greetings - eksid.re.kreksid.re.kr/pds/files/2013-23___________.pdf · -3-09:00-10:00...

Greetings

Dear colleagues and friends,

On behalf of the organizing committee of the annual meeting of Korean

Society for Investigative Dermatology (KSID), it is our great pleasure to cordially

invite you to the 23rd KSID Annual Meeting on March 22~23 of 2013.

This meeting has been organized to provide the participants with an excellent

scientific program, aiming at communicating leading-edge research on

immunology, lymphoma, atopic dermatitis, stem cell, hair and nail, melasma,

and cutaneous biology.

Celebrated Professors and Doctors from various countries, including Dr.

Hwang (USA), Dr. Iwatsuki, (Japan), Dr. Kabashima (Japan), Dr. Tokura (Japan),

Dr. Amagai (Japan), Dr. Nishigori (Japan), Dr. Ikeda (Japan), Dr. Zhang (China)

and distinguished Korean scholars will convey professional knowledge in their

fields of specialization.

We would like to appreciate all the participants who will graciously share

their invaluable knowledge and have an animated discussion. We also hope

that all of you will have the chance to enjoy the meeting, experience intellectual

interchange, and foster friendship.

We anticipate seeing many of you at the 23rd KSID meeting!

2013 March

Korean Society for Investigative Dermatology

President Kwang-Hyun Cho

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09:00-10:00 Free Communication Chairs: Jin Ho Chung, Kee Yang Chung

Program

22 March, 2013 (Fri)

08:30-09:00 Registration

FC-1 Silibinin induced down-regulation of type I collagen expression through blocking smad

2 /3-dependent signaling pathway in human skin fibroblasts from normal and keloid

tissues: its potential therapeutic use in the chemoprevention of keloid

Han-Won Ryu, Jun-Il Kwon, Jae-We Cho, Kyu-Suk Lee

Department of Dermatology, Keimyung University School of Medicine, Daegu, Korea 77

FC-2 Genetic variations associated with efficacy of dutasteride for male pattern hair loss

Seong Jin Jo1,2, Arang Rhie3,4, Seungbok Lee3,4, Bark-Lynn Lew5, Woo-Young Sim5, Kwang Hyun Cho1,2,

Jin Ho Chung1,2, Jong-Il Kim3,4, Oh Sang Kwon1,2

1Department of Dermatology, Seoul National University College of Medicine, Seoul, Korea2Institute of Human-Environment Interface Biology, Seoul National University, Seoul, Korea3Genomic Medicine Institute (GMI), Medical Research Center, Seoul National University, Seoul, Korea4Department of Biomedical Sciences, Seoul National University Graduate School, Seoul, Korea5Department of Dermatology, College of Medicine, Kyunghee University, Seoul, Korea 78

FC-3 Methyl- -cyclodextrin as a caveolin-1 inhibitor shows anti-aging activity in the skin:βinverse correlation between caveolin-1 and collagen I levels

Jung-Ae Lee1, Jee-Young Choi1, Da-In Choi1, Sun-Ouck Kim3, Suk-Jung Yun1, Kyung-A Cho2,

Jee-Bum Lee1, Seung-Chul Lee1

1Department of Dermatology, Chonnam National University Medical School,2Department of Biochemistry, Chonnam National University Medical School,3Department of Urology Chonnam National University Medical School 79

FC-4 Extracellular superoxide dismutase (EC-SOD) inhibits mast cell activation and allergic

responses

Yun Sang Lee and Tae-Yoon Kim

Department of Dermatology, College of Medicine, The Catholic University of Korea 80

FC-5 Sensitive skin: why is it sensitive?

Eun Ju Kim, Yeon Kyung Kim, Dong Hun Lee, Jung Yun Kim, Min-Kyoung Kim, Min Jung Lee,

Young Mee Lee, Hee Chul Eun, and Jin Ho Chung

Department of Dermatology, Seoul National University College of Medicine, Laboratory of Cutaneous Aging

Research, Biomedical Research Institute, Seoul National University Hospital, Institute of Human-Environment

Interface Biology, Seoul National University, Seoul, Korea 81

10:00-10:20 Coffee break

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Invited Lectures 1 Chairs:Min Geol Lee, Young Chul Kye

Invited Lectures 2 Chairs: Kwang Hyun Cho, Kwang Hoon Lee, Tae Yoon Kim

Invited Lectures 3 Chairs: Jun Mo Yang, Jeung Hoon Lee

10:20-10:50 EBV-associated T/ NK cell diseases, from indolent to aggressive proliferations

Young-Hyeh Ko (Sungkyunkwan University) 15

10:50-11:20 Remodeling of the cutaneous immune system and structures during viral infections

Keiji Iwatsuki (Okayama University, Japan) 17

11:20-11:50 Generation of new hair follicles by cell transplantation

Young Kwan Sung (Kyungpook National University) 19

11:50-12:20 Regulationmechanisms in gene expression ofATP2A2 and ATP2C1 (responsible for

Darier disease and Hailey-Hailey disease genes respectively)

Shigaku Ikeda (Juntendo Univ, Japan) 21

12:20-13:50 Lunch & Board meeting

13:50-14:00 Opening Ceremony

14:00-14:40 Induction of antigen-specific T Cell tolerance and its application to a variety of

immunologic disorders

Seong Hoe Park (Seoul National University) 26

14:40-15:10 Effects of Th17-derived cytokines on keratinocyte production of antimicrobial

peptides in psoriasis and adult T cell leukemia / lymphoma

Yoshiki Tokura (Hamamatsu University, Japan) 28

15:10-15:40 What we can learn from animal models of cutaneous T cell lymphoma

Sam T. Hwang (Medical College of Wisconsin, USA) 30

15:40-16:10 Coffee break

16:10-16:40 The threemusketeers of the epidermalbarrier and cutaneous sensitization to external

antigens

Masayuki Amagai (Keio University, Japan) 34

16:40-17:10 Molecular organization of synaptic junctions

Eunjoon Kim (KAIST) 37

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Invited Lectures 4 Chairs: Dongsik Bang, Chang Kwun Hong

17:10-17:40 Current trends of stem cell research, Where are we?

Il-Hoan Oh (Catholic University) 42

17:40-18:00 The concept of onychodermis (specialized nail mesenchyme) in the nail unit

Dong-Youn Lee (Sungkyunkwan University) 44

18:00- Welcome Reception

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09:00-10:00 Hot Posters Chairs: Il Hwan Kim, Eun So Lee

10:00-10:20 UAM Award Lecture Chair: Young Ho Won

Invited Lectures 5 Chairs: Kyoung Chan Park, Ai Young Lee

Invited Lectures 6 Chairs: Kee Chan Moon, Soo Chan Kim

14:00-17:00 피부생물학 연수강좌

23 March, 2013 (Sat)

The Effect of Adipose-Derived Stem Cell-Cultured Media on Oxazolone Treated Atopic

Dermatitis-Like Murine Model

Eung Ho Choi

Department of Dermatology, Yonsei University Wonju College of Medicine, Wonju, Korea 60

10:20-10:40 Coffee Break

10:40-11:10 Mechanismsofmelanomagenesis inrelationto signal transductionand transcriptionfactors

Chikako Nishigori (Kobe University, Japan) 48

11:10-11:40 Pathogenesis ofmelasma: What should be considered in treatment ofmelasma

Hee Young Kang (Ajou University) 50

11:40-12:10 Investigative dermatology in China: a decade's progress

Jianzhong Zhang (Peking University, China) 54

12:10-12:40 Visualization of skin inflammation

Kenji Kabashima (Kyoto University, Japan) 56

12:40-14:00 Photo, Lunch & General Assembly

모발연구 Chairs : 심우영 이원수,

Intra and extra-follicular regulation on the growth of hair follicles 상 서울의대( ) 64

Hair follicle stem cell 창덕 충남의대( ) 66

기저막연구 Chairs : 이승철 노주영,

Structure and Function of Basement Membrane Zone I 찬 연세의대( ) 68

Structure and Function of Basement Membrane Zone II 지 전남의대( ) 70

진균연구 Chairs : 안규중 서성준,

진균학연구에서분자생물학적방법의적용 남의대( ) 72

Malassezia and atopic dermatitis 양원 건국의대( ) 74

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Hot Posters

Posters

PO-1 TNS4 delayed wound healing through actin cytoskeletal regulation

Seon-Pil Jin, Eun Young Seo, Jin Ho Chung

Department of Dermatology, Seoul National University College of Medicine, Seoul, Korea 85

PO-2 Novel isonahocol E3 exhibits anti-inflammatory and anti-angiogenic effects in endothelin-1-stimulated human keratinocytes

Shyam K Sah and Tae-Yoon Kim

Department of Dermatology, College of Medicine, The Catholic University of Korea, Seoul, Korea 86

PO-3 TRPV1 inhibitory peptide prevents UV-induced skin responsesSo Min Kang, Sang Bum Han, Young Mee Lee, Yeon Kyung Kim, Chang Yup Shin and

Jin Ho Chung

Department of Dermatology, Seoul National University College of Medicine;

Laboratory of Cutaneous Aging Research, Clinical Research Institute, Seoul National University Hospital;

Institute of Dermatological Science, Seoul National University, Seoul, Korea 87

PO-4 Expression pattern of sortilin in human hair follicles and its essential role in hair growthLong-Quan Pi1, Xing-Hai Jin1, Sungjoo Tommy Hwang2, Won-Soo Lee11Department of Dermatology and Institute of Hair and Cosmetic Medicine, Yonsei University Wonju College

of Medicine, Wonju; 2Dr. Hwang’s Hair-Hair Clinic, Seoul, Korea 88

PO-5 Homoisoflavanone prevents allergic responses by inhibition of Syk signaling pathwayin mast cells



P-1 Prevention and treatment of alopecia areata with mesenchymal stem cells in the C3H/ HeJmouse model

Ji Won Byun, Myeong Shin Jeon1, Hyo Jin Kim, Jeonghyun Shin, Gwang Seong ChoiDepartment of Dermatology, Inha University School of Medicine1Department of Biomedical Sciences, Inha University School of Medicine 93

P-2 Differential expression of klotho in human scalp skin and hair folliclesXing-Hai Jin1, Long-Quan Pi1, Sungjoo Tommy Hwang2, Won-Soo Lee11Department of Dermatology and Institute of Hair and Cosmetic Medicine, Yonsei University Wonju College

of Medicine, Wonju; 2Dr. Hwang’s Hair-Hair Clinic, Seoul, Korea 94

P-3 A method to accurately evaluate hair growth in organ cultured hair folliclesXing-Hai Jin1, Long-Quan Pi1, Sungjoo Tommy Hwang2, Won-Soo Lee11Department of Dermatology and Institute of Hair and Cosmetic Medicine, Yonsei University Wonju College

of Medicine, Wonju2Dr. Hwang’s Hair-Hair Clinic, Seoul, Korea 95

P-4 Effect of the catagen transition induced by epidermal growth factor on a mouse modelof chemotherapy-induced alopecia

Ji-Seon Yoon1,2,3, Seung Hwan Paik1, JiYeon Lee2,3, Hyeong Ho Ryu1, Chang Yup Shin3,Kyung Hyun Min4, Seong Jin Jo1,2,3, Kyu Han Kim1,2,3, Oh-Sang Kwon1,2,3

1Department of Dermatology, Seoul National University College of Medicine, Seoul; 2Laboratory of Cutaneous

Aging and Hair Research, Clinical Research Institute, Seoul National University Hospital, Seoul; 3Institute

of Human-Environment Interface Biology, Seoul National University College of Medicine, Seoul; 4Bio Research

Laboratory, Life Science Research Institute, Daewoong Pharmaceutical Co., Ltd., Yongin, Korea 96

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P-5 Role of A20 in therapeutic effect of imiquimod on Squamous cell carcinoma diseasesLi Zheng Jun, Kyung-Cheol Sohn, Eun-Hwa Im, Myung Im, Young Lee, Chang Deok Kim,

Young-Joon Seo, and Jeung-Hoon Lee

Department of Dermatology, School of Medicine, Chungnam National University, Daejeon, Korea 97

P-6 Laser Cancer Prevention: Is the ablative laser for rejuvenation preventive againstultraviolet-induced skin cancer?

Jiwon Gye1, Jiyeon Yoo1,2, Ji Seok Kim1, Jee Young Kim1, Byung Cheol Park1, MyungHwa Kim1,

Seung Phil Hong1

1Department of Dermatology, College of Medicine, Dankook University, Cheonan, Korea2Department of Dermatology, Yonsei University Wonju College of Medicine, Wonju, Korea 98

P-7 Genomic variant landscape of Korean melanoma using whole-exome and transcriptomesequencing

Tae-Gyun Kim1,2,3, Young-Seok Ju4,5, Jong-Yeon Shin4, Byung-Ho Oh3, Hong Sun Jang3,

Mi-Kyoung Kim2, Hyoung-Pyo Kim1,2, Jeong-Sun Seo4,5,6,7, and Kee Yang Chung3

1Brain Korea 21 Project for Medical Science, Yonsei University, Seoul, Korea2Department of Environmental Medical Biology, Institute of Tropical Medicine, Yonsei University College of

Medicine, Seoul; 3Department of Dermatology, Yonsei University College of Medicine, Seoul, Korea4Genomic Medicine Institute, Medical Research Center, Seoul National University, Seoul, Korea5Macrogen Inc., Seoul; 6Department of Biochemistry, Seoul National University College of Medicine, Seoul;7

Department of Biomedical Sciences, Seoul National University Graduate School, Seoul, Korea 99

P-8 Role of Human Papilloma Virus Infection and RAS Mutation in KeratoacanthomaM.R. Roh1, J.H. Kim2, S.H. Lee1, K.H. Park2, K.Y. Chung1 and S.Y. Rha21Department of Dermatology and Cutaneous Biology Research Institute, Yonsei University College of Medicine,

Seoul; 2Yonsei Cancer Centre, Department of Internal Medicine, Yonsei University College of Medicine, Seoul,

Korea 100

P-9 P63 and TGF- 1&- 2 can be important markers in differentiation degree and malignancyβ βpotential of sebaceous/ follicular tumors

Su-Young Jeon, Seung-Min Ha, Dong-Yeob Ko, Jin-Woo Hong, Ki-Hoon Song, Ki-Ho Kim

Department of Dermatology, Dong-A University College of Medicine, Busan, Korea 101

P-10 Cilostazol inhibits the expression of hnRNP A2/ B1 and inflammatory factors in humandermal microvascular endothelial cells

Zhenlong Zheng, Sung Bin Cho, Do-Young Kim, Suhyun Cho, Min Ju Choi, and Dongsik BangDepartment of Dermatology and Cutaneous Biology Research Institute, Yonsei University College of Medicine,

Seoul, Korea 102

P-11 Capsiate inhibits the activation and differentiation of mouse CD4+ T cells throughsuppressed activation of Lck



P-12 Immune response-regulatory function of blood group antigen in HaCaT cellsJang-Hee Oh, Ji Young Jung, Min Kyeong Shin, Se-Rah Lee, Jin Ho ChungDepartment of Dermatology, Seoul National University College of Medicine; Laboratory of Cutaneous Aging

Research, Clinical Research Institute, Seoul National University Hospital; Institute of Dermatological Science,

Seoul National University, Seoul, Korea 104

P-13 Rhododendrin ameliorates skin inflammation through inhibition of NF- B, MAPK, andκPI3K /Akt signaling

Yoon-Jae Jeon and Tae-Yoon Kim

Department of Dermatology, College of Medicine, The Catholic University of Korea, Seoul, Korea 105

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P-14 Time course effects of topical Dermatophagoides farinae applications on the progressionof atopic dermatitis-like symptoms in NC/ Nga mice

Ji-Yun Kima, Mi Sook Jeonga, Kui Young Parka, Mi-Kyung Leeb, Seong Jun SeoaaDepartment of Dermatology, Chung Ang University College of MedicinebDepartment of Laboratory Medicine, Chung-Ang University College of Medicine 106

P-15 Bee venom ameliorates Dermatophagoides farinae-induced atopic dermatitis-like skin inNc/ NgA miceHeesu Kim, Shan Jin, Na Ra Lee, Hemin Lee, Jung U Shin, Kwang Hoon Lee

Department of Dermatology, Severance Hospital, Cutaneous Biology Research Institute, Yonsei University

College of Medicine, Seoul, Korea 107

P-16 Role of galanin in UV-induced inflammatory responses in human epidermal keratinocytesMin Jung Lee, Jin Ho ChungDepartment of Dermatology, Seoul National University College of Medicine; Institute of Dermatological Science,

Medical Research Center, Seoul National University; Laboratory of Cutaneous Aging Research, Clinical

Research Institute, Seoul National University Hospital, Seoul, Korea 108

P-17 Anacardic acid increases type I procollagen expression following ultraviolet irradiationvia inhibition of DNA methylation in the COL1A2 promoter region

Min-Kyoung Kim, Jin Ho ChungDepartment of Dermatology, Seoul National University College of Medicine; Laboratory of Cutaneous Aging

Research, Biomedical Research Institute, Seoul National University Hospital; Institute of Human-Environment

Interface Biology, Seoul National University, Seoul, Korea 109

P-18 Ethanol Extract of Peanut Sprout induces Nrf2 activation and expression of antioxidantand detoxifying enzymes in human dermal fibroblasts: implication for its protection

against UVB-irradiated oxidative stress

Jee-Young Choi1,2, Da-In Choi1,2, Jee-Bum Lee1,2, Suk-Jung Yun1,2, Dong-Ho Lee2, Jong-Bang Eun3,Seung-Chul Lee1,2*1Department of Dermatology of Chonnam National University Medical School, 2Chonnam National University

Hospital Research Institute of Clinical Medicine, 3Department of Food Science and Technology and Functional

Food Research Center, Chonnam National University, Gwangju, Korea 110

P-19 Comparison between Malassezia folliculitis and non-Malassezia folliculitisHyo Sang Song, Sue Kyung Kim, You Chan Kim

Department of Dermatology, Ajou University School of Medicine, Suwon, Korea 111

P-20 Use of Reverse Blot Hybridization Assay for Fast and Accurate Diagnosis of SuperficialFungal Infections

Sang-Yeon Park1, Bo-Kyung Kim1, Hyeyoung Lee2, Hye-young Wang3, Sunghyun Kim2,

Eung Ho Choi1

1Department of Dermatology, Yonsei University Wonju College of Medicine, Wonju, Korea2Department of Laboratory Medicine, Yonsei University, Wonju, Korea3M&D, Inc., Wonju Eco Environmental Technology Center, Wonju, Korea 112

P-21 Non-selective -blocker increases the expression of CCL20 in HaCaT cells stimulated withβTNF- a possible mechanism in exacerbation of psoriasisα

Heesu Kim, Sung hee Kim, Dae Suk Kim, Do Young Kim, Dashlkhumbe Byamba, Hyunjoong Jee,

Min-Geol Lee


College of Medicine, Seoul, Korea 113

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P-22 Intron A inhibits lymph node metastasis in melanoma via inhibition of lymphangiogenesisby downregulating Prox-1 protein expression

Zhenlong Zheng, Xianglan Zhang*, Junjie Piao, Tae Hyung Kim, Kee Yang Chung, Mi Ryung RohDepartment of Dermatology and Cutaneous Biology Research Institute, Yonsei University College of Medicine,

Seoul; *Oral Cancer Research Institute, College of Dentistry, Yonsei University, Seoul, Korea 114

P-23 Paracrine effect of melanogenesis by increased expression of stem cell factor andendothelin-1 in Keratinocytes via direct PAR-2 activation

Hyojung Sohn, Ji Young Kim, Dae Suk Kim, Sang Ho OhDepartment of Dermatology and Cutaneous Biology Research Institute, Yonsei University College of Medicine,

Seoul, Korea 115

P-24 Effect of ectopic expression of tyrosinase on wound healingMi Yoon Kim1, Dae-Kyoung Choi1, Kyung-Cheol Sohn1, Dongkyun Hong1, Myung Im1,Young Lee1, Chang Deok Kim1, Young-Joon Seo1, Tae-Jin Yoon2 and Jeung-Hoon Lee1

1Department of Dermatology and Research Institute for Medical Sciences, School of Medicine, Chungnam

National University, Daejeon; 2Department of Dermatology and Institute of Health Sciences, School of Medicine,

Gyeongsang National University, Jinju, Korea 116

P-25 Quantitative proteomics profiling of HaCaT cells after stimulation with estrogenJung U Shin, Yun Sun Lee, Heran Kim, Jihun Park, Ju Hee Lee, and Kwang Hoon LeeDepartment of Dermatology, Cutaneous Biology Research Institute, Yonsei University College of Medicine,

Seoul, Korea 117

P-26 Role of HMGB1 on lipid production in human sebocytesHyuk Chul Kwon, Kyung-Cheol Sohn, Hae-Eul Lee, Young Lee, Chang Deok Kim,Young-Joon Seo, Jeung-Hoon Lee, Myung Im

Department of Dermatology, School of Medicine, Chungnam National University, Daejeon, Korea 118

