistochemical study also demonstrated that SCCA1 was always present at high levels in parakeratotic epidermis.Conclusion: All of our findings indicate that SCCA1 plays an important role in the induction of epidermal barrier disruption. SCCA1 may be a critical determinant of barrier function in the epidermis.Up-regulation of serpin SCCA1 is associated with epidermal barrier disruptionChika Katagiri, Toshii Iida, Jotaro Nakanishi, Maki Ozawa, Setsuya Aiba, Toshihiko Hibino10.1016/j.jdermsci.2009.09.004Journal of Dermatological Science 57, 2 (2010)2010-02-01Journal of Dermatological Science2010-02-01572S0923-1811(10)X0002-0Regular articles95101http://www.jdsjournal.com/article/PIIS0923181109003351/abstract?rss=yesAbstract: Background: Dorfman–Chanarin syndrome (DCS), also referred to as neutral lipid storage disease with ichthyosis, is a rare autosomal recessive form of nonbullous congenital ichthyosiform erythroderma, characterized by the presence of intracellular lipid droplets in multiorgans. DCS patients often have mutations in CGI-58, which is an activator of adipose triglyceride lipase (ATGL), leading to accumulation of triglycerides (TG).Objective: To study whether a patient with DCS demonstrates TG accumulation in the epidermis and to analyze whether TG levels are correlated with skin disease activity.Methods: Skin specimen from a 62-year-old man with DCS was stained with oil red O, and analyzed on electromicrographs. Sequencing analysis of CGI-58 was performed using the patient's blood cells. The scales from the lesion were subject to lipid analysis by high-performance thin-layer chromatography (HPTLC).Results: The patient demonstrated ichthyoform erythroderma with a distinct seasonal fluctuation: his skin lesions were aggravated in summer but resolved during winter. Epidermis of the lesion showed intracellular lipid droplets. Sequencing analysis revealed a novel missense mutation in the exon 3 of CGI-58 gene. Lipid analysis of the scales from his lesions, compared with those from normal human control, revealed increased levels of triglycerides (TG) but, in turn, decreased levels of free fatty acids, suggesting dysfunction of adipose TG lipase. Notably, the TG levels in the scales from the patient were positively correlated with the severity of ichthyosis.Conclusion: These results suggest that TG accumulation by epidermal keratinocytes directly contributes to ichthyosiform phenotype of DCS.Epidermal triglyceride levels are correlated with severity of ichthyosis in Dorfman–Chanarin syndromeMayumi Ujihara, Kimiko Nakajima, Mayuko Yamamoto, Mika Teraishi, Yoshikazu Uchida, Masashi Akiyama, Hiroshi Shimizu, Shigetoshi Sano10.1016/j.jdermsci.2009.10.016Journal of Dermatological Science 57, 2 (2010)2010-02-01Journal of Dermatological Science2010-02-01572S0923-1811(10)X0002-0Regular articles102107http://www.jdsjournal.com/article/PIIS0923181109003612/abstract?rss=yesAbstract: Background: Glycolic acid (GA) is the most commonly used alpha-hydroxy acid (AHA) for dermatologic applications, and is considered as a versatile superficial peeling agent for facial rejuvenation. Its therapeutic effect includes acceleration of epidermal turnover without apparent inflammation, and its action is pH-dependent. However, little is known about the molecular mechanism of GA-induced peeling.Objective: To investigate the effects of topical application of GA on cell proliferation using a skin equivalent model and to examine the molecular mechanisms of GA-induced peeling.Methods: GA solution was applied on the surface of a skin equivalent model, and cell proliferation was measured by means of BrdU-incorporation and immunohistochemical methods. Release of chemical mediators such as ATP into the medium was examined. The effects of antagonists of ion channels were also analyzed.Results: At 24h after GA application, BrdU-incorporation into basal keratinocytes was significantly increased. Induction of keratinocyte proliferation was pH-dependent, and was inhibited by antagonists of TRPV1, an acid-sensitive ion channel. Furthermore, transient ATP release