P-27 Increased Expression of hypoxia-glycolysis-acidosis sequence related proteins: An importantrole in keloid pathogenesis

Zhenlong Zheng, Junjie Piao, Hye Rang On, Kee Yang Chung, Mi Ryung RohDepartment of Dermatology and Cutaneous Biology Research Institute, Yonsei University College of Medicine,

Seoul, Korea 119

P-28 Decreased Tissue and Serum Expression of Galectin-7 in Patients with Hypertrophic ScarsSung Bin Cho1, Jun-Sub Kim2, Zhenlong Zheng1, Min Ju Choi1, Ihn Geun Choi3,Hong Shik Oh4 and Keun Jae Ahn3,4

1Department of Dermatology and Cutaneous Biology Research Institute, Yonsei University College of Medicine,

Seoul, Korea; 2Department of Biotechnology, Korea National University of Transportation, Chungju, Korea,3Specialization Research Center, Hallym University Burn Institute, Hangang Sacred Heart Hospital, Hallym

University, Seoul, Korea; 4Department of Science Education, Jeju National University, Jeju, Korea 120

P-29 Investigation on animal models for acne vulgarisSang Lim Kim, Jin Sub Lee, Yoon Hyuk Choi, Yong Hyun Jang, Hyun Ho Son, Mi Yeung Sohn,

Seok-Jong Lee, Do Won Kim, Weon Ju Lee

Department of Dermatology, Kyungpook National University School of Medicine 121

P-30 Utility of eosinophil cationic protein levels in early diagnosis of intrinsic atopic dermatitisSong Youn Park, MD

1, Sohee Oh, PhD

2, EunJi Kim, MD

1, So Young Yoon, MD

1,

Hyun Sun Park, MD1, Hyun-Sun Yoon, MD, PhD1, Soyun Cho MD, PhD1

1Department of Dermatology, 2Department of Biostatistics, Seoul National University Boramae Hospital, Seoul,

Korea 122P-31 Clinical manifestations and skin barrier properties of Korean male patients with X-linked

recessive ichthyosis diagnosed by FISH analysis to detect STS deletionNoo Ri Lee, Bo-Kyung Kim, Na Young Yoon, Minyoung Jung, Eung Ho Choi

Department of Dermatology, Yonsei University Wonju College of Medicine, Wonju, Korea 123

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Invited Lectures 1

The 23rd

Annual Meeting of the Korean Society for

Investigative Dermatology

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Invited Lectures 1

Education:

1974-1980 M.D., Yonsei University College of Medicine, Seoul

1981-1982 M.S. in Medical Science: Yonsei University College of Medicine, Seoul

1983-1985 Completion of Ph.D. course in Medical science: Yonsei University College of Medicine,

Seoul

1991-1992 Ph.D. in Medical science: Yonsei University College of Medicine, Seoul

Thesis: Effect of glucocorticoid in the development of murine intestine

Supervisor: Professor Yoo-Bock Lee

Postdoctoral Training:

1980-2/1981 Rotating Internship, Yonsei University Severance Hospital, Seoul,

3/1981-1983 Resident, Department of Pathology, Yonsei University Severance Hospital, Seoul

Faculty Academic Appointment:

1984-1987 Instructor, Department of Pathology, Hanyang University College of Medicine, Seoul

1987-1993 Assistant Professor, Department of Pathology, Hanyang University College of Medicine,

Seoul

1994-1995 Associate professor, Department of Pathology, Hanyang University College of Medicine,

Seoul

1997-present Professor, Department of Pathology, Samsung Medical Center, Sungkyunkwan University

School of Medicine, Seoul

Appointment at Hospital:

03/1984-02/1995 Faculty, Department of Pathology, Hanyang University Hospital, Seoul

03/1995- Faculty, Department of Pathology, Samsung Medical Center, Seoul

09/2008- Chairperson, Department of Pathology, Samsung Medical Center, Seoul

09/2008- Director, Biobank, Samsung Medical Center

Other professional position

2012- Consultant, Samsung Advanced Institute of Technology

Young-Hyeh Ko, M.D., Ph.D.Department of Pathology, Samsung Medical Center, Sungkyunkwan University,

Seoul, Korea

CURRICULUM VITAE

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The 23rd Annual Meeting of the Korean Society for Investigative Dermatology

Societies including elected positions:

The Korean Society of Pathologists

Councillor, 2008-

Chairperson, Scientific Committee, 1998-2002

Chairperson, Publishing Committee, 2008-

Secretary General, Hematopathology Study Group, 1995-2010

Vice president, 2013-

The Korean Society of Cytopathology

Councillor, 2002-

The Korean Society of Hematology

Member, Steering Committee of Lymphoma Working Group

The International Academy of Pathologists

Convener the 7th Asia-pacific IAP, May 20-24, 2011, Taipei, Taiwan

The European Association of Hematopathology

Member, 1998-

Workshop Panel and Session Chair, XVI Meeting of EAHP, 2012

Society of International Lymphoma Study Group

Member, 2012-

Scholarly Service

2002- Editorial board, The Korean Journal of Pathology

2004-2010 Editorial board, The Korean Journal of Cytopathology

2008 - Editorial board, Journal of Hematopathology (ISSN 1865-5785)

2009- Pathology review panel for International T-cell Project ([email protected])

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Invited Lectures 1

EBV-associated T or NK cell lymphoproliferative diseases encompass several disease entities with

diverse clinical and pathologic findings. In the World Health Organization (WHO) classification,

aggressive NK cell leukemia (ANKL) and extranodal NK/T cell lymphoma (ENKTCL) have been

described as a prototype of EBV-positive NK/T cell neoplasm. In addition to ANKL and ENKTCL,

the Epstein-Barr virus (EBV) infected in T or NK cells can cause indolent or severe disease depending

on the immunological response of the individual. The term “T/NK cell chronic active EBV infection”

has been used in the literature to encompass a very broad spectrum of diseases, including a systemic

form that may be polyclonal, fulminant systemic EBV-positive T cell LPDs that are clonal, hydroa

vacciniforme (HV) of T cell derivation, and severe mosquito bite allergy usually of NK cell origin.

Among these, systemic EBV-positive T cell LPD of childhood (a clonal T cell LPD) and hydroa

vacciniforme-like T cell lymphoma are recognized and considered as neoplasm by the 2008 WHO

classification. However, there is significant overlapping of clinical and pathologic finding between

entities recognized by the 2008 WHO classification. Distinction between benign and malignant was

sometimes ambiguous in chronic active EBV infection and in clonal or atypical T-cell proliferations

in the setting of infectious mononucleosis. Alternative approach to the current classification of EBV-

positive T/NK LPD is required. This lecture would present spectrum of EBV-positive T/NK cell

LPD, the rationale for using the diagnostic terminology, and discuss selected cases as examples of

each diagnosis.

EBV-associated T/ NK cell diseases,

from indolent to aggressive proliferations

Young Hyeh Ko, M.D.

Department of Pathology, Samsung Medical Center, Sungkyunkwan University, Seoul, Korea

IL-1

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Education:

1978 Hokkaido University School of Medicine, Graduate

Career:

1978 Resident, Hamamatsu University School of Medicine

1979 Assistant Professor, Department of Dermatology,HamamatsuUniversity School ofMedicine

1984-85 Visiting Research Fellow, Hopital Ed-Herriot, Lyon (Prof. Jean Thivolet)

1991 Lecturer, Hamamatsu University School of Medicine

1992 Lecturer, Department of Dermatology, FukushimaMedical University School of Medicine

Professor and Chairman, Department of Dermatology, Okayama University School of

Medicine, Dentistry and Pharmaceutical Sciences

2011 Vice Director, Okayama University Hospital

Research Interest:

Cutaneous lymphoma, Autoimmune blistering diseases,

Collagen diseases, Oncogenic viruses,

Viral and bacterial infections

Keiji Iwatsuki, M.D., Ph.D.Department of Dermatology, Okayama University Graduate School of Medicine,

Dentistry and Pharmaceutical Sciences, Okayama, Japan

CURRICULUM VITAE

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Invited Lectures 1

Human papilloma virus-associated warts (HPV-warts) and molluscum contagiosum (MC) are

persistent, evading host immune surveillance. However, those lesions sometimes disappear spontane-

ously, following inflammation. To elucidate the immune evasion mechanisms of HPV and MC poxvirus

(MCV), we have examined the immunological and structural milieu of HPV-warts, HPV-Bowen

disease and MC, and the expression of MCV-encoded immunoregulatory genes.

The expression of various dendritic cell (DC) markers, MIP-3 , E-cadherin, and thymic stromalα

lymphopoietin (TSLP) was evaluated by immunohistochemistry. MIP-3 gene expression levelsα

were examined by in situ hybridization (ISH) and real-time quantitative polymerase chain reaction

(RT-qPCR). Apoptotic signals in HPV- and MCV-infected keratinocytes were examined by TUNEL

method. HPV infection patterns in HPV-Bowen disease were analyzed by APOT assay. After MCV

genotyping, we studied the expression of MCV-encoded gene products such as MC148mRNA, or

an antagonist for CCR8, and MC159mRNA, or a viral FLICE-inhibitory protein (vFLIP).

The numbers of CD1a+ or Langerin+ epidermal Langerhans cells (LCs), and the expression levels

of MIP-3 were markedly decreased in both HPV-warts and MC. The MIP-3 expression reappearedα α

in inflammatory HPV-warts, associated with dermal infiltrates composed of many cytotoxic T cells

and various subsets of DCs including Langerin+, DC-LAMP+, CD83+ DCs, and the lesser number

of CD123+ plasmacytoid DCs. By contrast, cellular infiltrates in HPV-Bowen disease contained

many B cells and plasma cells with sparse infiltration of DCs. The expression of TSLP was enhanced

in the lesional epidermis of HPV-warts and HPV-Bowen disease, whereas the expression was

induced locally in MC. All 14 MC samples examined harbored MCV type 1. Of the 14 samples,

MC148mRNA and MC159 mRNA was detected in all and 13 samples, respectively. No apoptotic

signals were observed in vacuolated cells in HPV-warts and molluscum bodies. TLR3 was expressed

by the lesional keratinocytes even in the non-inflamed HPV-warts and MC, associated with the

expression of type 1 interferons (IFNs).

HPV-warts and MC are protected from host immune responses and apoptotic signals because

they are surrounded by LC-depleted epidermal walls, and viral anti-apoptotic molecules. The up-

regulation of epidermal TLR3 signaling as well as type 1 IFNs might inhibit further viral spreading.

Remodeling of the cutaneous immune system

and structures during viral infections

Keiji Iwatsuki,M.D., Ph.D.

Department of Dermatology, Okayama University Graduate School of Medicine,

Dentistry and Pharmaceutical Sciences, Okayama, Japan

IL-2

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Education:

1988-1992 B.Sc. KyungpookNational University, Korea.

1993-1996 Ph.D. Imperial College, University of London, UK

Research Training

1996-1996 Post-doctoral fellow, University of Cambridge, UK

1996-2001 Post-doctoral fellow, The Johns Hopkins University School of Medicine, USA

Professional Experience

2001-2004 Research Professor, Biomolecular EngineeringCenter, KyungpookNational University,

Korea.

2004-2006 Assistant Professor, Bio-Medical Research Institute, Kyungpook National University

Hospital, Korea.

2006-2008 Assistant Professor, School of Medicine, Kyungpook National University, Korea

2008-present Associate professor, School of Medicine, Kyungpook National University, Korea

Memberships:

2006- Korean Society for Molecular and Cellular Biology

2006- Korean Society for Biochemistry andMolecular Biology

2011- Korean Tissue Engineering and Regenerative Medicine Society

2011- Korean Hair Research Society

2012- Tissue Engineering and RegenerativeMedicine International Society

Major research field

Hair follicle neogenesis (Cell therapy of hair loss), Mechanisms of hair loss and hair growth

Young Kwan Sung, Ph.D.Associate Professor, Department of Immunology and Hair Research Center,

School of Medicine, Kyungpook National University, Daegu, Korea

CURRICULUM VITAE

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Invited Lectures 1

Neogenesis of the hair follicle through cell implantation is a promising alternative for the treatment

of hair loss and is believed to depend significantly on the ability to reproducibly expand hair-

inductive dermal cells in vitro. There have been many attempts at neogenesis of hair follicles by

transplantation of cultured dermal cells. However, the hair-inductive capacities (trichogenicity) of

cultured dermal cells are lost during in vitro cultivation. Therefore, to achieve successful hair follicle

neogenesis, identification of cell culture supplements and/or culture conditions that enable dermal

cells to maintain trichogenicity is an important matter. In this lecture, I will discuss a few hair

reconstitution assays used to evaluate the trichogenicity of cultured dermal cells. I will also review

recent studies on the preservation of trichogenicity of cultured dermal cells. In addition, I will show

our recent data of maintenance/enhancement of trichogenicity by treatment with cell conditioned

media and small chemical compounds and by three dimensional spheroid cultivation.

Generation of new hair follicles by cell transplantation

Young Kwan Sung

Department of Immunology, School of Medicine, Kyungpook National University, Daegu, Korea

IL-3

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Education and professional training:

1982 MD, Juntendo University, School of Medicine, Tokyo

1986 Board certified dermatologist, Japanese Dermatological Association

1987 PhD, Juntendo University, Graduate School of Medicine, Tokyo

1993-95 Postdoctoral fellow, Department of Dermatology, UCSF, San Francisco, CA, USA

1995-96 Research associate professor, ibid

Professional background

1987-93 Lecturer, Department of Dermatology, Juntendo University, School of Medicine, Tokyo

1995-2002 Assistant professor, ibid

2002-04 Associate professor, ibid

2004- Professor and chair, ibid, and Department of Dermatology and Allergology, Juntendo

University Graduate School of Medicine,

2006- Vice director, Atopy (allergy) Research Center, Juntendo University Graduate School of

Medicine

Research fields

Keratinizing and bullous disorders (including psoriasis), Hair disorders, Medical mycology, Atopic

dermatitis

Awards

1993 Research Fellowship, Dermatology Foundation, USA

2000 Basic Medical Science-Shiseido award, Japanese Dermatological Association

Shigaku Ikeda, M.D., Ph.D.Department of Dermatology and Allergology,

Juntendo University Graduate School of Medicine, Tokyo, Japan

CURRICULUM VITAE

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Invited Lectures 1

Darier disease (DD) and Hailey Hailey disease (HHD) are classical genodermatoses, in which

mutations in the genes encoding calcium pumps are found to be responsible for the formation

of skin lesions. The genes responsible for DD and HHD are symbolized as ATP2A2 and ATP2C1

respectively. The pathomechanism underlying both diseases is assumed to be haploinsufficiency.

Because increased gene expression from intact alleles in both diseases is thought to help normali-

zation of lesional skin in the patients, we examined the regulation mechanisms in expression of

both genes by 1) 5’-RACE, 2) luciferase assay, 3) gel shift assay, 4) CHIP assay, 5) siRNA inter-

ference assay, and 6) cell culture and gene expression analysis.

We further analyzed the ameliorating effects of several types of drugs such as steroid, retinoid,

tacrolimus, and COX-2 inhibitors on the suppression of expression of both the genes by UVB

irradiation of cultured normal human keratinocytes.

These findings may provide novel therapeutic modalities for the treatment of both the diseases.

Regulation mechanisms in gene expression of

ATP2A2 and ATP2C1 (responsible for Darier disease

and Hailey-Hailey disease respectively)

Shigaku Ikeda

Department of Dermatology and Allergology, Juntendo University Graduate School of Medicine, Tokyo, Japan

IL-4

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The 23rd



Invited Lectures 2

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Invited Lectures 2

Education:

1983. 2 Seoul National University College of Medicine, Ph.D. (Pathology)

1979. 2 Seoul National University College of Medicine, M.S. (Pathology)

1975. 2 Seoul National University College of Medicine, M.D.

Professional Background

2012- Director of Transplantation Research Institute, MRC, Seoul National University

2004-2006 President of Center for Animal Resource Development, Seoul National University

2002-2006 Chair of the Graduate Program of Immunology, Seoul National University College

of Medicine

2000-2004 Chair of the Department of Pathology, Seoul National University College of Medicine,

and Director of the Department of Pathology, Seoul National University Hospital

2000-2001 Vice President and President of Korean Society of Immunology

1988 Assistant Professor of Seoul National University College of Medicine

1985-1987 Research Fellow of Harvard University Dana-Farber Cancer Institute

Awards

2001 National Academy of Science Award

1999 Emil von Behring Medical Award

1976 Pfizer Medical Research Award

Seong Hoe ParkProfessor of Medicine, Department of Pathology,

Seoul National University College of Medicine, Seoul, Korea

CURRICULUM VITAE

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Induction of antigen-specific T cell tolerance would aid treatment of diverse immunological

disorders and help prevent graft rejection and autoimmune disease. We developed an antibody

ligating a particular epitope on ICAM-1. Antibody-mediated ligation of ICAM-1 on dendritic cells

(DCs) led to the arrest of DCs in a semimature stage in vitro and in vivo. In islet xenograft model

of humanized mice, antigen-specific T cell tolerance was induced by administration of this

antibody, while T cell responses to unrelated antigens remained unaffected. The induction of T

cell tolerance was also achieved in non-human primates and we establish a protocol of allowing

long term survival of islet xenograft and allograft in diabetic Rhesus monkeys. Thus, in situ

induction of DC-mediated T cell tolerance using this method may represent a potent therapeutic

tool for preventing graft rejection including hair follicle graft. Furthermore, we will test the

therapeutic effect of MD-3 on autoimmune disease.

Induction of antigen-specific T cell tolerance and its

application to a variety of immunologic disorders

Seong Hoe Park

Department of Pathology & Transplantation Research Institute, Seoul National University College of Medicine

Seoul, Korea

IL-5

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Invited Lectures 2

Education and Training

1982 M.D., Hamamatsu University School of Medicine

1982 Resident, Department of Dermatology, Hamamatsu University School of medicine

1984 Instructor, Department of Dermatology, Hamamatsu University School of Medicine

1988 Ph.D., Hamamatsu University School of Medicine

1989 Visiting Researcher, Department of Dermatology, Yale University School of Medicine

Appointments

1992 Assistant Professor, Department of Dermatology, HamamatsuUniversity School ofMedicine

2000 Associate Professor, Department ofDermatology,HamamatsuUniversity School ofMedicine

2002 Professor and Chairman, Department of Dermatology, University of Occupational and

Environmental Health

2011 Professor and Chairman, Department of Dermatology, Hamamatsu University School of

Medicine

Society members

President: Japanese Society for Investigative Dermatology (JSID) 2008-2011

Board of Directors: Japanese Society for Dermatoallergology and Contact Dermatitis, Japanese

Skin Cancer Society, Japanese Society for Photomedicine and Photobiology (JSPP), Japanese

Committee for Sunlight Protection

Journal Editors

Journal of Dermatological Science, Editor-in-Chief Elect (May, 2013)

The Journal of Dermatology, Editor-in-Chief (-March, 2013)

Journal of Dermatological Science, Editorial Board

Experimental Dermatology, Editorial Board

Awards and Honors

JSPP Award (1999)

Visiting Professor, Department of Dermatology, Yale University School of Medicine (1999)

JSID Award (2001)

Current Research Activities

Immunology/Allergology, Photobiology, Cutaneous lymphomas

Yoshiki Tokura, M.D., Ph.D.Professor and Chairman, Department of Dermatology,

Hamamatsu University School of Medicine, Hamamatsu, Japan

CURRICULUM VITAE

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Th17-derived cytokines, IL-17A and IL-22, induce the production of antimicrobial peptides

(AMPs), human -defensin 2β (HBD-2) and cathelicidin, by keratinocytes. The close association of

IL-17 (and IL-22) with AMP production is seen in two different diseases, psoriasis and adult T

cell leukemia/lymphoma (ATLL).

It is well known that cathelicidin LL-37 play an important role as both an AMP and as an auto-

inflammatory mediator in psoriasis. Vitamin D3 (VitD3) analogues, widely used as topical applicants

for psoriasis, may modify the LL-37 production by IL-17A/IL-22-stimulated keratinocytes.

Cultivation of normal human epidermal keratinocytes (NHEKs) with IL-17A and IL-22 remarkably

increased LL-37 mRNA expression, and further addition of calcipotriol markedly enhanced the

IL-17A/IL-22-augmented expression of LL-37 in a dose-dependent manner. As to IL-8, the addition

of IL-17A and IL-22 markedly augmented its mRNA expression. On the contrary, calcipotriol

depressed the IL-17A/IL-22-enhanced IL-8 mRNA expression. When the culture supernatants were

measured for the concentration of LL-37, the extracellular production of cathelicidin LL-37 was

inhibited by calcipotriol in IL-17A/IL-22-stimulated NHEKs. Immunofluorescence microscopy

revealed that the overproduced cathelicidin LL-37 by calcipotriol resided within the cells. LL-37

has opposite aspects in the pathogenesis of psoriasis. LL-37 promotes psoriasis via interaction with

extracellular DNA, but it may suppress psoriasis by interfering cytosolic DNA. In this scenario,

the action of calcipotriol to increase intracellular cathelicidin LL-37 but rather to decrease extracellular

cathelicidin LL-37 is likely beneficial for the treatment of psoriasis.

Adult T cell leukemia/lymphoma (ATLL) is a malignancy of mature CD4+CD25+ T cells caused

by HTLV-1. Superficial dermatophytosis is quite common in ATLL patients, as approximately 50%

of the ATLL patients have tinea pedis/unguium/corporis, candidiasis and other cutaneous mycotic

infection. The frequencies of circulating CD4+CD25+ T cells and Th17 cells were inversely correlated

in ATLL patients. Whereas peripheral Th17 cells were significantly decreased, serum IL-10 and

TGF- 1 were increased in ATLL as compared to healthy controls. Furthermore, ATLL patientsβ

with dermatophytosis had higher IL-10 and TGF- 1 levels and lower IL-17 levels than did thoseβ

without dermatophytosis. Immunohistochemical study revealed that the epidermal expression of

both HBD-2 and LL-37 were significantly lower in ATLL patients with dermatophytosis than in

non-ATLL patients with dermatophytosis or healthy controls. Thus, the Th17-enhanced expression

of AMPs in keratinocytes is decreased in ATLL patients, leading to the perturbed innate immunity

and frequent occurrence of superficial dermatophytosis.

Effects of Th17-derived cytokines on keratinocyte

production of antimicrobial peptides in psoriasis

and adult T cell leukemia / lymphoma

Yoshiki Tokura, M.D., Ph.D.

Department of Dermatology, Hamamatsu University School of Medicine, Japan

IL-6

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Invited Lectures 2

Education:

1980-1984 MA, A.B., Harvard College, Cambridge

1984-1991 M.D., Harvard Medical School, Cambridge, MA

1986-1989 Ph.D., Dept. of Biochemistry, Univ. Basel (Switzerland)

Postgraduate Training and Fellowship Appointments:

1991-1992 Department of Internal Medicine, Brigham and Women's Hospital, Harvard

Medical School, MA

1992-1995 Resident, Department of Dermatology, Univ. of California (San Francisco) School

of Medicine, CA

1994-1997 Howard Hughes Physician Fellow, Department of Anatomy/Program in Immunology,

UCSF School of Medicine, CA

Faculty Appointments:

1995-1997 Clinical Instructor, Department of Dermatology, UCSF, CA

1997-2008 Senior (tenured) Investigator, Dermatology Branch, Center for Cancer Research,

National Cancer Institute, National Institutes of Health, Bethesda, MD

2009-Present Chair and Professor of Dermatology (Effective 12/1/2008), Medical College of

Wisconsin, Milwaukee, WI

Hospital Staff Privileges:

1994-1995 Dept. of Dermatology, Staff Attending, San Francisco General Hospital, CA

1995-1997 Staff Physician, Dept. of Dermatology, Univ. California San Francisco, CA

1997-2008 Clinical Center, National Institutes of Health, MD

2009-Present Froedtert Memorial Lutheran Hospital, Milwaukee, WI

2009-Present Milwaukee Veteran's Administration Hospital, Milwaukee, WI

Samuel Tzen-yue Hwang, M.D., Ph.D.Chair and Professor, Department of Dermatology,

Medical College of Wisconsin, USA

CURRICULUM VITAE

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Murine models of cancer have markedly advanced our knowledge of many human cancers, but

mouse models of CTCL have been lacking. Several murine models of CTCL will be described in

this presentation along with their corresponding advantages and disadvantages. Because the

inflammatory microenvironment likely plays a role in the pathogenesis of CTCL, including mycosis

fungoides, we have sought to develop a murine skin T cell lymphoma model in which inflam-

mation is a critical regulator of tumorigenesis. To this end, we have developed a model in which

MBL2 T lymphoma cells are injected into the ear skin of syngeneic C57BL/6 mice. In the absence

of topical application of di-nitro-fluorobenzene (a well known contact allergen), no tumor formation

is observed and the MBL2 cells gradually die. With a single topical application of DNFB, however,

immediately after MBL2 implantation, high grade tumors develop in the ear skin within 14-20

days. Several known topical treatments for early stage MF (specifically, corticosteroids and imiquimod)

block tumor development in this model. Using this model, we have found a requirement for

macrophages and have identified cytokine expression pathways that are expressed early during

tumorigenesis. This murine model of CTCL, albeit having its own limitations, is simple, highly

reproducible, and bears similarities to plaque/tumor development in humans with CTCL. This

model may be a convenient means to identify novel agents that will improve therapy for CTCL.

What we can learn from murine models of

cutaneous T cell lymphoma

Sam T. Hwang, M.D., Ph.D.

Chair and Professor, Department of Dermatology, Medical College of Wisconsin, USA

IL-7

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The 23rd



Invited Lectures 3

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Invited Lectures 3

Education:

1979-1985 Keio University School of Medicine (MD)

1985-1989 Department of Dermatology and Molecular Biology, Keio University, Graduate

School of Medicine (PhD)

Fellowship Appointments:

1989-1992 Visiting research fellow, Dermatology Branch (John R. Stanley’s lab), National Cancer

Institute, National Institutes of Health

Faculty Appointments:

1996-2005 Assistant Professor, Department of Dermatology, Keio University School of Medicine

2005- Professor and Chair, Department of Dermatology, Keio University School of

Medicine

2007- Vice Director, Keio University Hospital

Awards and Honors:

1991 The Minami Prize from Japanese Dermatological Association

2000 The JSID Award from Japanese Society for Investigative Dermatology

2002 AlfredMarchionini Award at World Congress of Dermatology, Paris

2002 Morris H. Samitz Lecture from University of Pennsylvania, Department of Dermatology

2003 William Montagna Lectureship Award from the Society for Investigative Dermatology

2005 CE.R.I.E.S. Research Award

2006 JSPS Prize from Japan Society for the Promotion of Science

2006 JSI Award from Japanese Society for Immunology

2010 Honorary Membership of the Austrian Society of Dermatology and Venereology

2012 Wälz Prize

Masayuki Amagai, M.D., Ph.D.Professor and Chair, Department of Dermatology, Keio University School of Medicine,

Tokyo, Japan

CURRICULUM VITAE

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Classic atopic dermatitis is complicated by asthma, allergic rhinitis, and food allergies, cumulatively

referred to as atopic diseases. Recent discoveries of mutations in the filaggrin gene as predisposing

factors for atopic diseases have refocused investigators’ attention on epidermal barrier dysfunction

as a causative mechanism. The three musketeers of the epidermal barrier are as follows: the stratum

corneum (air-liquid barrier), tight junctions (liquid-liquid barrier), and the Langerhans cell network

(immunological barrier). Clarification of the molecular events underpinning epidermal barrier

function and dysfunction should lead to a better understanding of the pathophysiological mechanisms

of atopic diseases.

To evaluate the impact of filaggrin deficiency on skin barrier function, we generated filaggrin

knockout (KO) mice. Filaggrin KO mice exhibited dry and scaly skin, but did not develop any

spontaneous dermatitis. Despite of prominent decrease in NMF, water content and transepidermal

water loss (TEWL) in SC of filaggrin KO mice was unaffected. Permeability assay using calcein-

encapsulating liposomes demonstrated that filaggrin-deficiency allows its penetration through SC.

This impairment in SC barrier appears to be a consequence of increased fragility and premature

detachment of cornified layers. Barrier defect in filaggrin KO mice led to enhanced hapten-induced

contact hypersensitivity responses and humoral responses to topically immunized protein antigens.

Using 3D visualization method of epidermal TJs in mouse ear skin, we demonstrated that activated

Langerhans cells (LC) extend their dendrites beyond tight junctions (TJ) to capture external antigens.

To demonstrate pathophysiological relevance of this percutaneous antigen capture, we took

advantage of a model for staphylococcal scaled skin syndrome (SSSS), a severe blistering disease

caused by skin infection of exfoliative toxin (ET)-producing Staphylococcus aureus. Patch-immuni-

zation of ET did not affect epidermal integrity of immunization site, but led to ET-specific IgG1

production, indicating that antigen uptake by LCs via tight junctions had taken place. Strikingly,

in contrast to control mice that developed SSSS upon intraperitoneal ET challenge, mice that were

patch-immunized with ET were protected from disease. Mice that were depleted of LCs prior to

immunization failed to elicit anti-ET IgG1 and developed SSSS upon challenge. Percutaneous humoral

responses elicited by LCs highlight an efficient mechanism by which immunity to potentially

pathogenic skin-surface microbes is provided without disrupting tight junction barriers, and

demonstrate an important role for LCs in host defense in vivo.

The three musketeers of the epidermal barrier and

cutaneous sensitization to external antigens

Masayuki Amagai

Department of Dermatology, Keio University School of Medicine

IL-8

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Invited Lectures 3

Research Interests

1. Mechanisms underlying synapse formation with focus on synaptic adhesion, spine morphogenesis,

and structural and functional synaptic plasticity.

2. Association of synaptic proteins with various neuropsychiatric disorders including autism

spectrum disorders, ADHD, schizophrenia, and intellectual disability.

Educational Background

1982. 3-1986. 2 B.S., Dept of Pharmacology, Busan National University, Korea.

1986. 3-1988. 2 M.S., Dept of Biological Engineering, Korea Advanced Institute of Science and

Technology (KAIST), Korea.

Advisor: Moo Young Pack, Ph.D.

1991. 9-1994.12 Ph.D., Dept of Pharmacology and Toxicology, Michigan State University.

Advisor: James L. Bennett, Ph.D.

Professional Career

1988. 3-1991. 8 Research Associate, Korea Research Institute of Bioscience and Biotechnology,

Daejeon, Korea

1995. 1-1997. 2 Postdoc, Dept of Neurobiology and Howard Hughes Medical Institute,

Harvard Medical School

P.I.: Morgan Sheng

1997. 3-2000. 2 Assistant Professor, Dept of Pharmacology, Busan National University, Korea.

2000. 3-present Assistant, Associate, & Full Professor, Dept of Biol. Sci., KAIST, Korea.

2003. 7-2012. 5 Director, National Creative Research Initiative Center for Synaptogenesis,

Korea

2012. 6-present Director, Center for Synaptic Brain Dysfunctions, Institute for Basic Science

(IBS), KAIST, Korea

Honors and awards

2012 Inchon Award, Dong-A Ilbo

2012 Life Science Award, Korean Society for Molecular and Cell Biology

Eunjoon KimDirector, Center for Synaptic BrainDysfunctions, Institute for Basic Science (IBS), andProfessor,

Department of Biological Sciences, KoreaAdvanced Institite of Science and Technology (KAIST)

CURRICULUM VITAE

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2011 Chair Professor, KAIST

2011 Best Research Award, KAIST.

2010 Member, Korean National Academy of Sciences.

2005 BPS Award, Korean BioPharmacal Society.

2004 Young Investigator Award, Korean Ministry of Science and Technology.

2003 Academic Award, KAIST.

1991 Governmental Fellowship for Studies Abroad, Korean Ministry of Education.

Editorial board

2012-present eLife (a new open access journal, sponsored by HHMI, Welcome Trust and the

Max Planck Society)

2012-present Experimental Neurobiology

2012-present Molecules and Cells

2009-present Neurosignals

2008-present Molecular Brain

2007-present Frontiers in Molecular Neuroscience

2006-2009 Journal of Biochemistry

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Invited Lectures 3

Understanding the mechanisms underlying brain functions is the ultimate challenge in neuro-

science research. A potential way to get closer to this seemingly unreachable goal would be to

take a reductionist approach. That is to split complex brain functions into the simplest possible

units, for which synaptic transmission would be a strong candidate. Neuronal synapses, where

synaptic transmission occurs, however, are formed and regulated by a large number of synaptic

proteins, ranging from hundreds to thousands. Deciphering detailed functions of these proteins

would be a daunting task. However, some of the synaptic proteins would be more important than

the others, and their defects would cause significant abnormalities in neural circuits and brain

functions, which has been termed “synaptopathy”. Synaptopathies are thought to underlie diverse

neuropsychiatric disorders including schizophrenia, attention deficit/hyperactivity disorder,

intellectual disability, autism, and emotional disturbances. Exploring disease-causing mechanisms

along the hierarchy of synaptopathies is another main challenge in neuroscience. Luckily, however,

animal models including transgenic mice carrying human mutations are providing important clues

to synaptopathies. These key mechanisms will help us better diagnose and treat mental illnesses,

and eventually understand higher brain functions that lie on the flip sides of mental illnesses,

including consciousness, attention, intellect, sociability, and emotion.

Molecular organization of synaptic junctions

Eunjoon Kim

Department of Biological Sciences, KAIST, Korea

IL-9

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The 23rd



Invited Lectures 4

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Invited Lectures 4

Education:

1986 M.D. The Catholic University of Korea, College of Medicine

1997 Ph.D. Temple University, U.S.A.

Major Activities:

Academic & Governmental (Present)

Professor, Chairman, Dept. of Medical Lifescience, Catholic University of Korea

Director, Catholic High-Performance Cell Therapy Center

Director, Center for Evaluation of Stem Cell Therapeutics (Korean FDA)

President-Elect, Korean Society of Stem Cell Research

Representative Special, Korean Society of Blood and Marrow

Representative, National Center for Bioethics Policy of Korea

Drug Evaluation Committee for Korean Food & Drug Administration

Executive Committee for Health Technology Planning, Ministry of Health and Welfare, Korea

Editorial Appointment (Present)

Editorial Board, "Stem Cells"

Associate Editor, "International Journal of Hematology"

Associate Editor, "Korean J. of Hematology"

Editorial Writer (invited) for Mai-Kyung Daily News paper (present-)

Honors and Awards:

2007 Excellent Research Performance (Ministry of Science & Technology)

2009 Outstanding Contribution to Health Technology (Minister of Health & Welfare)

2010 Award for Mythics of Life (Archidiocese of Seoul, Korea)

Il-Hoan Oh, M.D., Ph.D.Director, Catholic High-Performance Cell Therapy Center,

The Catholic University of Korea, College of Medicine, Seoul, Korea

CURRICULUM VITAE

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Stem cell-based regeneration of diseased organs constitutes an integral part of regenerative

medicine emerging as new alternatives to treat intractable diseases. With promise for creating

future biotechnological values as well as for use in the regenerative medicine, the research and

development on stem cell therapies are being actively promoted with coordinated efforts from

multi-ministry program of Korean government. These efforts included a total coordination of the

pipe-line for stem cell therapeutics, which included basic, translational and clinical studies in the

various area of medical conditions. In particular, clinical studies to evaluate the safety and efficacy

of stem cell therapeutics have rapidly increased over past decades, mostly in the era of adult stem

cells. While traditional stem cell therapy have been mostly performed utilizing hematopoietic stem

cells for reconstitution of myeloid and immune reconstitution, recent clinical cell therapies have

grown up mostly for cell therapeutic utilization of mesenchymal stromal cells (MSCs) to facilitate

regeneration of cardiovascular system, bone and cartilage, gastro-intestinal tracts as well as to

suppress immune reactions such as graft vs. host disease or auto-immune disease. Promising

results have been obtained for safety issues out of such clinical trials, revealing a feasibility of

cell therapies using cells produced in most of industrial settings. However, accumulating experiences

in a variety of cell therapeutic trials now point that recent cell therapeutic development in the

area of MSCs needs to be further improved in their therapeutic efficacy to be able to become more

meaningful therapeutic modalities.

On the other hand, stem cell-based therapies utilizing induced pluripotent stem cells (iPS), although

mostly at the stages of basic study level, are being actively developed for clinical applications.

In addition, reprogramming of somatic cells for direct conversion of desired tissue type cells are

emerging as a new alternative to enhance the therapeutic efficacy of stem cell therapies. Further

studies on the basic and translational areas of stem cell research will shed light on the stem

cell-based therapeutic approaches and bring up fruitful outcomes for patients in the difficult

conditions.

Current Trends of Stem Cell Research,

Where Are We?

Il-Hoan Oh, M.D., Ph.D.

Director, Center for Evaluation of Stem Cell Therapeutics, The Catholic University of Korea, College of Medicine,

Seoul, Korea

IL-10

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Invited Lectures 4

Education:

Graduate

1986-1992 Seoul National University, College of Medicine, Seoul, Korea

Postgraduate training and education:

1992 Degree: M.D.

1992-1993 Internship, Seoul National University Hospital

1993-1997 Resident, Department of Dermatology, Seoul National University Hospital

1997 Dermatology Board

1998-2000 Chief, Department of Dermatology, Seoul District Army Hospital

2000-2003 Ph.D., Seoul National University, College of Medicine

2002-2007 Assistant Professor, Department of Dermatology, Samsung Medical Center,

Sungkyunkwan University School of Medicine, Seoul

2004 Diplomate, International Board of Dermatopathology

2006-2008 Visiting scholar, Department of Dermatology, UCSD, San Diego, CA, USA

2007-present Associate Professor, Department of Dermatology, Samsung Medical Center,

Sungkyunkwan University School of Medicine, Seoul

Member in Academic Society:

Korean Society for Investigative Dermatology

Korean Dermatopathology Society

Korean Hair Research Society

Korean Vitiligo Society

Society for Investigative Dermatology

American Academy of Dermatology

Council for Nail Disorders

American Society of Dermatopathology

International Society of Dermatopathology

Invited Lecture (selected):

Mar 1, 2013. The 71st Annual Meeting of the American Academy of Dermatology, Maimi, USA.

Nail Symposium. Onychodermis: Hot Spot Research.

Dong-Youn Lee, M.D., Ph.D.Associate Professor, Department of Dermatology, Samsung Medical Center,

Sungkyunkwan University School of Medicine, Seoul, Korea

CURRICULUM VITAE

- 44 -


The nail and hair have many attributes in common mainly in terms of their origin, anatomical

structures and common involvement in many diseases. They exclusively express hard keratin. The

hair follicle develops as a result of the epithelial-mesenchymal interaction. In the hair follicle, the

follicular dermal papilla, which is located at its base, and the follicular dermal sheath, which

surrounds its outer part, represent a specialized part of the hair mesenchymes that are distinct

from the dermis of the adjacent skin. Follicular papilla cells and follicular dermal sheath cells are

specialized hair mesenchymal cells that are distinguished from dermal fibroblasts. These cells can

induce hair follicle development in vivo.

Due to its limited availability there has been very little research on the mesenchyme of the nail

unit. Previously, we discovered specialized mesenchymal cells beneath the nail matrix and proposed

to call them onychofibroblasts. In this study, to precisely localize and characterize the nail

mesenchyme, we investigated the histology and immunohistochemistry.

Thirty extradigits were obtained during polydactyly operations. Longitudinal, transverse and

horizontal sections were made from formalin-fixed paraffin-embedded blocks. In hematoxylin and

eosin staining, there was a mesenchymal area that showed much more cellularity and less eosinophilic,

loose connective tissue beneath the nail matrix and nail bed. By Alcian blue staining, mucin was

detected in the mesenchymal area below the nail matrix and nail bed. Immnunohistochemically,

CD10 was strongly expressed in the mesenchyme containing onychofibroblasts under the nail matrix

and nail bed. Versican was expressed diffusely in the nail mesenchyme containing onychofibroblasts.

These results demonstrate the presence and localization of a specialized nail mesenchyme

containing onychofibroblasts in a well-defined area beneath the nail matrix and nail bed. Thus,

we propose the terminology onychodermis for the specialized nail mesenchyme because it is

histologically and immunohistochemically distinct from the dermis of other parts of the nail unit.

In a previous study using organotypic cultures, nail matrical fibroblasts induced hard keratin

expression in the non-nail-matrical keratinocytes through epithelial-mesenchymal interactions.

However, the characteristics of the specialized mesenchymal cells in vivo, such as their localization

and the existence of a marker for these cells, were not determined. Based on this finding and

our results, the specialized nail mesenchyme (onychodermis) containing onychofibroblasts may play

an important role in nail formation through epithelial-mesenchymal interaction.

In addition, we found the presence of onychodermis in MRI, which was correlated with

histopathology. We also found the presence of onychodermis in adult nail unit and ectopic nails.