was detected in the culture medium after GA stimulation, and this was also suppressed by TRPV1 antagonists.Conclusion: These results suggest that one of the mechanisms of GA-induced epidermal proliferation is a growth response of basal keratinocytes to the local elevation of H+-ion concentration by infiltrated GA. This response is mediated by TRPV1 activation and ATP release. Activation of P2 receptors by the released ATP may also be involved.Glycolic acid induces keratinocyte proliferation in a skin equivalent model via TRPV1 activationSumiko Denda, Mitsuhiro Denda, Kaori Inoue, Toshihiko Hibino10.1016/j.jdermsci.2009.11.007Journal of Dermatological Science 57, 2 (2010)2010-02-01Journal of Dermatological Science2010-02-01572S0923-1811(10)X0002-0Regular articles108113http://www.jdsjournal.com/article/PIIS0923181109002989/abstract?rss=yesAbstract: Background: UVB irradiation (290–320nm) is the most damaging component of the UV spectrum and causes both direct and indirect damage to the basal cell layer of the epidermis; this results in the activation of a number of signaling pathways involved in pathophysiological processes in the skin, such as photoaging and inflammation. In photoaging UVB irradiation promotes degradation of the extracellular matrix (ECM) by matrix metalloproteinases (MMPs) and, in inflammation, UVB irradiation promotes the expression of inducible cyclooxygenase (COX-2), leading to overproduction of inflammatory mediators.Objective: We first investigated the protective effects of macelignan from Myristica fragrans Houtt. on immortalized human keratinocytes (HaCaT) against UVB damage. We then explored the inhibitory effects of macelignan on UVB-induced MMP-9 and COX-2 and investigated the molecular mechanism underlying those effects.Methods: HaCaT cells were treated with macelignan for the indicated times followed by irradiation with UVB. Secretion of MMP-9 was measured by gelatin zymography. Expression of COX-2, mitogen-activated protein kinases (MAPKs), phosphatidylinositol 3-kinase/Akt (PI3K/Akt), c-Fos, c-Jun, and CREB were assayed by western analysis.Results: Macelignan at a concentration of 0.1–1μM increased the viability of HaCaT cells following UVB irradiation and inhibited MMP-9 secretion and COX-2 expression in a concentration-dependent manner. An inhibitory effect was also seen in the signal transduction network, where macelignan treatment reduced the activation of UVB-induced MAPKs, PI3K/Akt, and their downstream transcription factors.Conclusion: These results suggest that macelignan protects skin keratinocytes from UVB-induced damage and inhibits MMP-9 and COX-2 expression by attenuating the activation of MAPKs and PI3K/Akt.Effects of macelignan isolated from Myristica fragrans Houtt. on UVB-induced matrix metalloproteinase-9 and cyclooxygenase-2 in HaCaT cellsAnggakusuma, Yanti, Jae-Kwan Hwang10.1016/j.jdermsci.2009.10.005Journal of Dermatological Science 57, 2 (2010)2010-02-01Journal of Dermatological Science2010-02-01572S0923-1811(10)X0002-0Regular articles114122http://www.jdsjournal.com/article/PIIS0923181109003405/abstract?rss=yesAbstract: Background: Although the function of human melanocytes is well characterized at cellular and molecular levels, the mechanism of the regulation of the life cycle (proliferation, differentiation, and cell death) of human melanocytes is not fully understood.Objective: This study aims to clarify what factors are involved in regulating the life cycle of human melanocytes using serum-free culture system.Methods: Human epidermal melanocytes were cultured in a serum-free growth medium supplemented with several kinds of growth factors, cytokines, and hormones and the effects of these factors on the life cycle of melanocytes were investigated in detail.Results: Of the factors tested, endothelin-1 (ET-1) stimulated the proliferation of melanoblasts and melanocytes in the presence of cyclic AMP (cAMP)-elevating factor such as dibutyryl cAMP (DBcAMP) and of basic fibroblast growth factor (bFGF). ET-1 also stimulated the proliferation and differentiation of human melanocytes