The concept of onychodermis

(specialized nail mesenchyme) in the nail unit

Dong-Youn Lee

Department of Dermatology, Samsung Medical Center, Sungkyunkwan University School of Medicine,

Seoul, Korea

IL-11

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The 23rd



Invited Lectures 5

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Invited Lectures 5

Education:

1949-1980 Kobe University, School of Medicine

1983-1987 Kyoto University graduate school of Medicine, Department of Dermatology

Professional experience:

1980 Kyoto University Hospital : Resident in Dermatology

1981-1982 Osaka Red Cross Hospital Dermatologist

1987-1988 Department of Experimental Radiology Kyoto University; Instructor

1988-1994 and 1995-1999 Department of Dermatology Kyoto University; Instructor

1994-1995 Department of immunology MD Anderson Cancer Center: Postdoctoral fellow

1999-2002 Department of Dermatology, Graduate School of Medicine, Kyoto University:

Assistant Professor

2002-2003 Department of Dermatology, Graduate School of Medicine, Kyoto University:

Associate Professor

2003- Division of Dermatology, Graduate School of Medicine, Kobe University:

Professor and Chairman

Professional Specialty: Dermatology and Photobiology, Pigment Cell Research

Memberships:

The Japanese association of Dermatology : councilor

The Japanese Society for investigative dermatology : councilor

The Japanese Society for photomedicine and photobiology : council

The Japanese Society for pigment cell research : president

The Japanese Society for skin cancer : council

The Japanese Cancer Association

American Society for Photobiology

Chikako Nishigori, M.D., Ph.D.Professor and Chairman, Division of Dermatology, Department of Internal Related,

Kobe University Graduate School of Medicine, Kobe, Japan

CURRICULUM VITAE

- 48 -


The Ras/raf/MEK/ERK pathway has been shown to the main stream of melanomagenesis. Recently

ectopic expression of metabotropic glutamate receptor-subtype 1 (mGluR1) in mouse melanocytes

induces melanoma formation. Using novel transgenic mice, which conditionally express mGluR1

in melanocytes, we analyzed the involvement of mGluR1 in melanomagenesis. We found pigmented

lesions on the ears and tails of the transgenic mice began to appear 29 weeks after activation of

the mGluR1 transgene, and tumor frequency reached 100% at 52 weeks. Subsequent inactivation

of the mGluR1 transgene in melanoma-bearing mice inhibited melanoma growth with reduction

of immunoreactivity to phosphorylated ERK1/2, while mice with persistent expression of mGluR1

developed larger melanoma burdens. mGluR1 expression is thus required not only for melanoma

development but also for melanoma growth in vivo.

Many melanoma cells constitutively produce interleukin-8 (IL-8). We found that the levels of

IL-8 production correlated well with the level of phosphorylated (activated) a transcription factor,

signal transducer and activator of transcription 3 (STAT3), in human melanoma cell lines. Introduction

of the constitutively activated form of STAT3 into melanoma cells, WM35, with low levels of IL-8

production and phosphorylated STAT3, enhanced IL-8 production. Knockdown of STAT3

suppressed IL-8 production and its growth in vitro in melanoma cells, WM1205Lu producing a

high level of IL-8 accompanying STAT3 activation. STAT3 is considered to behave as oncogene

and it has been generally thought that Tyr705 activation is a hallmark of STAT3 activations

whereas Ser727 activation is a secondary event after Tyr705 activation. In normal cells, the duration

of STAT3 activation is temporary, lasting from a few minutes to several hours. Unexpectedly we

found that Ser727 was constitutively activated both in normal melanocytes and melanoma cells

irrespective of Tyr705 phosphorylation. The constitutive Ser727 activation in melanoma cells was

partially mediated by the B-Raf-MEK-ERK1/2 pathway. Immunohistochemical studies on specimens

of primary lesions of acral lentiginous melanoma revealed that Ser727 activation precedes Tyr705

activation in the early stages of melanoma progression. Our results indicate that Ser727 activation

on STAT3 is not necessarily a secondary event after Tyr705 activation and suggest that it has

Tyr705 and Ser727 has its differential role in the regulation of cell survival activity and nuclear

translocation of STAT3 in melanocytic cells.

Mechanisms ofMelanomagenesis in relation to

signal transduction and transcription factors

Chikako Nishigori, Massanobu Sakaguchi, Yoko Funasaka, Atsu Aiba,

Masahiro Oka

Division of Dermatology, Graduate School of Medicine, Kobe University

IL-12

- 49 -

Invited Lectures 5

Education:

1988-1994 M.D. in Medicine, Ajou University School of Medicine

1997-1999 M.S. in Dermatology, Ajou University Graduate School

2001-2003 Ph.D. in Dermatology, Ajou University Graduate School

Professional Experience:

1994-1995 Internship in Ajou University Hospital

1995-1997 Research fellow in Department of Life Science, Postech, Korea

1997-2001 Residency in Department of Dermatology, Ajou University Hospital

2001-2002 Fellowship in Department of Dermatology, Ajou University School of Medicine

2002-2004 Instructor in Department of Dermatology, Ajou University School of Medicine

2004-2008 Assistant professor in Department of Dermatology, Ajou University School of

Medicine

2008. 5-2009. 8 Visiting scholar (Enseignant-chercheur) in Department of Dermatology,

University of Nice, France

2008-Present Associate professor in Department of Dermatology, Ajou University School of

Medicine

Major interest:

Melasma and pigmentary disorders

Melanocyte biology

Hee Young Kang, M.D., Ph.D.Department of Dermatology, Ajou University School of Medicine,

Korea

CURRICULUM VITAE

- 50 -


Melasma is a common acquired hyperpigmentary disorder characterized by hyperpigmented

patches on sun-exposed areas. Its treatment remains a challenge.

Increased pigmentation is the main target of treatment. Our studies showed melasma is

characterized by epidermal hyperpigmentation. Some patients have dermal melanin as well as

epidermal melanin in the lesion, but the amount is not significant. Moreover, its distribution is

very heterogeneous in the lesional skin. It seems that the small amount of dermal melanin is a rather

common finding in patients with the darker skin type. The increased epidermal pigmentation is

due to enhanced melanogenesis in individual melanocytes. Transcriptomics and immunohistochemical

studies showed that mRNA and protein expressions of melanogenesis- associated markers such

as silver and tyrosinase were up-regulated in the lesional skin.

Factors that activate melanocytes in melasma are other important targets for treatment. Prominent

solar elastosis in melasma skin implies that solar damage may influence development of hyperpig-

mentation in the lesion. We have shown that expressions of SCF around fibroblasts and its receptor,

c-kit, on the melanocytes were increased in the lesional skin. We have also noticed that the lesional

skin of melasma is characterized by an augmented vasculature. Immunohistochemistry for vascular

markers revealed an increased number of vessels in the upper dermis. There was a significant

positive correlation between pigmentation and the number of vessels. Clinical studies have also

supported the role of vasculatures in development of melasma. The studies showed targeting vascular

structures as well as pigmentation is beneficial for treatment. The altered dermal structures such

as fibroblast and vasculature may work in conjunction to stimulate melanocytes resulting in the

epidermal hyperpigmentation of melasma.Another interesting target of treatment is the altered basement membrane. This finding drew

our attention when we observed “protruding melanocytes” in the lesional skin. Type IV collagen

immunostaining was very weakly positive around those cells, suggesting that loosened basement

membrane may be related to the pendulous feature of the melanocytes. Moreover, the overall type

IV collagen expression was significantly reduced in the lesional skin, which implicated the basementmembrane structure of melasma is not intact and disrupted. It may be assumed that the disrupted

basement membrane facilitates the interaction between dermal structures and epidermal melanocytes.

In pigmented areas, a certain kind of melanogenesis-stimulating factor, such as SCF or vasculaturerelated factor may easily penetrate from dermis to epidermis through the DEJ.

In summary, melasma is characterized by increased epidermal pigmentation due to increased

melanogenesis in individual melanocytes. The altered dermal structures and impaired basement

membrane may have an influence on development of epidermal hyperpigmentation in melasma.

The cellular network between fibroblasts, and perhaps vasculatures and melanocytes, througha disrupted basement membrane may contribute to development of melasma. For treatment, we

need to consider targeting all of the above-mentioned changes.

Pathogenesis ofmelasma: What should be

considered in treatment ofmelasma

Hee Young Kang

Department of Dermatology, Ajou University School of Medicine, Korea

IL-13

- 51 -

The 23rd



Invited Lectures 6

- 53 -

Invited Lectures 6

Dr. Jianzhong Zhang Graduated from Peking University School of Medicine in 1986. He worked

in Department of Dermatology, Peking University First Hospital from 1986 through 1992 as

resident and attending physician. He was a visiting scholar in Fukushima Medical University Japan

from 1992 through 1994. From 1994 through 1996, he worked in Department of Dermatology, Peking

University First Hospital where he was promoted to be associate professor in 1995. He then

worked in Department of Dermatology, Peking University People’s Hospital since 1996 and became

professor and chairman of the department in 2000. He is currently the director, College of

Dermatology and Venereology Peking University and is also professor and chairman, department

of dermatology, Peking University People`s Hospital.

He has been actively involved in Chinese Society of Dermatology, Chinese Medical Association.

He was the secretary General of Chinese Society of Dermatology from 2006 through 2009 and president-

elect from 2009 through 2012. He is currently the president of Chinese Society of Dermatology.

Dr. Zhang is interested in atopic dermatitis, psoriasis, cutaneous lupus erythematosus, alopecia,

mycobacterial infections and epidemiology of skin diseases. He is involved in board of editors

of more than 10 journals. He has published over 300 peer-reviewed articles and is the editor or

contributor of over 30 books.

Jianzhong ZhangDepartment of Dermatology, Peking University People’s Hospital

CURRICULUM VITAE

- 54 -


Although Chinese investigative dermatology began at early 1930s, it had nearly no publications

in international journals in subsequent 50 years. In 1986, Dr. Hong-Duo Chen published his paper

in Journal of Investigative Dermatology, which started a new page of Chinese investigative

dermatology. In 2002, only 21 papers from China were published in international journals. In 2007,

105 papers were published. In 2012, totally 371 papers were published, which was 18 times that

of ten years ago. These papers were from 108 hospitals, suggesting that more and more Chinese

dermatology departments are able to do clinical and basic investigations. From 1986 till 2012, over

1800 papers were published with basic research accounting for 58.3% and clinical research

accounting for 41.7%. In recent years, a number of high-level papers had been published in top

journals such as New England Journal of Medicine, Nature Genetics, Science and Immunity. A

number of pathological genes have been found by Chinese dermatologists and scientists including

SCN9A gene for erythermalgia, ribosomal protein L21 gene (RPL21) for hereditary hypotrichosis

simplex, MVK gene for disseminated superficial actinic keratosis and U2RH gene for Marie Unna

hereditary hypotrichosis. Moreover, Chinese dermatologists found and named several new skin

diseases such as fatal bacterial granuloma after trauma, AD-like cutaneous GVHD and gluteofemoral

erythema of pregnancy. In recent years, research grants in Chinese dermatology increased rapidly,

which enable Chinese dermatologists and researchers to perform high level researches. We can

expect more contributions from Chinese dermatology to global dermatology.

Investigative dermatology in China:

a decade's progress

Jian-Zhong Zhang

Department of Dermatology, Peking University People’s Hospital

IL-14

- 55 -

Invited Lectures 6

Education:

1996 Kyoto University, Faculty of Medicine (MD)

2003 Kyoto University, Faculty of Medicine (PhD)

Occupation:

1996- Intern, United States Naval Hospital, Yokosuka

1997- Resident/Visiting clinical fellow, University of Washington, Department of Internal

Medicine/Dermatology

1998- Clinical Fellow, Department of Dermatology, Kyoto University

2003- Assistant Professor, Department of Dermatology, Kyoto University

2003- Research Associate, Department of Microbiology and Immunology, University of

California, San Francisco

2005- Associate Professor, Department of Dermatology, University of Occupational and

Environmental Health

2008- Associate Professor, Department of Dermatology, Kyoto University Graduate School of

Medicine

Editorial Board Members:

J. Invest. Dermatol., J. Derm. Sci., Exp. Dermatol., J. Dermatol. etc

Board of Directors:

Japanese Society of Investigative Dermatology

Kenji Kabashima, M.D., Ph.D.Associate Professor, Department of Dermatology,

Kyoto University Graduate School of Medicine, Japan

CURRICULUM VITAE

- 56 -


The skin is not merely a physical barrier but an active immune organ, and a variety of immune

responses are induced therein. Previously, the evaluation of the inflammatory status of the skin

was based on the histological analysis; however, three-dimensional or chronological evaluation was

difficult in that traditional way.

In this presentation, we aimed to analyze the spatio-temporal behavior of T cells and dendritic

cells in contact hypersensitivity (CHS) response. These effector T cells were labeled and transferred

into DNFB-sensitized mice and the ear was challenged. Once they transmigrated to the dermis,

they started to move around rather rapidly (6~9 m/min). We also analyzed the cell behavior ofμ

antigen-specific T cells prepared from DNFB-sensitized mice and observed the arrest of cell

migration and reduction of mean velocity of T cells in an antigen-specific manner.

These observations introduce a new concept that T cells perform similar motile activities upon

specific antigen exposure in the skin as well as in the lymph nodes.

Visualization of skin inflammation

Kenji Kabashima, M.D., Ph.D.

Associate Professor, Department of Dermatology, Kyoto University Graduate School of Medicine, Japan

IL-15

- 57 -

The 23rd



UAM Award Lecture

- 59 -

UAM Award Lecture

Education:

1982-1988 Yonsei University Wonju College of Medicine, Wonju, Korea (M.D. degree)

1989-1992 Master degree from Yonsei University Graduate School

1995-1998 Ph.D degree from Yonsei University Graduate School

Post-Graduate Training:

1988-1992 Intern & Resident, Department of Dermatology, Wonju Christian Hospital, Yonsei

University Wonju College of Medicine

Academic Appointments:

1995-2007 Fellow, Instructor, Assistant & Associate Professor, Yonsei University Wonju College

of Medicine

2003-2005 Postdoc Research Fellow & Visiting Scientist, Department of Dermatology

(Dr. Elias' Lab), University of California San Francisco, San Francisco, CA, USA

2008-present Professor, Yonsei University Wonju College of Medicine

Professional Affiliations:

Korean Society for Skin Barrier Research: The chief director (2006. 9-2008.9)

Korean Society for Skin Barrier Research: Vice chair (2010.9-present)

Pan Asian Pacific Skin Barrier Research Society: General Secretary (2010.9-present)

Korean Atopic Dermatology Association: Publication Secretary (2011.10-present)

Korean Society for Investigative Dermatology Society for Investigative Dermatology

Research Interests:

1. Skin barrier, 2. Atopic dermatitis, 3. Skin aging

Eung Ho Choi, M.D., Ph.D.Professor, Department of Dermatology, Yonsei University Wonju College of Medicine,

Wonju, Korea

CURRICULUM VITAE

- 60 -


The Effect ofAdipose-Derived StemCell-Cultured

Media onOxazolone Treated Atopic

Dermatitis-LikeMurineModel

Hae-Jin Lee, Minyoung Jung, Jae-Hong Kim, Na Young Yoon, Eung Ho Choi

Department of Dermatology, Yonsei University Wonju College of Medicine,

Wonju, Korea

A stem cell is an undifferentiated cell that has the potential for self-renewal and differentiation.

Among them adipose derived stem cells (ADSCs) have advantages in accessibility and abundance

compared to other kinds of stem cells, and produce many growth factors and hormones. Therefore,

we investigated whether ADSC cultured media could be used as a therapy for atopic dermatitis.

ADSC cultured media was topically applied twice daily for 5 days to oxazolone-treated atopic

dermatitis-like hairless mice. Topical application of ADSC cultured media improved the epidermal

permeability barrier and keratinocyte differentiation, and restored the predominant Th2 phenotype

when compared to vehicle. ADSC cultured media treated epidermis also showed an increase in

the expression of antimicrobial peptides such as cathelin-related antimicrobial peptide and mouse

beta-defensein 3. Collectively, topical ADSC cultured media could be useful in the treatment of

atopic dermatitis.

UAM Award Lecture

- 61 -

The 23rd



피부생물학

- 63 -

피부생물학

Education:

2002. 8-2005. 2 Graduate School, Seoul National University, Seoul, Korea (Ph.D.)

1997. 3-1999. 2 Graduate School, Seoul National University, Seoul, Korea (M.S.)

1988. 3-1994. 2 College of Medicine, Seoul National University, Seoul, Korea (M.D.)

Postgraduate Training & Academic Appointment

2010. 4-present Associate Professor, Department of Department of Dermatology, Seoul

National University College of Medicine, Seoul, Korea

2007. 7-2009. 7 Visiting Scholar, Department of Dermatology, University of Pennsylvania,

Philadelphia PA, USA

2005. 3-2010. 3 Assistant Professor, Department of Dermatology, Seoul National University

College of Medicine, Seoul, Korea

2003. 4-2005. 2 Clinical Instructor, Department of Dermatology, Seoul National University

Hospital, Seoul, Korea

2003. 3-2003. 4 Visiting Fellowship, Elective Course for Dermatological Surgery, Department

of Dermatology, Oregon Health Science University, Portland OR, USA.

2002. 5-2003. 2 Research Fellowship, Department of Dermatology, Seoul National University


1995. 3-1999. 2 Resident, Department of Dermatology, Seoul National University Hospital,

Seoul, Korea

Memberships and Committees

2010. 5-present Korean Hair Research Society (KHRS)

Board director for Publication and Information

2011. 4-present Korean Society of Investigative Dermatology (KSID) Board director for

Publication

2011. 12-present Organizing Committee for 8th World Congress for Hair Research in 2014,

Jeju, Korea

Oh Sang Kwon, M.D., Ph.D.Associate Professor, Department of Dermatology,

Seoul National University College of Medicine, Seoul, Korea

CURRICULUM VITAE

- 64 -


Mammalian hair follicle is a composite mini-organ with a complex structure and function. It

involves several types of cells from different embryonic origins; keratinocytes, melanocytes and

specialized fibroblasts such as dermal papilla cells and connective tissue sheath cells. The cells

shape the highly organized, multilayered hair follicles which produces the hair, their functional

endpoint.

Hair follicles continuously progress through cycling stages (anagen-catagen-telogen) during whole

postnatal life owing to the persistent integration of inputs from intrinsic follicular and extrinsic

environmental signals. Recently, it has become revealed that interdependent relationships among

cell populations residing in and around the hair follicle. These interactions between different

lineages of stem cells are crucial for hair follicle growth and cycling and point to a complex

crosstalk in stem cell niches.

The follicular stem cell niche, or the bulge, is composed of heterogeneous population of self-

renewing multipotent cells including both epithelial and melanocyte stem cells. Inside the hair

follicles, hair follicle epithelial stem cells located in bulge interact with dermal papilla located at

the lowermost area to produce hair fibers. In addition, numerous extrafollicular cell types can

influence the activity and characteristics of bulge cells. The activation of hair follicle stem cells has

been shown to be modulated by the activator/inhibitor signals released from intradermal adipose

tissue, perifollicular peripheral nerves as well as immune system and various hormones. The

balance and interplay among intrafollicular and extrafollicular signals would modulate the function

of bulge stem cells during hair cycling and control the growth of hair follicles. Our new

understanding on these interactive network would be able to provide new insights for regenerative

medicine and new strategies for the treatment of hair diseases.

Intra and extra-follicular regulation

on the growth of hair follicles

Oh-Sang Kwon

Department of Dermatology, Seoul National University College of Medicine, Seoul, Korea

피부생물학 1

- 65 -

피부생물학

Education:

1986. 3-1990. 2 Department of Zoology, School of Natural Sciences, Seoul National University,

Seoul, Korea (BS)

1990. 3-1992. 2 Department of Molecular Biology, School of Natural Sciences, Seoul National

University, Seoul, Korea (MS)

1992. 3-2002. 8 School of Biological Sciences, Seoul National University, Seoul, Korea (PhD)

Career:

1992. 1-2001. 1 LG Household & Health Care Ltd., Daejeon, Korea (Researcher)

2002. 9-2003. 8 OBM Lab Ltd., Daejeon, Korea (Researcher)

2003. 9-2006. 2 Department of Dermatology, School of Medicine, Chungnam National

University, Daejeon, Korea (Postdoctoral researcher)

2006. 3-present Department of Dermatology, School of Medicine, Chungnam National

University, Daejeon, Korea (Associate professor)

2010.10-2012. 3 Department of Dermatology, University of Pennsylvania School of Medicine,

Philadelphia, PA (Visiting Scholar)

Chang Deok Kim, Ph.D.Department of Dermatology, School of Medicine, Chungnam National University

CURRICULUM VITAE

- 66 -


Hair follicles are formed during the embryogenesis by interaction between epithelium and

underlying mesenchyme. Once established, hair grows in a cyclical manner, characterized by

anagen, catagen and telogen. To maintain its cyclic property, hair follicle cells should be provided

repeatedly from stem cells. In 1990, Dr. Cotsarelis discovered that hair stem cells reside in bulge

region of hair follicle using label retaining cell (LRC) technique. It has been demonstrated that hair

follicle stem cells are self-renewing and multipotent, possessing the ability to generate all epithelial

layers of the hair follicle throughout life. Many investigators have identified important molecules

and signaling pathways that play pivotal roles in the development of hair follicles and the

maintenance of hair growth cycle. Those include Wnt/ -catenin, sonic hedgehog, and BMPβ

signaling pathways. Besides, many new molecular players that control hair growth cycle has been

identified recently. In this presentation, I will talk about recent findings on molecular mechanism

underlying hair growth regulation.

Hair follicle stem cell

Chang DeokKim

Chungnam National University

피부생물학 2

- 67 -

피부생물학

교육경력

1972. 3-1978. 2 연세대학교 의과대학 의학사,

1979. 3-1981. 2 연세대학교 대학원 의학석사,

1981. 3-1987. 2 연세대학교 대학원 의학박사,

수련경력

1979. 3-1983. 2 전공의 세브란스병원 피부과,

1988.10-1990. 7 리서치 휄로우 존스홉킨스의대 피부과,

교직경력

1986. 5-1988. 2 전임강사 연세의대 피부과학교실,

1988. 3-1994. 2 조교수 연세의대 피부과학교실,

1994. 3-1999. 2 부교수 연세의대 피부과학교실,

현재2000. 3- 교수 연세의대 피부과학교실,

현재2001. 3- 강남세브란스병원 피부과장

면허 및 학회활동

대한피부과학회 정회원 현재: 1983. 3-

정회원 현재The Society for Investigative Dermatology : 1990. 6-

정회원 현재European Academy of Dermatology and Venereology : 2004. 10-

European Academy of Dermatology and Venereology Working Group :

대한피부연구학회 정회원 현재: 1991. 6-

대한피부연구학회 간행이사 : 1995. 3-1997. 2

대한피부연구학회 총무이사 : 1999. 3-2001. 2

대한피부과학회 홍보이사 : 2001. 11-2003. 10

대한 코스메틱 피부과학회 이사장 : 2006. 6-2008.5

대한 화장품 연구분과위원회 학술이사 : 2006. 10-2008. 9

현재Journal of Dermatology International Advisory Board : 2000-

현재Journal of Dermatological Science Editorial Board : 2003-

제 차 세계피부과학회 조직위원회 사무총장22 : 2007. 10-2011.5

대한피부과학회 학술위원장 : 2011.10

대한피부연구학회 정보위원장 : 2012.4-2013.3

대한피부연구학회 차기 이사장 : 2012.4-2013.3

Soo-Chan Kim강남세브란스병원 피부과

CURRICULUM VITAE

- 68 -


피부에서 기저막대 는 표피와 진피 사이를 연결하는 구조물로서(basement membrane zone; BMZ)

표피와 진피를 굳게 결합시켜 주는 역할을 할 뿐 아니라 표피의 구조를 지지해 주고 표피와 진피를,

나누는 장벽의 역할을 한다 전자현미경으로 보면 기저막대는 기저세포 투명판 치밀. , (lamina lucida),

판 치밀판 하부로 부위를 나눌 수 있다 기저막대를 구성하는 단백은 여러 종류가 있는(lamina densa), .

데 기저세포의 케라틴 가 반교소체 와 연결되어 있으며 반교소체를 구성하는 단5/14 (hemidesmosome) ,

백으로 세포질 내에 존재하는 과 이 있으며 세포막을 관통하는 단백으로BPAG1(BP230) plectin BPAG2

와 이 있다 와 은 투명대를 가로 지르는(BP180) 6 4 integrin . BPAG2 6 4 integrin anchoringα β α β filament

를이루는 단백이기도하다 는 투명판과치밀판에걸쳐존재하는데위로는. Laminin 332 BPAG2 및 6 4α β

과 결합하고 있고 아래로는 을 이루는 과 결합하고integrin anchoring fibril type VII collagen 있다.

치밀판은 으로 구성되어 있으며 치밀판 아래에는type IV collagen, nidogen, perlecan type VII collagen

이 있다 기저막대를 이루고 있는 단백에 돌연변이가 생기거나 자가항체가 생기게 되면 표피와. 진피의

결합에 장애가 생겨 수포가 발생하게 된다 기저막대 단백의 돌연변이에 의한 유전성 수포성 질환을.

수포성표피박리증 이라고 하는데 돌연변이를 일으킨 단백의 종류에 따라 여러(epidermolysis bullosa)

가지 종류의 수포성표피박리증으로 구분할 수 있다 및 유전자에 변이가 생기면 단순. BPAG1 plectin

형 수포성표피박리증이 발생하고 와 및 유전자에 변이가 생기면BPAG2 6 4 integrin laminin 332α β

경계형 수포성표피박리증이 발생하며 에 변이가 생기면 이 양형 수포성표피박리type VII collagen

증이 발생한다 또한 과 에 대한 자가항체가 생기면 유사천포창이 발생하고. BPAG1 BPAG2 , laminin

또는 에 대한 자가항체가 생기면 점막유사천포창이 발생할 수 있으며332 6 4 integrin type VIIα β

에 대한 자가항체가 생기면 후천성 수포성표피박리증이 발생한다 이상과 같이 피부기저막대collagen .

는 여러 질환의 병인과 직접적인 관계가 있으므로 피부 기저막대의 구조와 기능을 이해하는 것이

중요하다.

Structure and Function of Basement

Membrane Zone I

김수찬

연세의대피부과학교실

피부생물학 3

- 69 -

피부생물학

교육 및 경력

년 월1989 2 전남대학교 의과대학 졸업

년 월2000 2 전남대학교의과대학에서 박사학위 취득

년 월1998 3 피부과 전문의 취득

년 월현재1999 2 - 전남대학교 의과대학과 전남대학교병원에서 근무 현재 교수임,

해외연수 경력2.

년 월 년 월1) 2002 3 -2003 5

일부 후쿠오카 구루메 의과대학 및 미국 에서- NIH (National Institute of Health) Research

로 연수fellow

년도 월 년 월 개월2) 2007 10 -2008 2 (5 ): University of Missouri Health Care Hospital Visiting scholar

로 연수

연구분야3. : 수포성질환 여드름 광의학 피부종양 혈관종양, , , ,

학회활동4.

대한피부과학회 정회원

미국피부과학회 정회원(American Academy of Dermatology)

대한피부과학회 고시위원 위원 년부터 현재까지(2007 - )

대한피부과학회 학술위원회 위원 년부터(2012 - )

대한피부과학회 신의료기술위원회 전산정보통신위원회 용어집위원회의 위원, ,

대한여드름학회 학술이사

대한의진균학회 간행이사

대한미용피부외과학회 간행홍보이사

이 지 범전남대학교 의과대학 피부과학교실

CURRICULUM VITAE

- 70 -


피부의 basement membrane zone 은 복합체(BMZ) 1) keratin filament-hemidesmosome , 2) lamina

구조densa 3), microfibrillar 로 이루어져 있다 이들은 기저세(anchoring fibrils, anchoring plaques) .

포와 망상진피간 연속적인 부착기능 및 여러 기능을 제공하기 위해서 여러 들로 구성되어molecules

있다 이 시간에는 이 분자들 중 의 구조와 기능 그리고 질. collagen VII, laminin 332, integrin 6 4 ,α β 환

과의 연관성에 대해서 논의하고자 한다.

는 의 주된 성분으로 각질형성세포와 섬유모세포 둘 모두로부터 합성Collagen VII anchoring fibrils

된다 이는 중 가장 길고 인 와 양쪽에 와. collagen , collagenous domain triple helical domain NC-1

인 로 구성되어 있다 의 은 내에서NC-2 globular domains . Collagen VII NC-1 domains lamina densa

위치하여 있고 와 와 결합한다 그리고 와 인근 진피에 고정을, laminin 332 collagen IV . lamina densa

위해서 과 공유 교차결합한다 환자의 표적이 되는 항원이 되고collagen I . EBA, bullous SLE , DEB

환자에서는 의 유전자 에서 돌연변이collagen VII COL7A1 이 관찰되는데 지금까지 개(mutation) 300

이상의 돌연변이가 발견되고 있고 와 이 매우 다양하고 광범위하다, genotype phenotypes .

은 세 가지 가 로 결합하여 구성되어 있다 그 중Laminin , , subunit chains disulfide-bond . 3, 3,α β γ α β γ

2 삼합체 가 로 알려져 있는 이다 이는 내와(trimer) laminin 5 laminin332 . lamina lucida/lamina densa

에 존재한다 의 과 비공유 결합을 통해 서로 상호작용하anchoring filament . Collagen XVII ectodomain

며 기능은 와 다른 세포표면 성분들과 상호작용하여 세포의 결합 이동 증식 극성 등의integrins , , ,

세포활성을 조절한다 또는 의 돌연변이가 에서 발견되고. 3, 3, 2 chains junctional EB , cicatricialα β γ

pemphigoid 에서는 표적항원이 된다(CP) .

는 와 높은 친화성을 가져서 을 밑에 존재하는 기저막대와Integrin 6 4 laminin332 hemidesmosomeα β

기질을 통합시키는데 필수적인 분자이다 동반한 환자에서 또는. Pyloric atresia junctional EB 6 4α β

에 돌연변이가 발견되고 에서 표적항원이 되기도 한다chains , CP .

Structure and function of basement membrane zone II:

collagen VII, laminin 332, Integrin 6 4α β

이지범

전남대학교의과대학피부과학교실

피부생물학 4

- 71 -

피부생물학

경력

1979 연세의대 졸업

1983 피부과학 전문의 취득

1988 의학박사 취득

1983-2013 현재 남대학교 피부과학교실 교수

1990-1991 미국 분교 연수University of California San Francisco

1997-1998 미국 연수Center for Disease Control & Prevention

2008-2009 네덜란드 연수CBS Fungal Biodiversity Centre

최 종 수남대학교 의과대학 피부과학교실

CURRICULUM VITAE

- 72 -


Molecular biologic techniques are developing very fast, and replaced traditional identification

method of fungi. Nucleic acid detection methods such as PCR and sequencing have become a

common tool for microbial identification and diagnosis. They are fast, sensitive and reproducible.

With phylogenetic analysis, new species are identified and new classification of fungi is being

established. Molecular typing techniques provide a information to detect their infection routes, and

to differentiate reinfection and recurrence of infection. Mating type locus was found in several

dermatophytes, and it is possible to identify the mating type by PCR Comparison of RNA expres-

sion among antifungal agents will provide action mechanism and targets of the new drugs. The

comparative genomic analysis of dermatophytes may help for understanding in dermatophyte

pathogenesis. There are lots of techniques and each method has advantage and limitation, and

proper selection is essential. We review the several molecular methods in mycology.

Application ofmolecular biologic

methods in mycology

최종수

남대학교의과대학피부과학교실

피부생물학 5

- 73 -

피부생물학

Education:

Feb. 1996 B.S. in genetic engineering, College of biomedical science, Kyunghee University

Feb. 2000 Doctor of Medicine (MD), School of Medicine, Konkuk University

Feb. 2006 Ph.D. Konkuk University School of Medicine Graduate School

Academic Appointments:

2000-2001 Residency training (internship), Konkuk University Hospital

2001-2005 Residency training in Dermatology, Konkuk University Hospital

2005-2006 Fellowship training in Dermatology, Konkuk University Hospital

2006-2007 Clinical assistant professor in Dermatology, Konkuk University Hospital

2007-2011 Assistant professor in Dermatology, Konkuk University Hospital

2010-2011 Visiting professor in Department of Biomechanical Engineering, Michigan State

University

2011-present Associate professor in Dermatology, Konkuk University Hospital

Academic Award:

2002 Best Paper Award, The 9th Korean Society for Medical Mycology

2003 Best Poster Award, The 55th Spring Meeting, Korean Dermatological Association

2003 Top graduate (Presidential citation), The Graduate School of Konkuk University

2006 Best Paper Award, The 13th Korean Society for Medical Mycology

2006 Scholarship, The 65th annual meeting of American Academy of Dermatology

2007 Research Award, Korean Dermatological Association.

2008 Research Grant for young investigators, Korea Research Foundation

2008 Travel grants, The 5th Georg Rajka International Symposium on Atopic Dermatitis

2009 Travel grants, The 17th Congress of The International Society for Human and

Animal Mycology

Social Activities:

2011-The present Planning director, Korean Society for Medical Mycology

2006-The present Member of International society for human and animal mycology

(ISHAM) Malassezia working group

2013-The present Planning director, Korean Society for Aesthetic and Dermatologic Surgery

2010-The present Member of board of directors, The Korean Hair Research Society

Yang-Won LeeDepartment of Dermatology, Konkuk University Hospital,

Seoul, Korea

CURRICULUM VITAE

- 74 -


아토피피부염 은 주로 유아기에 시작하는 가려움을 동반하는 만성재발성 습진(atopic dermatitis)

질환으로 연령에 따라 특징적인 병변의 분포와 양상을 보인다 아토피피부염의 임상양상은 매우 다양.

하며 특이한 검사소견이 없어 임상양상을 종합한 아토피피부염 진단기준에 따라 진단한다 아토피피.

부염은 전 세계적으로 증가추세에 있으며 국내의 정확한 발생 빈도는 추정하기는 어렵지만 유병률은

꾸준히 증가하고 있으며 대략 정도로 본다, 10~20% .

아토피피부염의 원인은 아직 확실히 밝혀져 있지 않으나 유전학적인 측면 알레르기 및 면역학적,

측면 약리 생리학적 측면 그리고 피부장벽의 이상 등 다양한 원인들이 제시되어 왔으며 최근에는,

아토피피부염과 Malassezia 효모균의 병인적 연관성이 중요하게 대두되고 있다.

Malassezia 효모균은 피부의 정상균총으로 존재하는 진균 중 가장 많은 빈도를 차지하며 그 중에서

도 M. resticta와 M. globosa가 가장 많은 빈도로 존재한다. Malassezia 효모균의 집락은 정상인보다

아토피피부염 환자에 배 많은 것으로 알려져 있으며 흥미로운 것은 경도와 중등도의 아토피피부2~5

염 병변에서는 M. resticta가 가장 많은 빈도로 발견되지만 중증의 아토피피부염에서는 M. globosa

의 비율이 많아져 M. resticta와 거의 같은 비율로 발견된다는 점이다 아토피피부염에서. Malassezia 효

모균은 정상 상재균으로 병적인 감염원이 아니라 알러젠 으로서 만성적인 염증반응을 유발하(allergen)

게 되고 아토피피부염의 만성화와 악화 요인으로 작용하는 것으로 알려져 있다 최근. M. sympodialis

이 아토피피부염 환자의 에 강한 교차반응을 일으키는 것이 밝thioredoxin-specific T cell thioredoxin

혀져 이러한 사실을 뒷받침하고 있으며 M. furfur 등 다른 균종들에서도 다양한 알러젠들이 계속

동정되고 있다 또한. Malassezia 효모균은 스스로 지질을 합성할 수 없어 숙주인 사람의 지질을 분해

흡수하여 양원으로 사용하게 되는데 이 과정에서 사람의 피부지질 장벽에 손상을 유발하여 아토피

피부염을 악화시킬 수 있다는 가능성이 제시되고 있다.

Malassezia and atopic dermatitis

이양원

건국대학교의학전문대학원피부과학교실

피부생물학 6

- 75 -

The 23rd



Free Communication(FC-1 ~ FC-5)

- 77 -

Free Communication

FC-1

Silibinin induced down-regulation of type I collagen expression through

blocking smad2/3-dependent signaling pathway in human skin fibroblasts

from normal and keloid tissues: its potential therapeutic use in the

chemoprevention of keloid

Han-Won Ryu, Jun-Il Kwon, Jae-We Cho, Kyu-Suk Lee

Department of Dermatology, Keimyung University School of Medicine, Daegu, Korea

Inhibition of the Smad2/3 pathway is the key step involved in the down-regulation of type I collagen

synthesis, eventually preventing keloid formation in the tissue. In this study, we investigated the

effect of silibinin on the proliferation of human skin fibroblasts (HSF), expressions of type I

collagen, matrix metalloproteinase-1, and Smad2/3. Our data showed that the proliferation rates

of fibroblasts were not markedly decreased in a dose and time-dependent manner of silibinin. Even

though silibinin did not exert any cytotoxic effect on HSF, the expression of type I collagen was

markedly decreased in a dose and time dependent manner in silibinin-treated HSF. Consistent with

this finding, decreased promoter activity of type I collagen was observed in HSF by silibinin treatment.

MMP-1 and MMP-2 expression levels were increased in silibinin-treated HSF. Moreover, silibinin-

induced down-regulation of type I collagen was associated with the inhibition of Smad2/3 activation

in TGF- 1-treated HSF. We further demonstrated that silibinin attenuated the translocationβ of Smad

2/3 into the nucleus in TGF- 1-treated HSF. These results were similar to in keloid fibroblasts.β

Now, we tried to confirm these anti-fibrotic effects of silibinin in bleomycin-induced sclerotic mice

models. Taken together, our data indicated that silibinin has the potential to protect the fibrotic

change of skin through inducing the down-regulation of type I collagen expression, which is partly

mediated by inhibition of the smad2/3-dependent signaling pathway.

- 78 -


FC-2

Genetic variations associated with efficacy of dutasteride for male pattern hair

loss

Seong Jin Jo1,2, Arang Rhie

3,4, Seungbok Lee

3,4, Bark-Lynn Lew

5, Woo-Young Sim

5, Kwang Hyun Cho

1,2,

Jin Ho Chung1,2, Jong-Il Kim3,4, Oh Sang Kwon1,2

1Department of Dermatology, Seoul National University College of Medicine, Seoul, Korea2Institute of Human-Environment Interface Biology, Seoul National University, Seoul, Korea3Genomic Medicine Institute (GMI), Medical ResearchCenter, Seoul National University, Seoul, Korea4Department of Biomedical Sciences, Seoul National University Graduate School, Seoul, Korea5Department of Dermatology, College of Medicine, Kyunghee University, Seoul, Korea

Male pattern hair loss (MPHL) is an androgen-induced progressive hair loss caused by shortening

of anagenduration representing as miniaturization of involved hair follicles. A main treatment

target for MPHL is inhibition of 5 á-reductase (5AR) because dihydrotestosterone (DHT) which

is converted from testosterone by 5AR in hair follicles and sebaceous glands is the most responsible

androgen for MPHL. However, the effect of 5AR inhibition depends on each individual and the

genetic causes of the individual difference in the treatment efficacy have not been identified. In

this study, we aimed to search for exonic variants associated with response to dutasteride, a dual

inhibitor of type I and II 5AR.

A total of 42 men with MPHL who had been treated with dutasteride for 6 months were recruited

and classified into good- (over the 75 percentile in efficacy, n=10) and poor-efficacy group (below

the 25 percentile in efficacy, n=10) according to the change of hair count after treatment. Quantitative

regression analysis on all subjects yielded 16 single nucleotide variants (SNVs) to be associated

(p<0.05) and quantitative regression analysis by classifying good- and poor responding group left

10 SNVs out of 16. Treating the poor/good responding groups as cases and controls, 3 SNVs were

significant to be associated. A novel SNV (chr7:91763660:T > C) was located on 7q21.2, the first exon

of CYP51A1. The others were rs72623193 on 2q31 and rs1064796 on 19p13.12 and the associated

genes were DHRS9 and CYP4F11, particularly. Our results suggested CYP51A1, DHRS9, and

CYP4F11 are potential candidate genes associated to the efficacy of dutasteride on MPHL.

- 79 -

Free Communication

FC-3

Methyl-β-cyclodextrin as a caveolin-1 inhibitor shows anti-aging activity in

the skin: inverse correlation between caveolin-1 and collagen I levels

Jung-Ae Lee1, Jee-Young Choi

1, Da-In Choi

1, Sun-Ouck Kim

3, Suk-Jung Yun

1, Kyung-A Cho

2,

Jee-Bum Lee1, Seung-Chul Lee1

1Department of Dermatology, Chonnam National University Medical School,2Department of Biochemistry, Chonnam National University Medical School,3Department of Urology Chonnam National University Medical School

Aged skin is characterized by decreased thickness due to loss of dermal collagen (COL). This

study evaluated the role of caveolin-1 (Cav-1) in relation with COL expression in the skin. There

was an inverse correlation between collagen I (COL I) and Cav-1 levels in the chronologically aged

skin of humans and mice in vivo and senescent human dermal fibroblasts (HDF) in vitro, which

was confirmed by Cav-1 siRNA transfection and knock-out experiments. Treatment of HDF with

methyl- -cyclodextrinβ (M CD), a Cav-1 inhibitor, dose-dependently up-regulated COL I mRNAβ

and protein, as it up-regulated mRNA levels of transforming growth factor (TGF)- 1, TGF-β β

receptors of TGF- 1 receptor Iβ (T RI) and T RII, and Smad2, indicating M CD-mediated activationβ β β

of TGF- /Smad2 pathway. In hairless mice, repetitive intra-dermal injection of 2.5% M CD forβ β

3 months induced down-regulated Cav-1 and up-regulated COL I levels of mRNA and protein,

leading to skin thickening. There were no adverse reactions in the skin and major internal organs

in M CD-injected mice. The data indicate that Cav-1 negatively modulates COL I expression inβ

the skin and that intra-dermal injection of M CD results in anti-aging effect via its anti-Cav-1β

activity. Cav-1 inhibitors can be developed as novel anti-aging agents through their COL-stimulating

activity in the skin.