in the presence of DBcAMP. Moreover, stem cell factor (SCF) stimulated the proliferation of melanoblasts and melanocytes synergistically with ET-1. The removal of ET-1 and SCF from the culture medium greatly inhibited the proliferation of melanocytes followed by apoptotic cell death.Conclusion: These results suggest that the life cycle of human melanocytes is regulated by ET-1 and SCF in synergy with cAMP and bFGF.Life cycle of human melanocytes is regulated by endothelin-1 and stem cell factor in synergy with cyclic AMP and basic fibroblast growth factorTomohisa Hirobe, Tsuneo Shinpo, Kazuhiko Higuchi, Tomohiko Sano10.1016/j.jdermsci.2009.11.006Journal of Dermatological Science 57, 2 (2010)2010-02-01Journal of Dermatological Science2010-02-01572S0923-1811(10)X0002-0Regular articles123131http://www.jdsjournal.com/article/PIIS0923181109003260/abstract?rss=yesWoolly hair (WH) belongs to a group of disorders characterized by hair shaft anomalies that presents clinically with tightly curled hair . Patients with woolly hair can be divided into two categories. In the first group, woolly hair occurs in the setting of associated cutaneous and/or systemic anomalies. In the second, woolly hair presents as an isolated feature. The distinction between the two categories is critical because woolly hair can occur in the setting of syndromes that can be lethal at early ages due to cardiac arrythmias. Naxos (OMIM 601214) and Carvajal syndromes (OMIM 605676) are conditions that dermatologists should be aware of when managing the woolly hair and cardiologists consultation is mandatory. These syndromes are clinically characterized by woolly hair, palmoplantar keratoderma (usually striate type), right ventricular cardiac disease in the case of Naxos syndrome with mutation in plakoglobin, and left ventricular cardiac disease in the case of Carvajal syndrome with mutation in desmoplakin I . Non-syndromic woolly hair can be inherited either in an autosomal recessive (ARWH; OMIM 278150) or autosomal dominant pattern (OMIM 194300) . Until recently, genes associated with non-syndromic woolly hair were unknown. We and others have recently shown that P2RY5 and Lipase H (LIPH) are associated with ARWH and/or hypotrichosis . Mutations in both genes result in a clinically indistinguishable phenotype which can range from woolly hair to hypotrichosis and complete loss of hair . Histology is consistent with decreased number of hair follicles with miniaturization , however, all biopsies performed were from patients with later stages of hypotrichosis and not from patients with the early stages of woolly hair.A missense mutation in the P2RY5 gene leading to autosomal recessive woolly hair in a Syrian patientM. Kurban, S. Ghosn, O. Abbas, Y. Shimomura, A. Christiano10.1016/j.jdermsci.2009.10.015Journal of Dermatological Science 57, 2 (2010)2010-02-01Journal of Dermatological Science2010-02-01572S0923-1811(10)X0002-0Letters to the Editor132134http://www.jdsjournal.com/article/PIIS0923181109003065/abstract?rss=yesAdipose tissue-derived stem cells (ADSCs) can display multi-lineage plasticity and share similar characteristics with bone marrow-derived mesenchymal stem cells . Moreover, ADSCs have various cytokine-secreting properties and beneficial paracrine effects on surrounding cells or tissues . Recently, paracrine function is considered one of the most important therapeutic benefits of therapy using mesenchymal stem cells .Hair growth promoting effects of adipose tissue-derived stem cellsChong Hyun Won, Hyeon Gyeong Yoo, Oh Sang Kwon, Mi Young Sung, Yong Jung Kang, Jin Ho Chung, Byung Soon Park, Jong-Hyuk Sung, Won Serk Kim, Kyu Han Kim10.1016/j.jdermsci.2009.10.013Journal of Dermatological Science 57, 2 (2010)2010-02-01Journal of Dermatological Science2010-02-01572S0923-1811(10)X0002-0Letters to the Editor134137http://www.jdsjournal.com/article/PIIS0923181109003375/abstract?rss=yesFood-induced anaphylaxis is one of the most common causes of anaphylaxis . Establishing the cause of recurrent anaphylaxis is one of the most important goals of management because