- 80 -


FC-4

Extracellular superoxide dismutase (EC-SOD) inhibits mast cell activation

and allergic responses


Department of Dermatology, College of Medicine, The Catholic University of Korea

Extracellular superoxide dismutase (EC-SOD), also known as SOD3, is an enzyme that is present

in the extracellular matrix and catalyzes the dismutation of superoxide anions. It is a multi-functional

molecule, containing reactive oxygen species scavenging, anti-angiogenic, anti-inflammatory, anti-

chemotatic, and anti-tumoric activity. Recently, we demonstrated that EC-SOD inhibited ovalbumin-

induced allergic airway inflammation in mice. However, the role of EC-SOD in mast cell activation,

which is important for allergic responses was not well studied. In this study, we demonstrated

whether EC-SOD could inhibit mast cell activation and allergic responses using primary mouse

mast cells generated from bone marrow cells of wild type, EC-SOD transgenic, and knock-out mice.

The expression of pro-inflammatory cytokines increased in EC-SOD KO mast cells and decreased

in EC-SOD over-expressing mast cells. Consistent results were obtained in the secretion of pro-

inflammatory cytokines. EC-SOD KO mast cells also showed increased histamine release after

antigen/IgE stimulation or PMA/A23187, suggesting that EC-SOD inhibits mast cell activation.

A passive cutaneous anaphylaxis experiment showed more blood leakage from EC-SOD KO mouse

ear skin, implying that the lack of EC-SOD increases allergic responses. These results suggest that

an altered expression of EC-SOD could cause allergic diseases.

- 81 -

Free Communication

FC-5

Sensitive skin: why is it sensitive?

Eun Ju Kim, Yeon Kyung Kim, Dong Hun Lee, Jung Yun Kim, Min-Kyoung Kim,

Min Jung Lee, Young Mee Lee, Hee Chul Eun, and Jin Ho Chung

Department of Dermatology, Seoul National University College of Medicine, Laboratory of Cutaneous

Aging Research, Biomedical Research Institute, Seoul National University Hospital, Institute of

Human-Environment Interface Biology, Seoul National University, Seoul, Korea.

Although sensitive skin, which is defined as an exaggerated reaction of prickling, burning,

itching, stinging, or tingling sensation to environmental factors, became one of the most prevailing

complaints from those who use cosmetics, the etiology of sensitive skin is not yet fully understood.

In this study, we investigated gene sets and signaling pathway implicated in the pathogenesis

of sensitive skin by using microarray. Sensitive skin individuals (n=9) were discriminated from

normal control skin (n=9) by self-assessment questionnaires and 10% lactic acid sting test. Interestingly,

sensitive skin showed a decreased gene expression profile involved in muscle composition and

contraction, energy metabolism, and ion transport and ionic balance and such downregulated gene

expression led to alteration of physiological factors such as muscle contractility, ATP, Ca2+, and

H+. Moreover, we found that enhanced protons in sensitive skin can provoke pain through

transcriptional activation of TRPV1, ASIC3, and CGRP or aberrant muscle contraction. We selected

three candidate signal pathway regulatory genes (activin A receptor 1C, adiponectin, and

phosphodiesterase 3B) and performed siRNA knockdown analysis in RD cells. The transient

transfection of these genes siRNA in RD cells recapitulated the distinct gene expression profile

and physiologic alterations shown in sensitive skin in vivo. Taken together, our finding suggest

that sensitive skin may be associated with dysregulation of muscle contraction and relaxation

process provoked by exaggerated physiological changes such as abnormal muscle compositions,

reduction of ATP production, aberrant Ca2+ regulation, and impairment of maintaining pH

resulting from altered expressions of related genes. Adiponectin, phosphodiesterase 3B, and activin

A receptor 1C may play crucial roles in the pathogenesis of sensitive skin. Therefore, some specific

activators and ligands against these genes may have the potential as a bioactive molecule in the

treatment of sensitive skin.

- 83 -

The 23rd



Hot Posters(Po-1 ~ Po-5)

- 85 -

Hot Posters

PO-1

TNS4 delayed wound healing through actin cytoskeletal regulation

Seon-Pil Jin, Eun Young Seo, Jin Ho Chung

Department of Dermatology, Seoul National University College of Medicine, Seoul, Korea

Tensin proteins are known to play a pivotal role in cell migration, wound healing and tumorigenesis.

TNS4 is one of the four tensin family members, but little is known about its role in skin epidermal

migration and wound healing. In this study, TNS4 was over-expressed in primary cultured normal

human epidermal keratinocytes (NHEK) in vitro or epidermis in vivo using a GFP tagged adenoviral

over-expression system. We examined the role of TNS4 in the skin through a wound healing assay.

In the TNS4 over-expressed NHEK, TNS4 was observed in the peripheral cytoplasms, and the

morphology and the size of the keratinocytes differed from that of the GFP controls. Consistent

with the morphological change, F-actin polymerization was decreased where TNS4 was over-expressed

on immunocytofluorescent staining. When in vitro scratch assay was performed, scratched area

was remained significantly larger in the TNS4 over-expressed cell layer after 48 hours compared

to the GFP control group (59% VS. 26%, respectively, n=3, p=0.05) indicating that cell migration was

diminished by TNS4 over-expression. Cdc42 have well known associations with F-actin polymeri-

zation and cell migration. We found that Cdc42 protein level was reduced by 50% when TNS4

was over-expressed, in addition to the downstream signals of Cdc42 being reduced. Cdc42 level

was restored when treated with a proteasome inhibitor was treated. When TNS4 was over-

expressed, the proportion of S phase was reduced in TNS4 over-expressed group. Finally, we

confirmed a delay in wound healing in vivo using mice back skin with punch injury. Four days

after wounding, the injured area was 1.7-fold (p<0.05) wider in the TNS4 over-expressed group

compared to the GFP control group. In conclusion, our study suggested that TNS4 over-expression

triggers Cdc42 degradation through a proteasome pathway and eventually affects the cytoskeletal

system, which leads to aberrant cell migration, proliferation, and delayed wound healing.

- 86 -


PO-2

Novel isonahocol E3 exhibits anti-inflammatory and anti-angiogenic effects

in endothelin-1-stimulated human keratinocytes

Shyam K Sah and Tae-Yoon Kim

Department of Dermatology, College of Medicine, The Catholic University of Korea, Seoul, Korea

Endothelin-1 (ET-1) is reported to be a potent mitogenic and pro-angiogenic factor that plays

a vital role in both physiological and pathological processes. ET-1 is implicated in dermal cell pro-

liferation and skin disorders, such as psoriasis and atopic dermatitis. ET-1 and its receptors ET-A

and ET-B could be potential targets for developing specific therapeutics to treat such disorders.

Here, we provide the first report that the brown algae Sargassum siliquastrum produces an

isonahocol [2,-5-dihydroxy-3-(13-hydroxy-3,-7,-11,-15-tetramethyl-12-oxo-hexadeca-2,-6,-14-trienyl)-

phenyl]-acetic acid methyl ester (isonahocol E3) that has functional antagonistic activities against

ET-1 induced inflammatory and pro-angiogenic effects. Isonahocol E3 significantly inhibited ET-1-

induced cell proliferation, as well as inflammatory mediators, such as interleukin-6 (IL-6) and

interleukin-8 (IL-8) and tumor necrosis factor-α (TNF- ), and pro-angiogenic factors includingα

metalloproteinases in immortalized human keratinocytes. We also found that isonahocol E3

suppressed ET-A and -B expression levels and ET-1-induced extracellular signal-regulated kinase

phosphorylation. Experiments with known ET-1 receptor inhibitors BQ123 and BQ788 indicated

that the activity of isonahocol E3 was similar. Taken together, our results suggest that isonahocol

E3 exerts anti-inflammatory and anti-angiogenic activities against ET-1 signaling by regulating the

expression of its receptors and extracellular signal-regulated kinase signaling pathway activation.

- 87 -

Hot Posters

PO-3

TRPV1 inhibitory peptide prevents UV-induced skin responses.

So Min Kang, Sang Bum Han, Young Mee Lee, Yeon Kyung Kim, Chang Yup Shin and

Jin Ho Chung

Department of Dermatology, Seoul National University College of Medicine; Laboratory of Cutaneous

Aging Research, Clinical Research Institute, Seoul National University Hospital; Institute of Dermatological

Science, Seoul National University, Seoul, Korea.

Transient receptor potential vanilloid 1 (TRPV1) channel can be activated by vanilloids, exposure

to ultraviolet (UV) light, heat, or protons, and conditions that occur during tissue injury. In the

present study, we designed new TRPV1 inhibitory peptide mimicking the phosphorylated site by

both protein kinase C (PKC) and Ca2+/calmodulin-dependent protein kinase (CAMK) in TRPV1 (a.a

701-709 : QRAITILDT), and investigated whether this TRPV1 inhibitory peptide can reduce

UV-induced responses.

Treatment with this TRPV1 inhibitory peptide (a.a.701-709) prevented UV-induced mRNA and

protein expression of MMP-1 and pro-inflammatory cytokines such as IL-6 and TNF- in HaCaTα

cells. Moreover, this peptide prevented heat-induced MMP-1 expression in HaCaT cells. Treatment

with this peptide also inhibited capsaicin-induced calcium influx in HaCaT cells. TRPV1 inhibitory

peptide (a.a.701-709) prevented UV-induced skin thickening and also prevented UV-induced

apoptosis in the skin of hairless mice. The mRNA and protein level of UV-induced MMP-13 tended

to be reduced by this peptide. The UV-induced MMP-9 increase was also inhibited by TRPV1

inhibitory peptide (a.a.701-709). Our data suggest that this this TRPV1 inhibitory peptide can be

prevent UV-induced inflammation and skin damages.

Keywords: TRPV1, TRPV1 inhibitory peptide, UV irradiation

- 88 -


PO-4

Expression pattern of sortilin in human hair follicles and its essential role in

hair growth

Long-Quan Pi1, Xing-Hai Jin

1, Sungjoo Tommy Hwang

2, Won-Soo Lee

1

1Department of Dermatology and Institute of Hair and Cosmetic Medicine, Yonsei University Wonju

College of Medicine, Wonju, Korea2Dr. Hwang’s Hair-Hair Clinic, Seoul, Korea

Pro-nerve growth factor (proNGF) and its apoptosis-promoting high-affinity receptor (p75NTR)

regulate the apoptosis in human hair follicles. Sortilin is well known as a required component

for transmitting proNGF-dependent death signals via p75NTR. However, the expression and role

of sortilin in human hair follicles have not yet been clearly shown. In this study, we showed that

human hair follicles express sortilin at the mRNA and protein levels. Sortilin immunoreactivity

was detected both in anagen hair follicles and in the extra-follicular structures. During the transfor-

mation from anagen to catagen, sortilin expression appeared to be up-regulated in the hair matrix

and epithelial strand. In outer root sheath (ORS) keratinocyte culture, proNGF reduced cell viability

and induced cell apoptosis. In human hair follicle organ culture, proNGF significantly inhibited

human hair growth and promoted apoptosis. Moreover, sortilin-neutralizing antibody blocked the

action of proNGF in cultured ORS kerationcytes and human hair follicles. Altogether, these results

indicate that sortilin is involved not only in the termination of anagen in human hair follicles,

but is also involved in proNGF induced apoptosis in human hair follicles.

- 89 -

Hot Posters

PO-5

Homoisoflavanone prevents allergic responses by inhibition of Syk signaling

pathway in mast cells



Mast cells play important roles in allergic inflammatory responses because they produce leukotrienes

(LTs), prostaglandins (PGs), and a variety of inflammatory cytokines. Thus, pharmacological inter-

ventions for allergies have focused on inhibiting mast cell activation. Homoisoflavanone (HIF),

isolated from Cremastra appendiculata Makino, has anti-angiogenic activities; however, its effects

on allergic reactions have not been determined. Thus, we investigated the effects of HIF on allergic

inflammatory reactions and the underlying mechanisms. HIF down-regulated PGD2, LTB4 and

LTC4 production, and inhibited the production of pro-inflammatory cytokines, such as interleukin-6

and tumor necrosis factor-a in activated mouse primary mast cells. The molecular mechanisms

by which HIF caused these inhibitory effects were determined to be the inactivation of spleen tyrosine

kinase (Syk) signaling and the concurrent suppression of cyclooxyganase-2 (COX-2) and 5-lipoxiganase

(5-LOX). HIF inhibited allergic responses in vivo in PCA and compound 48/80-induced ear swelling

mouse models. The efficacy of HIF was better than that of dexamethasone and zileuton. These

results suggested that decreased activation of the Syk pathway together with dual inhibition of

5-LOX and COX-2 in mast cells by HIF may be an effective therapy for allergic diseases.

- 91 -

The 23rd



Posters(P-1 ~ P-31)

- 93 -

Posters

P-1

Prevention and treatment of alopecia areata with mesenchymal stem cells in

the C3H/HeJ mouse model

Ji Won Byun, Myeong Shin Jeon1, Hyo Jin Kim, Jeonghyun Shin, Gwang Seong Choi

Department of Dermatology, Inha University School of Medicine1Department of Biomedical Sciences, Inha University School of Medicine

Alopecia areata (AA) is a common autoimmune disease characterized by non-scarring hair loss.

Current therapeutic options for AA are limited, and there is no effective prevention for recurrent

AA. Emerging evidence of the potent immunosuppressive activity of mesenchymal stem cells

(MSCs) by modulation immune responses enables MSCs to be developed as a promising therapeutic

modality for immune-related or inflammatory diseases. In this study, we first investigated the

effects of MSCs on AA development and treatment in C3H/HeJ mice. We identified potentially

important cytokines and chemokines in the treatment of AA by mcMSCs. Mice with skin graft

induction of AA were injected with PBS, bone marrows from wild type C3H/HeJ mice and mcMSCs

from wild type C3H/HeJ mice. Serum of C3H/HeJ mice was collected at 0, 7, 35 and 49 days

after treatment and assessed for alterations in hematopoietic cytokine secretion using Luminex

assays. In the result, Mice with AA development had increased secretion of IP-10 and MIG induced

by IFN- in serum. mcMSCs injection resulted in a significant decrease in AA development, asγ

compared with that with PBS and bone marrows injection. This result also correlated with signifi-

cant decreases in IP-10 (interferon-gamma-induced protein 10: CXCL10), MIG (Monokine induced

by gamma interferon: CXCL9) after msMSCs injection. In conclusion, our results demonstrated that

mcMSCs provided effective prevention of onset of AA in the C3H/HeJ model, and warrant further

studies to determine whether mcMSCs might be developed as a cell therapy for AA.

Keywords: Alopecia areata, C3H/HeJ, Stem cell therapy

- 94 -


P-2

Differential expression of klotho in human scalp skin and hair follicles

Xing-Hai Jin1, Long-Quan Pi


2, Won-Soo Lee

1


College of Medicine, Wonju, Korea2Dr. Hwang’s Hair-Hair Clinic, Seoul, Korea

Background: Klotho is a newly identified anti-aging protein that plays a pivotal role in regulating

ageing. However, whether klotho expresses in human hair follicles (HFs) and whether klotho

expression correlates with hair growth have not yet been clearly shown.

Objectives and methods: In this study, we examined the expression of klotho in human scalp skin,

human HFs and its expression change in organ cultured human HFs using reverse transcriptase-

polymerase chain reaction and immunofluorescence.

Results: Klotho was expressed in human scalp skin and HF both gene and protein levels. In human

scalp skin, prominent klotho expression was observed in the epidermis. Klotho expression

in the epidermis was increased with keratinization from basal layer to stratrum corneum. In

human anagen HFs, prominent klotho expression was observed in the epithelium. Klotho

expression in the epithelium was increased with keratinization in henle layer and hair cuticle.

Conclusion: Altogether, these results indicate that klotho might be an important regulatory factor

for human hair growth and hair cycle change.

- 95 -

Posters

P-3

A method to accurately evaluate hair growth in organ cultured hair follicles

Xing-Hai Jin1, Long-Quan Pi


2, Won-Soo Lee

1


College of Medicine, Wonju, Korea.2Dr. Hwang’s Hair-Hair Clinic, Seoul, Korea.

Background: Hair follicle (HF) organ culture techniques are widely used in the hair biology research.

In HF organ culture, hair growth is commonly employed as a measurement of follicular activity.

For measurement of hair growth, the microscope fitted with an eyepiece graticule is routinely

used. However, using this method, it is difficult to measure the crooked hair growth which

is always showing in the cultured HFs. Furthermore, even in same anagen phase, individual

HFs are not consistent and showing different hair growth ability, dependent on the hair bulb

size.

Objectives and methods: In this study, we propose an improved method that is designed to

accurately measure the HF length in organ cultured HFs. The improvement focused on the

measurement of crooked hair growth and the detection of effective hair growth relative

parameters to minimize the difference in hair length of individual HFs in same phase.

Results: We showed that there is a significant difference in HF length between linear length which

is measured by routine method and crooked length which is measured by improved method

using in this study. Auber’s line was the most effective hair growth relative parameters to

minimize the difference in hair length of individual HFs in same phase. With this improvement,

the discrete trend of individual HFs was significantly reduced.

Conclusion: Altogether, these results indicate that the current novel method should be more

accurate measurement of hair growth.

- 96 -


P-4

Effect of the catagen transition induced by epidermal growth factor on a

mouse model of chemotherapy-induced alopecia

Ji-Seon Yoon1,2,3

, Seung Hwan Paik1, JiYeon Lee

2,3, Hyeong Ho Ryu

1, Chang Yup Shin

3,

Kyung Hyun Min4, Seong Jin Jo1,2,3, Kyu Han Kim1,2,3, Oh-Sang Kwon1,2,3

1Department of Dermatology, Seoul National University College of Medicine, Seoul, Korea2Laboratory of Cutaneous Aging and Hair Research, Clinical Research Institute, Seoul National University

Hospital, Seoul, Korea3Institute of Human-Environment Interface Biology, Seoul National University College of Medicine, Seoul,

Korea4Bio Research Laboratory, Life Science Research Institute, Daewoong Pharmaceutical Co., Ltd., Yongin, Korea

Chemotherapeutic agents primarily damage highly proliferative anagen hair follicles and thus

it would be worthwhile to investigate whether transition of hair follicle to less proliferative stage

(i.e. catagen) may have beneficial effects in the prevention of chemotherapy-induced alopecia (CIA).

The aim of the present study was to investigate the effect of the catagen transition induced by

epidermal growth factor (EGF) on C57BL/6 mouse model of CIA. We pretreated hair follicles with

a vehicle or EGF encapsulated with nano-liposome system (50 g/ml or 100μ g/ml) which has beenμ

reported to enhance the localization of EGF in skin, before treatment with a chemotherapeutic

agent. To validate the catagen-inducing property of EGF and damage response after chemotherapy,

we evaluated the hair cycle score in histological sections and the number of TdT-mediated dUTP

nick end labeling (TUNEL)-positive cells in the hair bulbs of control and EGF-treated mice. It was

noted that topical EGF application induced early catagen-like stage, representing with a narrower

dermal papilla compared with anagen VI hair and increased apoptotic cells as observed by TUNEL

staining. In addition, after injection of a chemotherapeutic agent (cyclophosphamide 120 mg/kg),

hair follicles treated with EGF entered to less severe chemotherapeutic insult of the dystrophic

anagen pathway followed by primary recovery, whereas hair follicle treated with vehicle entered

to more severe chemotherapeutic insult of the dystrophic catagen pathway followed by secondary

recovery. Thus, the results of this study suggest that catagen inducers could be useful as a new

alopecia-protection strategy, especially in the context of CIA.

- 97 -

Posters

P-5

Role of A20 in therapeutic effect of imiquimod on Squamous cell carcinoma

diseases

Li Zheng Jun, Kyung-Cheol Sohn, Eun-Hwa Im, Myung Im, Young Lee, Chang Deok Kim,

Young-Joon Seo, and Jeung-Hoon Lee

Department of Dermatology, School of Medicine, Chungnam National University, Daejeon, Korea

Squamous cell carcinoma (SCC) is a malignant cancer of the skin epidermal cells. The first line

of treatment for SCC is surgical excision, but some people may not be suitable to this treatment.

Imiquimod is a topical small-molecule immune response modifier and Toll-like receptor 7 (TLR7)

agonist, which has been shown the efficacy against SCC in clinical trials. Although imiquimod

can induces apoptosis in SCC cell, however its mechanism of action is not well understood. The

deubiquitinating enzyme A20 is a key regulator of antiviral and apoptotic signaling pathways.

Thus, we investigate whether A20 can regulate signaling pathway involved in imiquimod’s action

on SCC. In our study, we found that the high expression of A20 in SCC12 cells, and treatment

with imiquimod reduced the A20 expression in a dose-time dependent manner. Treatment with

imiquimod resulted in a strong signal for active caspase-3 and PARP, but after transfected with

A20 adenovirus, caspase-3 and PARP expression were significantly decreased. Phosphorylation

levels of JNK were significantly abolished by overexpression of A20. Furthermore, knockdown of

A20 significantly increased phosphorylation levels of JNK and P38 that were induced by imiquimod.

These results suggested that knock down of A20 (which was induced by imiquimod) will enhance

apoptosis.in SCC12 cells.

- 98 -


P-6

Laser Cancer Prevention: Is the ablative laser for rejuvenation preventive

against ultraviolet-induced skin cancer?

Jiwon Gye1, Jiyeon Yoo

1,2, Ji Seok Kim

1, Jee Young Kim

1, Byung Cheol Park

1, MyungHwa Kim

1,

Seung Phil Hong1

1Department of Dermatology, College of Medicine, Dankook University, Cheonan, Korea2Department of Dermatology, Yonsei University Wonju College of Medicine, Wonju, Korea

Background: Non-melanoma skin cancers, one of the most commonly diagnosed cutaneous malign-

ancies in human, are mainly caused by prolonged ultraviolet (UV) exposure. However, there

is no effective prevention other than avoiding sun exposure. Recently, ablative fractional

photothermolysis (FP) laser treatment is actively being carried out for facial rejuvenation.

Objective: We elucidated whether the occurrence of skin tumor caused by exposure to ultraviolet

light can be decreased by with multi-sessions of ablative FP with CO2 laser.

Materials and Methods: Two groups of hairless mice were treated with either FP or nothing at

3-weeks interval during the 20 weeks of UV exposure period, simultaneously exposed to 60mJ/

cm2 of UVB and 1.8 J/cm2 of UVA three times per week for first 20 weeks. The other group

was treated with only FP without UV exposure. In the following 10 weeks, mice were examined

for tumor development every 2 weeks without any treatments. At the 30-week, termination

of the experiment, representative tumors were taken to evaluate the type of tumor. In addition,

we evaluated the change of skin barrier function, thickness, elasticity at 12 week, 20week.

Results: At 30weeks, FL treated group showed significantly lower average size and the number

of tumors than UV exposed group. Tumor occurred in FL treated group 2~3 weeks later than

UV exposed group. There was no tumor development in the FL-only treated group, and their

skin looked more smooth, tightened. All mice of UV exposed group developed skin tumor,

but 64.3% mice of FL treated group developed skin tumor. And UV exposed group showed

significantly increased in trans-epidermal water loss than FL-treated group.

Conclusion: Ablative FP can be effective for not only the rejuvenation but also the prevention

against skin tumors induced by UV.

Key words: photocarcinogenesis, photoaging, photothermolysis, skin cancer, prevention

- 99 -

Posters

P-7

Genomic variant landscape of Korean melanoma using whole-exome and

transcriptome sequencing

Tae-Gyun Kim1,2,3

, Young-Seok Ju4,5, Jong-Yeon Shin

4, Byung-Ho Oh

3, Hong Sun Jang

3,

Mi-Kyoung Kim2, Hyoung-Pyo Kim1,2, Jeong-Sun Seo4,5,6,7, and Kee Yang Chung3

1Brain Korea 21 Project for Medical Science, Yonsei University, Seoul, Korea2Department of Environmental Medical Biology, Institute of Tropical Medicine, Yonsei University College

of Medicine, Seoul, Korea3Department of Dermatology, Yonsei University College of Medicine, Seoul, Korea4Genomic Medicine Institute, Medical Research Center, Seoul National University, Seoul, Korea5Macrogen Inc., Seoul, Korea6Department of Biochemistry, Seoul National University College of Medicine, Seoul, Korea7Department of Biomedical Sciences, Seoul National University Graduate School, Seoul, Korea

Melanoma is a malignant skin cancer originating from unregulated growth of melanocytes. It

is more prevalent in Caucasians compared to dark-skinned Asians and predominant melanoma

subtypes among the races are considerably different, suggesting that genetic background is an

important factor for melanomagenesis. The identification of molecular events in melanoma that

govern cancer transformation and growth is the fundamental question for developing new targeted

therapy. However, most current studies on melanoma genome have been conducted using

Caucasian samples. To characterize comprehensive genomic variants in Korean melanoma, we

performed a combined analysis of massively parallel whole-exome and transcriptome sequencing

for cancers and paired normal tissues acquired from 2 Korean melanoma patients. We demon-

strated that the cancers displayed 200-300 somatic point mutations such as Q61K in NRAS; however,

other well-known somatic mutations in either KIT or BRAF were completely absent. Copy number

variation analysis revealed that various gains and losses of exonic loci were present. Transcriptome

sequencing analysis showed previously unidentified novel fusion genes that might affect

melanomagenesis. Interestingly, the mutational signature of acral melanoma genome was not

highly compatible with damage due to ultraviolet light exposure, suggesting that other mutational

mechanisms may contribute to the acral melanoma pathogenesis. Further dissection of melanoma

genomes in Asian population may shed light on the development of a promising molecular target

for personalized treatment of Asian melanoma patients.

- 100 -


P-8

Role of Human Papilloma Virus Infection and RAS Mutation in Keratoacanthoma

M.R. Roh1, J.H. Kim

2, S.H. Lee

1, K.H. Park

2, K.Y. Chung

1and S.Y. Rha

2

1Department of Dermatology and Cutaneous Biology Research Institute, Yonsei University College of

Medicine, Seoul, Korea2Yonsei Cancer Centre, Department of Internal Medicine, Yonsei University College of Medicine, Seoul, Korea

RAS gene activation and its association with human papillomavirus (HPV) infection have been

extensively studied in various cancers. However, the correlation between RAS mutations and HPV

in keratoacanthoma (KA) has not yet been investigated. The aim of the present study was to

determine the presence of RAS mutations and their correlation with HPV infection in KA. HPV

DNA was detected by nested PCR in 28 KA specimens. Molecular analysis was also performed

to identify oncogenic mutations (HRAS, KRAS, NRAS, BRAF). Statistical analyses were performed

using the Fisher’s exact tests. HPV DNA was detected in 7 (25%) of the 28 samples, and RAS

mutations were detected in 8 (28.5%). Six samples had an HRAS mutation and two showed the

NRAS mutation. The presence of a RAS mutation was significantly correlated with a history of

chronic sun damage (p=0.033). However, no significant correlation was observed between HPV

infection and RAS mutation. Our findings suggest that mutational activation of the RAS gene is

a common event in KA and that HPV infection and oncogene activation appear to represent two

independent factors in the development of KA.

- 101 -

Posters

P-9

P63 and TGF-β1&-β2 can be important markers in differentiation degree

and malignancy potential of sebaceous/follicular tumors

Su-Young Jeon, Seung-Min Ha, Dong-Yeob Ko, Jin-Woo Hong, Ki-Hoon Song, Ki-Ho Kim

Department of Dermatology, Dong-A University College of Medicine, Busan, Korea

The epidermal stem cells located at the bulge region are responsible for replenishing the hair

lineage, while the stem cells at the isthmus (the junction between the infundibulum and hair follicle)

regenerate interfollicular epidermis (IFE) and sebaceous glands (SG). Among the epidermal appendage

tumors, certain tumors may show any stages of differentiation such as hyperplasia (hamartoma),

adenoma, benign epithelioma, primordial epithelioma and malignant tumor.

The p63 gene is expressed in normal human epidermal appendages, and its correlation with

tumor grading and/or aggressive behavior in epithelial tumors was well studied. During catagen

development in ORS and epithelial strands of the hair, TGF- 1 is increased. Also, a recent studyβ

suggested that TGF- signaling plays an important role in regulating the proliferation, differentiation,β

and apoptosis of distinct epithelial stem cell populations in hair follicles. But, during the carcino-

genesis process, TGF- 1&- 2 as tumor suppressors may also have pro-oncogenic activities in aβ β

complex manner.

We planned to elucidate the expressions of TGF- 1&- 2 and p63 in benign and malignant tumorsβ β

toward hair and sebaceous gland directions and their importance in differentiation degrees of the

corresponding tumors. So, we performed immunohistochemistry studies with some antibodies such

as of Gli1 (a marker for sebaceous tumors), PHLDA-1 (a marker for hair follicle ORS cells), p63,

TGF- 1 and TGF- 2 in trichofolliculomaβ β (n=1), desmoplastic trichoepithelioma (n=3), trichilemmal

carcinoma (n=4), morpheaform BCC (n=3); nevus sebaceous (n=4), sebaceous hyperplasia (n=3),

sebaceous adenoma (n=3), sebaceous epithelioma (n=3), and sebaceous carcinoma (n=5).

Gli1 proteins were expressed in the basaloid cells, sebocytes, sebaceous carcinoma cells, and were

decreased with the higher differentiation. PHLDA-1 were expressed in the ORS cells and some

cells of follicular tumors. The p63 was expressed in nuclei of the outermost basaloid cells (seboblasts)

and poorly-differentiated sebaceous carcinoma cells and was also seen in tumor cells toward hair

direction. Remarkably, TGF- 1 was expressed exclusively in nuclei of benign and malignantβ (hair)

follicular tumors in correlation with the differentiation degree, but not so in sebaceous tumors.

And, TGF- 2 was seen focally in the structures of dermal papilla.β

In conclusion, we propose the usefulness of p63 and/or TGF- 1 in differentiation degree andβ

malignancy potential of sebaceous/follicular tumors and in discerning between trichilemmal

carcinoma and sebaceous carcinoma, for an example.

Keywords: Gli-1, PHLDA-1, p63, TGF- 1, morphogenesis, follicular tumor, sebaceous tumorβ

- 102 -


P-10

Cilostazol inhibits the expression of hnRNP A2/B1 and inflammatory factors

in human dermal microvascular endothelial cells

Zhenlong Zheng, Sung Bin Cho, Do-Young Kim, Suhyun Cho, Min Ju Choi, and Dongsik Bang

Department of Dermatology and Cutaneous Biology Research Institute, Yonsei University College of Medicine,

Seoul, Korea

hnRNP A2/B1 has been identified as a target antigen of anti-endothelial cell IgA antibody in

patients with Behçet’s disease (BD). In addition, cellular hnRNP A2/B1 is increased by the stimulus

of the sera from BD patients or Streptococcus sanguinis. In this study, we aim to investigate the

effects of cilostazol on the expression of hnRNP A2/B1 and inflammatory factors such as CXCL1,

CXCL2, CXCL8 and IL-1 in human dermal microvascular endothelial cells (HDMECs). Expressionβ

of hnRNP A2/B1 and chemokines in HDMECs were induced by tumor necrosis factor (TNF)- ,α

interleukin (IL)-1 , and lipopolysaccharideβ (LPS). mRNA expression of inflammatory factors were

detected by quantitative real-time polymerase chain reaction and found that all four inflammatory

factors significantly increased in HDMECs treated by any stimulators. By contrast, mRNA expression

of hnRNP was significantly increased in HDMECs treated with IL-1 or LPS, but not in TNF-β α

treated cells. Interestingly, mRNA expression of hnRNP A2/B1 and inflammatory factors in HDMECs

treated with various stimulators were significantly inhibited by cilostazol treatment except IL-1β

-induced IL-1 expression and TNF- -induced CXCL-8 expression. Significantly increased proteinβ α

expression of hnRNP A2/B1 was found in HDMECs treated with all three stimulators using

immunocytochemistry. Nuclear and cytoplasmic expression of hnRNP A2/B1 was found in

HDMECs and was effectively inhibited by cilostazol treatment regardless of stimulator and protein

localization. Taken together, we concluded that cilostazol effectively inhibits the expression of hnRNP

A2/B1 and inflammatory factors in HDMECs and the reagent may prove useful in treatment

modalities for BD.

- 103 -

Posters

P-11

Capsiate inhibits the activation and differentiation of mouse CD4+ T cells

through suppressed activation of Lck



Capsaicin exhibits antioxidant, anticancer, and anti-angiogenic effects, but it is rarely used due

to its high pungency. It was reported that capsiate [4-hydroxy-3-methoxybenzyl (E)-8-methyl-6-

nonenoate], isolated from the fruits of a cultivar of Capsicum annuum L. (CH-19 Sweet) is a non-

pungent capsaicin analog with an ester bond instead of the amide bond between the vanillyl

moiety and fatty acid chain and has multiple biological effects, similar to those of capsaicin without

causing irritation. However, the effect of capsiate on T cells is not well studied. In this study,

we investigated the effect of capsiate on mouse CD4+ T cells. Purified mouse naïve CD4+ T cells

were activated with anti-CD3 and anti-CD28 and cultured with or without capsiate for 4days to

determine the anti-proliferative effect of capsiate on activated CD4+ T cells. The result showed

that capsiate inhibited CD4+ T cell proliferation in a dose-dependent manner. Consistently, capsiate

inhibited production of IL-2 from activated CD4+ T cells. Furthermore, our results showed that

the anti-proliferative activity of capsiate was through the inhibition of Lck phosphorylation, which

is necessary for CD4+ T cell activation. The phosphorylation of AKT and NF- B, and Th1 and Th17κ

differentiation were also inhibited by capsiate in CD4+ T. These results suggest the possibility

of further developing capsiate as an immunosuppressive drug for CD4+ T cell-mediated diseases,

such as psoriasis.

- 104 -


P-12

Immune response-regulatory function of blood group antigen in HaCaT cells

Jang-Hee Oh, Ji Young Jung, Min Kyeong Shin, Se-Rah Lee, Jin Ho Chung


Aging Research, Clinical Research Institute, Seoul National University Hospital; Institute of

Dermatological Science, Seoul National University, Seoul, Korea

Since ABH blood group antigen was found on the surface of red blood cells in 1900, many

tissues of human body have been demonstrated to express ABH blood group antigen and their

precursors, including skin. Human skin tissue expresses A or B antigens only in the granular layer,

and H antigen in the granular layer and the upper spinous layer. H antigen is the precursor for

A or B antigen, synthesized by addition of N-D-acetylgalactosamine or D-galactose to H antigen,

respectively, mediated by transferase A or B, coded by the individual’s polymorphism of ABO

gene. Individuals who has non-functional gene are to be O blood type. The synthesis of H antigen

is generally mediated by fucosyltransferase 1 (FUT1) or fucosyltransferase 2 (FUT2), responsible

for type 2 H antigen or type 1 H antigen, respectively. Type 2 H antigen is known as the major

form in human skin, but type 1 H antigen is not detected. However, physiological function of

ABH antigen has not been well elucidated, except in transplantation. Therefore, in this study, we

investigated the inflammatory function of ABH antigens in HaCaT cells by transfection of FUT1

siRNA. B antigen expressed by HaCaT cells was down-regulated by transfection of FUT1 siRNA.

Thereafter, interferon (IFN) -induced intercellular adhesion molecule 1γ (ICAM-1) and human

leukocyte antigen (HLA)-DR protein expression were also down-regulated by transfection ofα

FUT1 siRNA. However, their mRNA levels were not down-regulated by transfection of FUT1

siRNA. Decrease of ICAM-1 protein was found to be caused by accelerated protein degradation

by transfection of FUT1 siRNA, which was inhibited by treatment with MG132, a proteasome

inhibitor. Decrease of HLA-DR protein was found to be caused by decrease of protein level ofα

Cathepsin S, an upstream regulator of HLA-DR, by transfection of FUT1 siRNA. In conclusion,

ABH blood group antigens may play roles in interferon (IFN) -induced ICAM-1 and HLA-DRγ

induction in human skin.

- 105 -

Posters

P-13

Rhododendrin ameliorates skin inflammation through inhibition of NF-κB,

MAPK, and PI3K/Akt signaling

Yoon-Jae Jeon and Tae-Yoon Kim

Department of Dermatology, College of Medicine, The Catholic University of Korea, Seoul, Korea

A wide range of active compounds isolated from nature are used in clinical applications and

as a source of lead compounds for drug development. It is well known that Rhododendron

brachycarpum exerts anti-inflammatory effect in skin diseases; however, the molecule responsible

for these effects has not been identified. In this study, we found that rhododendrin, isolated from

R. brachycarpum leaves has a potent anti-inflammatory effect. Rhododendrin showed intracellular

reactive oxygen species (ROS) scavenging activity and suppressed nuclear translocation of nuclear

factor- Bκ (NF- B) by inhibiting phosphorylation of NF- B, inhibitor of NF- Bκ κ κ (I B ), and I Bκ α κ α

kinase (IKK / ). Furthermore, rhododendrin inhibited mitogen-activated protein kinasesα β (MAPKs),

including ERK1/2, p38, and decreased c-Jun N-terminal kinase (JNK) and phosphoinositide 3-kinase

(PI3K)/Akt signaling. As a result, rhododendrin reduced expression of pro-inflammatory mediators,

such as cyclooxygenase-2 (COX-2), intracellular adhesion molecule-1 (ICAM-1), interleukin-1α (IL-1

), IL-1 , IL-6, IL-8, tumor necrosis factor-α β α (TNF- ), interferon-α γ (IFN-γ), chemokine (C-X-C) motif

ligand 1 (CXCL1), and chemokine (C-C motif) ligand 17 (CCL17) in TNF- /IFN-α γ-stimulated

keratinocytes. Notably, we demonstrated that topically applied rhododendrin alleviated skin

inflammation in trinitrochlorobenzene (TNCB)-treated mouse ear skins. Collectively, these results

indicate that rhododendrin is a biologically active compound that exhibits anti-inflammatory activity

and is a promising candidate molecule to treat inflammatory skin diseases, such as psoriasis

- 106 -


P-14

Time course effects of topical Dermatophagoides farinae applications on the

progression of atopic dermatitis-like symptoms in NC/Nga mice

Ji-Yun Kima, Mi Sook Jeong

a, Kui Young Park

a, Mi-Kyung Lee

b, Seong Jun Seo

a

aDepartment of Dermatology, Chung Ang University College of MedicinebDepartment of Laboratory Medicine, Chung-Ang University College of Medicine

Atopic dermatitis (AD) is not a simple inflammatory skin disease but is a quite complicated skin

syndrome influenced by genetic background and different types of environmental factors such as

allergens and microbes. Although various animal models have been suggested to analyze the

pathogenesis of AD and the development of therapeutic drugs for the disease, there are few reports

to evaluate each stage of the skin condition occurring in the course of AD. In this study, we

identified the correlation between the expressions of immunologic factors and each stage of AD

progression. To evaluate the time course effects of topical allergen stimulations on the onset and

duration of AD-like symptoms, we applied Dermatophagoides farinae extract (DfE) together with skin

barrier disruption on the upper dorsal skin of NC/Nga mice twice a week for 8 weeks.

Repeated application of DfE rapidly elevated the dermatitis score followed by histologic changes

of the skin at the each stage of AD progression in a time-dependent manner. From the 2nd week

of the DfE application, the skin surface appeared the dryness and hemorrhage, and edema and

excoriation occurred from the 3rd week. Interestingly, we found that skin barrier disruption with

4% sodium dodecyl sulfate (SDS) twice a week failed to develop the AD-like skin lesions in

NC/Nga mice. We also identified the correlation between the expressions of AD-related immune

regulatory factors, such as immunoglobulin (Ig) subclasses and cytokines, and the each stage of

AD progression. The changes in the expressions of total and D. farinae-specific Ig E, G1, G2a in

plasma as well as splenic Th1, 2, 17 cytokines affected the change at the each stage of AD-like

skin symptoms.

In conclusion, our results suggest that we should pay attention to the characteristics of each

stage of AD progression and choose the suitable stage of animal model not only to elucidate the

pathogenesis of AD but also to develop and evaluate the therapeutic drugs for AD.

- 107 -

Posters

P-15

Bee venom ameliorates Dermatophagoides farinae-induced atopic dermatitis-

like skin in Nc/NgA mice

Heesu Kim, Shan Jin, Na Ra Lee, Hemin Lee, Jung U Shin, Kwang Hoon Lee



Atopic dermatitis (AD) is a chronically relapsing inflammatory skin disease that is accompanied

by severe itching. Bee venom (BV) has long been used as an oriental traditional medicine to relieve

pain and to treat chronic inflammation. Recently it was reported that BV might be an effective

treatment for allergic diseases. However, clinical effect of BV in treating AD hasn’t been investigated

in depth. This study aimed to address both clinical efficacy and mechanism of BV concerning the

anti-inflammatory effect on AD-like skin lesions in Nc/NgA mice. After AD-like skin lesions were

induced by repeated application of the extract of Dermatophagoides farinae, the NC/Nga mice

were randomly allocated into four treatment groups; non-treatment (AD), bee venom treatment

(BV), vehicle treatment (Vehicle), and methylprednisolone aceponate treated group (MethylP). Each

solution was applied to the AD-like skin once a day for 14 days. The clinical dermatitis score was

significantly improved in BV group than in AD group, whereas the level of serum total Ig E was

not positively correlated with the clinical improvement. Histological analysis showed that BV

didn’t only decrease hypertrophy and hyperkeratosis in the epidermis, but also reduced the

infiltration of inflammatory cells in the dermis. RT-PCR revealed that IL-4 and TSLP decreased

in the skin of BV group, compared to AD control group and vehicle group. However, IL-17 has

relatively increased in BV group, compared with other groups. Also, IFN- was increased in theγ

skin of BV group.

In conclusion, BV appears to be relatively safe and effective for treating of AD-like skin lesions

in Nc/NgA mice, and may be an alternative topical medicine for topical steroid. Furthermore,

BV may affect to modulate immune functions such as Th2 and Th17 related cytokines in the skin

of AD-like skin lesions.