identification of the responsible allergens allows avoidance of further exposure.Food-dependent anaphylaxis with serum IgE immunoreactive to dairy products containing high-molecular-weight proteinsShoko Abe, Kenji Kabashima, Tatsuya Moriyama, Yoshiki Tokura10.1016/j.jdermsci.2009.11.003Journal of Dermatological Science 57, 2 (2010)2010-02-01Journal of Dermatological Science2010-02-01572S0923-1811(10)X0002-0Letters to the Editor137140http://www.jdsjournal.com/article/PIIS0923181109003387/abstract?rss=yesMalignant melanoma is one of the most aggressive cancers. Recently, an increasing number of biomarkers for malignant melanoma like S100, MART-1, and gp100/HMB45 have been identified . We also provided the possibility that Zinc finger protein 28 could be a biomarker for malignant melanoma . These biomarkers are useful for a more detailed diagnostic categorization for malignant melanoma.CD109 expression levels in malignant melanomaYuichiro Ohshima, Ichiro Yajima, Mayuko Y. Kumasaka, Takeshi Yanagishita, Daisuke Watanabe, Masahide Takahashi, Yuji Inoue, Hironobu Ihn, Yoshinari Matsumoto, Masashi Kato10.1016/j.jdermsci.2009.11.004Journal of Dermatological Science 57, 2 (2010)2010-02-01Journal of Dermatological Science2010-02-01572S0923-1811(10)X0002-0Letters to the Editor140142http://www.jdsjournal.com/article/PIIS0923181109003363/abstract?rss=yesMetabolic syndrome is a constellation of multiple risk factors including central obesity, dyslipidemia, glucose intolerance, and elevated blood pressure. The syndrome is associated with cardiovascular disease and type 2 DM , and non-alcoholic steatohepatitis (NASH) . Several reports indicate the association between psoriasis and DM, hypertension, obesity, and metabolic syndrome in Caucasian and Chinese psoriasis . Although we have shown the increased prevalence of obesity and adiposity in Japanese psoriasis , the incidence of DM, hypertension, cardiovascular disease, and the metabolic syndrome remains to be determined.Prevalence of metabolic syndrome in Japanese psoriasis patientsHidetoshi Takahashi, Ichiro Takahashi, Masaru Honma, Akemi Ishida-Yamamoto, Hajime Iizuka10.1016/j.jdermsci.2009.11.002Journal of Dermatological Science 57, 2 (2010)2010-02-01Journal of Dermatological Science2010-02-01572S0923-1811(10)X0002-0Letters to the Editor143144http://www.jdsjournal.com/article/PIIS0923181109003594/abstract?rss=yesDystrophic epidermolysis bullosa (DEB) is a group of inherited mechano-bullous disorders with a broad range of clinical severity characterized by blistering. Ultrastructurally, DEB shows abnormalities of the anchoring fibrils, which are composed of type VII collagen . On the basis of the mode of inheritance and the clinical manifestations, DEB is classified into 3 major forms: one dominant (DDEB) and two recessive (RDEB), the severe generalized RDEB subtype (RDEBsg) and “RDEB generalized other” (RDEB-O) which designates the other groups of generalized RDEB . All forms of DEB are known to be caused by mutations in the COL7A1 gene encoding type VII collagen. This gene consists of 118 exons, and over 300 COL7A1 mutations have been reported , most of them being family specific.Mutational survey of recessive dystrophic epidermolysis bullosa in Tunisian families unveils a spectrum of private, ethnic specific and world wide recurrent mutationsHouyem Ouragini, Faïka Cherif, Sabrine Ahlem Ben Brick, Sonia Nouira, Giovanna Floriddia, Monica Pascucci, Rym Kefi, Wafa Daoud, Nabiha Mahdhaoui, Selma Kassar, Ridha Mrad, Mohammed Ridha Kamoun, Amel Ben Osman-Dhahri, Mohamed Denguezli, Kamel Monastiri, Hassen Seboui, Mourad Mokni, Samir Boubaker, Daniele Castiglia, Sonia Abdelhak10.1016/j.jdermsci.2009.12.001Journal of Dermatological Science 57, 2 (2010)2010-02-01Journal of Dermatological Science2010-02-01572S0923-1811(10)X0002-0Letters to the Editor144146http://www.jdsjournal.com/article/PIIS0923181110000125/abstract?rss=yesAnnouncements10.1016/S0923-1811(10)00012-5Journal of Dermatological Science 57, 2 (2010)2010-02-01Journal of Dermatological Science2010-02-01572S0923-1811(10)X0002-0147147