- 108 -


P-16

Role of galanin in UV-induced inflammatory responses in human epidermal

keratinocytes

Min Jung Lee, Jin Ho Chung

Department of Dermatology, Seoul National University College of Medicine; Institute of Dermatological

Science, Medical Research Center, Seoul National University; Laboratory of Cutaneous Aging Research,

Clinical Research Institute, Seoul National University Hospital, Seoul, Korea

The skin is the largest human organ of the body that is directly exposed to the environment.

Ultraviolet (UV) irradiation from the sun is the major environmental cause of skin damage such

as inflammation. Galanin is a biologically active neuropeptide that is widely distributed in the

nervous system. Recently, the neuropeptide galanin is known to be expressed in nonneuronal cells

in the skin as well as neuronal cells. The aim of this study was to investigate the role of galanin

on UV-induced pro-inflammatory cytokine (IL-1 , and IL-6), MMP-1 and COX-2 expression inβ

human epidermal keratinocytes. We demonstrated that UV irradiation increased the expression

of galanin mRNA and protein expression in human epidermis in vivo and cultured keratinocytes

in vitro. We next demonstrated that transfection of galanin siRNA prevented significantly UV-

induced expression of pro-inflammatory cytokines (IL-1 , and IL-6), COX-2 and MMP-1, respecβ -

tively. Galanin siRNA tranfection also significantly inhibited UV-induced phosphorylation of ERK

and JNK, and UV-induced expression of c-Jun and c-Fos proteins. We also observed that galanin

siRNA transfection prevented UV-induced translocation of c-Jun and c-Fos proteins, and NF-kB/

p65 protein into the nucleus, respectively. Therefore, our data suggest that galanin may play an

important role in UV-induced phosphorylation of ERK1/2 and JNK, and also activation of AP-1

and NF-kB transcription factors and their translocation into the nucleus, resulting in increased

expressions of pro-inflammatory cytokines, MMP-1 and COX-2 in human skin.

- 109 -

Posters

P-17

Anacardic acid increases type I procollagen expression following ultraviolet

irradiation via inhibition of DNA methylation in the COL1A2 promoter region

Min-Kyoung Kim, Jin Ho Chung


Aging Research, Biomedical Research Institute, Seoul National University Hospital; Institute of

Human-Environment Interface Biology, Seoul National University, Seoul, Korea

Skin is continuously exposed to many hazardous environmental stimuli, including ultraviolet

(UV) light. The photoaged skin following repeated exposure to solar ultraviolet irradiation shows

largely accumulated damage in cutaneous connective tissue, which is composed mainly of type

I procollagen. UV radiation decreases procollagen production mainly by inhibiting TGF- /Smadβ

signaling pathway. Although histone modification and DNA methylation may plays a crucial role

in transcriptional regulation of type I procollagen, relationship between UV-induced histone

modification and DNA methylation with type I procollagen expression is not clear.

In the present study, we demonstrated the roles of DNA methylation and histone acetylation

in UV-induced regulation of COL1A2 transcription in human dermal fibroblasts (HDFs) by using

AA. UV irradiation decreased type I procollagen expression and decrease phosphorylation of Smad3.

Using chromatin immunoprecipitation assays, we observed that the recruitment of acetyl-H3, p300,

and Smad3 were consistently decreased by UV to a distinct region (-1446/-1320) adjacent to the

p300 binding site (-1406/-1393) in the COL1A2 promoter. However, the recruitment of acetyl-H3,

p300, and Smad3 was increased by anacardic acid (AA) treatment to this region of COL1A2

promoter. Using bisulfite modification and methylation specific PCR (MSP), we observed that DNA

methylation was increased by UV at a distinct region (-1450/-1349) adjacent to the putative p300

binding site (-1406/-1393) in COL1A2 promoter, while the UV-induced DNA methylation was

inhibited by AA, indicating that AA may be inhibitor of DNA methyltransferase. Inhibition of

UV-induced DNA methylation by treatment with a DNMT inhibitor (5-AZA-2'-deoxycytidine; 5-

AZA-DC) resulted in increased recruitment of acetyl-H3 and p300 to this region of COL1A2

promoter. Also, at this region, a decreased DNA methylation was observed by 5-AZA-DC.

These results indicate that methylation of the putative p300 binding site (-1406/-1393) in COL1A2

promoter inhibits recruitment of p300 and acetyl-H3 to this site, leading to less binding of Smad3

to its response elements and decreased synthesis of procollagen. Our results suggest that DNA

methylation plays a critical role in the COL1A2 transcription by UV irradiation.

- 110 -


P-18

Ethanol Extract of Peanut Sprout induces Nrf2 activation and expression of

antioxidant and detoxifying enzymes in human dermal fibroblasts:

implication for its protection against UVB-irradiated oxidative stress

Jee-Young Choi1,2, Da-In Choi

1,2, Jee-Bum Lee

1,2, Suk-Jung Yun

1,2, Dong-Ho Lee

2, Jong-Bang Eun

3,

Seung-Chul Lee1,2*

1Department of Dermatology of Chonnam National University Medical School,2Chonnam National University Hospital Research Institute of Clinical Medicine,3Department of Food Science and Technology and Functional Food Research Center, Chonnam National

University, Gwangju, Korea

A peanut sprout is known to contain a significant level of resveratrol, which was reported to

have beneficial effects in our body due to its antioxidant activities. The purpose of this study was

to evaluate the cytoprotective activity of ethanol extract of peanut sprout (EPS) from ultraviolet

B (UVB)-induced oxidative stress in human dermal fibroblasts (HDF). EPS was revealed to contain

54.2 g/g of trans-resveratrol. The DCF-DA-positive reactive oxygen speciesμ (ROS) level was

increased by 50 mJ/cm2 of UVB irradiation (2150 ± 450% of non-irradiated control), which was

markedly suppressed by EPS treatment (180 ± 42% of control). Annexin V-positive apoptotic cell

death induced by UVB irradiation (16.4 ± 4.5%) was also significantly inhibited by EPS treatment

(6.7 ± 2.5%). EPS induced up-regulation and nuclear translocation of Nrf2, a transcription factor

for antioxidant and detoxifying enzymes, in HDF as a dose-dependent manner. UVB irradiation

up-regulated Nrf2-dependent enzymes of heme oxygenasse-1, NAD(P)H:quinine oxidoreductase-1

and glutathione-S-transferase pi, and they were further stimulated by EPS treatment. Taken together,

EPS is an efficient cytoprotective agent against UVB-induced oxidative stress by activation of Nrf2

and up-regulation of Nrf2-relating antioxidant and detoxifying enzymes in HDF.

- 111 -

Posters

P-19

Comparison between Malassezia folliculitis and non-Malassezia folliculitis

Hyo Sang Song, Sue Kyung Kim, You Chan Kim

Department of Dermatology, Ajou University School of Medicine, Suwon, Korea

Folliculitis is inflammation of hair follicles characterized by erythematous papule and pustules

on beaded area. Causes of folliculitis are various such as bacterial infection, yeast infection, and

drug ingestion. Among various folliculitis, differentiation of malassezia folliculitis from other

folliculitis is important in that treatment is different using antifungal agent mainly. Retrospectively,

we reevaluated the tissues diagnosed previously as folliculitis through serial section of the tissue

and Diastase/Periodic acid-Schiff (D-PAS) staining. Among 100 of folliculitis cases, 20 cases were

already diagnosed as malassezia folliculitis and 80 cases were non-malassezia folliculitis. 80 cases

with non-malassezia folliculitis were reevaluated by serial section of tissue into 10 slices each

stained with hematoxylin and eosin (H&E). Through H&E stain, 10 cases showed many round to

oval yeast organisms in hair follicles that confirmed malassezia folliculitis. Finally, D-PAS stain

was applied to detect yeast organisms at the rest of tissues. Interestingly, in 6 cases tissue, PAS-

positive organisms were detected and diagnosed as malassezia folliculitis. As a result, diagnosis

of 16 cases changed into malassezia folliculitis from non-malassezia folliculitis. Comparing with

non-malassezia folliculitis and malassezia folliculitis, malasseizia folliculitis showed major

involvement on the trunk, and lesser involvement on face and legs with male predilection. Through

this study, we suggest that physician consider serial section and, or D-PAS staining in folliculitis

patients even though no yeasts are detected initially. These additional results enable physicians

to prescribe proper medication to patients.

- 112 -


P-20

Use of Reverse Blot Hybridization Assay for Fast and Accurate Diagnosis

of Superficial Fungal Infections

Sang-Yeon Park1, Bo-Kyung Kim

1, Hyeyoung Lee

2, Hye-young Wang

3, SunghyunKim

2,

Eung Ho Choi1

1Department of Dermatology, Yonsei University Wonju College of Medicine, Wonju, Korea2Department of Laboratory Medicine, Yonsei University, Wonju, Korea3M&D, Inc., Wonju Eco Environmental Technology Center, Wonju, Korea

Superficial fungal infections are very common problems in dermatologic clinics, which are usually

caused by the infection of dermatophytes or yeasts on superficial skin, hair, nails, and oral mucosa.

Conventionally, potassium hydroxide (KOH) preparation and fungus culture have been used for

its diagnosis. However, both of these methods have inconsistent sensitivity and many false negative

results. Also the fungus culture using Sabouraud medias needed at least 2 weeks for species

identification. Therefore, a novel method for fast and accurate diagnosis of superficial fungal

infections has been needed for clinicians.

REBA fungus-ID test (M&D, Korea) is based on a reverse blot hybridization assay (REBA)

principle, that performs the PCR using DNAs extracted from the specimens such as scales, nails

and hair to prepare DNA templates and gives us the results within 48 hours. It can provide us

not only whether the patient is infected, but also which species of fungus are pathogens.

Forty five patients diagnosed as superficial fungal infections by KOH smear or fungus culture

were examined withREBA fungus-ID test (M&D, Korea). Clinical diagnosis was oral candidiasis

(28.9%), onychomycosis (24.4%), tinea corporis (13.3%) and tinea pedis (13.3%), etc. 39 of all patients

(86.7%) showed positive results in KOH preparation while 8 patients (20.0%) of them were negative

in fungus culture. REBA fungus-ID test showed that all of the patients were infected by

dermatophytes or candida. Thirty two patients (88.9%) among 36 patients with fungus culture(+)

had consistent results between fungus culture and REBA fungus-ID test.

Based on these results, REBA fungus-ID test based on REBA principle can be used a sensitive

and specific diagnostic method for superficial fungal infections. Furthermore, REBA fungus-ID

test can identify the causative fungus within 48 hours, much faster than fungus culture. We suggest

that REBA can be used for the fast and accurate diagnosis of superficial fungal infections in the

clinics.

Key words: Superficial fungal infection, Dermatophyte, Candida, Reverse blot hybridization assay

- 113 -

Posters

P-21

Non-selective β-blocker increases the expression of CCL20 in HaCaT cells

stimulated with TNF-αa possible mechanism in exacerbation of psoriasis

Heesu Kim, Sung hee Kim, Dae Suk Kim, Do Young Kim, Dashlkhumbe Byamba, Hyunjoong Jee,

Min-Geol Lee



Both cardioselective and non-cardioselective -blockers are known as drugs that aggravate orβ

induce psoriasis. A possible mechanism is that the decrease of cyclic adenosine monophosphate

induced by -blockers leads to a decrease in intracellular calcium, which consequently increasesβ

cellular proliferation and lack of differentiation, as seen in psoriasis. However, the immunologic

roles of non-selective -blockerβ (NSBB) on the epidermis of psoriasis hasn’t been investigated in

depth. An effort to elucidate these effects of NSBB was made using the HaCaT keratinocytes in

vitro. To induce psoriatic keratinocytes, HaCaT cells were stimulated with TNF- and IL-23,α

fundamental cytokines previously noted for their elementary roles in psoriatic skin. After 24 hours

of incubation, NSBB was added to each TNF- - and IL-23-treated HaCaT keratinocytes. Via ELISA,α

CCL20 expression was shown to be increased in TNF- -treated HaCaT keratinocytes with NSBB,α

when compared to the other pre-treatment groups (p<0.05), whereas the expression of CCL20 of

IL-23-treated HaCaT keratinocytes remained unchanged indifferent to the addition of NSBB.

Meanwhile, up-regulation of IL-1 was observed in TNF- -stimulated keratinocytes regardless ofβ α

NSBB with no significant difference between the groups. ELISA results of CXCL8 NSBB in TNF-α

-treated keratinocytes showed an additive effect, though there were no significant statistical

differences between the other pre-treatment groups. Confocal laser microscopy revealed that NSBB

induced significant translocations of NF-kB p65 into the nuclei in TNF- stimulated keratinocytes.α

In conclusion, although we did not find definitive evidence as to whether NSBB may induce

psoriatic keratinocytes by itself, it was observed that NSBB may increase CCL20 expression in

psoriatic keratinocytes stimulated with TNF- . Furthermore, it seems that NSBB may exacerbateα

psoriasis through the control of the transcription of DNA.

- 114 -


P-22

Intron A inhibits lymph node metastasis in melanoma via inhibition of

lymphangiogenesis by downregulating Prox-1 protein expression

Zhenlong Zheng, Xianglan Zhang*, Junjie Piao, Tae Hyung Kim, Kee Yang Chung,

Mi Ryung Roh

Department of Dermatology and Cutaneous Biology Research Institute, Yonsei University College of

Medicine, Seoul, Korea

*Oral Cancer Research Institute, College of Dentistry, Yonsei University, Seoul, Korea

Intron A is the most commonly used biologically active cytokine in the treatment for high risk

patients with melanoma, but the mechanism of molecular basis of intron A in melanoma are not

fully understood yet. Lymph node metastasis is an independent and reliable prognostic factor for

melanoma and tumor-induced lymphangiogenesis is known to play an important and active role

in the promotion of cancer metastasis to lymph nodes in melanoma. The purpose of this study

is to investigate the effect and mechanism of Intron A on lymphangiogensis. Intron A effectively

inhibited tube formation of lymphatic endothelial cells and reduced Prox-1 protein expression, a

lymphatic endothelial cell marker. Moreover, lymphatic endothelial cells with Intron A treatment

or knockdown of Prox-1 showed significantly decreased motility and invasiveness in co-culture

system (bottom chamber: melanoma cell and melanoma-associated fibroblast; upper chamber:

lymphatic endothelial cells). Nevertheless, in melanoma xenograft mice, frequency of LN metastasis

and lymphatic vessel density were significantly reduced in intron A treated group compared to

control group. In conclusion, intron A effectively inhibits lymph node metastasis in melanoma via anti-

lymphangiogenic activity, and we suggest that prox-1 may be a target for anti-lymphangiogenic

activity in melanoma.

- 115 -

Posters

P-23

Paracrine effect of melanogenesis by increased expression of stem cell

factor and endothelin-1 in Keratinocytes via direct PAR-2 activation

Hyojung Sohn, Ji Young Kim, Dae Suk Kim, Sang Ho Oh



Keratinocytes secrete many mitogenic or melanogenic molecules for melanocytes. Among several

keratinocyte-derived factors, SCF and ET-1 are regarded as main paracrine mediators involved in

skin pigmentation. Protease-activated receptor (PAR)-2 is a member of G-protein coupled seven

transmembrane receptor family. PAR-2 is known to be involved in the production of inflammatory

mediators as well as melanosomes transfer. Thus, in this study, we would like to investigate

whether direct activation of PAR-2 by PAR-2 agonist can induce the production of SCF and ET-1

in keratinocytes.

The expression of SCF and ET-1 in HaCaT cells was examined after PAR-2 activation with PAR-2

activating peptide (PAR-2 AP, SLIGKV-NH2) and kallikrein 5 in western blotting and real time

RT-PCR. After treatment of PAR-2 AP and kallikrein 5, SCF and ET-1 in HaCaT cells were increased

in the levels of protein and mRNA. To confirm if the increase of SCF and ET-1 by PAR-2 AP

and kallikrein 5 was directly associated with PAR-2 activation, incubation of PAR-2 AP and

kallikrein 5 after pretreatment of PAR-2 antagonist and knockdown of PAR-2 expression by PAR-2

siRNA technique were performed. After treatment with PAR-2 antagonist, increased SCF and ET-1

after kallikrein 5 was not observed. In addition, treatment with PAR-2 AP did not increase SCF

and ET-1 in PAR-2 siRNA-treated HaCaT cells contrary to scrambled siRNA-treated HaCaT cells.

In conclusion, our study suggested that PAR-2, which is known to act as a gate of melanin

transfer might directly mediate skin pigmentation via production of keratinocyte-derived mediators

such as SCF and ET-1.

- 116 -


P-24

Effect of ectopic expression of tyrosinase on wound healing

Mi Yoon Kim1, Dae-Kyoung Choi

1, Kyung-Cheol Sohn

1, Dongkyun Hong

1, Myung Im

1,

Young Lee1, Chang Deok Kim

1, Young-Joon Seo

1, Tae-Jin Yoon

2and Jeung-Hoon Lee

1

1Department of Dermatology and Research Institute for Medical Sciences, School of Medicine, Chungnam

National University, Daejeon, Korea2Department of Dermatology and Institute of Health Sciences, School of Medicine, Gyeongsang National

University, Jinju, Korea

The wound healing process involves unexplained mechanisms. An aberration in this process is

known to cause dermal disorders such as keloid or hypertrophic scars, but the mechanism by

which these scars are formed remains to be elucidated. According to previous reports, black skin

have more and larger fibroblasts and melanosomes than white skin. Tyrosinase is a key enzyme

of melanin synthesis. It is found in melanosomes of melanocytes, and is essential for pigmentation.

Tyrosinase is also known to be involved in wound healing and primary immune response. In this

study, we investigate whether ectopic expression of tyrosinase may affect the collagen expression

in human skin dermal fibroblasts. Overexpression of tyrosinase in dermal fibroblasts resulted in

decrease of reactive oxygen species (ROS), and increase of PPAR gamma expression via mTOR

singling pathway. Moreover, overexpression of tyrosinase induced the expression of Bcl-2 and

Beclin-1 (anti-autophagic and anti-apoptotic gene), inhibiting the autophagy and reducing the

expression of collagen. Together, these results suggest that ectopic expression of tyrosinase can

lead to abnormal wound healing via the modulation of collagen expression.

- 117 -

Posters

P-25

Quantitative proteomics profiling of HaCaT cells after stimulation with estrogen

Jung U Shin, Yun Sun Lee, Heran Kim, Jihun Park, Ju Hee Lee, and Kwang Hoon Lee

Department of Dermatology, Cutaneous Biology Research Institute, Yonsei University College of Medicine,

Seoul, Korea

Aging of the skin is associated with skin thinning, atrophy, dryness, wrinkling, and delayed

wound healing. These undesirable aging effects are exacerbated by declining estrogen levels in

postmenopausal women. Replacement of estrogen can restore skin thickness by increasing collagen

synthesis and accelerate wound healing in mouse model. Also wrinkling and dryness can be

improved with estrogen replacement therapy. Furthermore, estrogen modulates local inflammation,

granulation, re-epithelization and possibly wound contraction.

Stable-isotope labeling by amino acids in cell culture (SILAC) is one of the quantitative proteomics

and has emerged as a simple and powerful analysis tool. It involves growing two populations

of cells, one in a medium that contains a ‘light’ (normal) amino acid and the other in a medium

that contains a ‘heavy’ amino acid. Incorporation of the heavy amino acid into a peptide leads

to a known mass shift compared with the peptide that contains the light version of the amino

acid. By this approach, SILAC can be a simple and powerful quantitative proteomics.

To find novel proteins associated with estrogen effects on keratinocyes, we attempted SILAC.

Using SILAC, we identified about one thousand proteins expressed in two groups. Among these

proteins HMGB1 has been validated as a functional protein after estrogen stimulation.

Key words: estrogen, keratinocyte, proteomics

- 118 -


P-26

Role of HMGB1 on lipid production in human sebocytes

Hyuk Chul Kwon, Kyung-Cheol Sohn, Hae-Eul Lee, Young Lee, Chang Deok Kim,

Young-Joon Seo, Jeung-Hoon Lee, Myung Im

Department of Dermatology, School of Medicine, Chungnam National University, Daejeon, Korea

HMGB1 (High Mobility Group Box 1) has been implicated in a variety of biological processes,

including transcription, DNA repair, differentiation, development and extracellular signaling.

However, there is no evidence for potential role of HMGB1 in human sebocytes. In this study,

we demonstrated that HMGB1 in acne tissue was more strongly expressed than normal tissue.

In addition, testosterone increased HMGB1 expression in cultured human sebocytes. To investigate

the effect of HMGB1 on lipogenesis in sebocytes, we evaluated the lipid production by Oil red

O staining and thin layer chromatography. As a result, we showed that HMGB1 induced lipogenesis

and this phenomenon was enhanced in the presence of testosterone. Our findings provide

compelling evidence that HMGB1 has potent lipid-producing effect, and it is tempting to propose

that blocking agents of HMGB1 could be an interesting candidate for the treatment of skin

disorders with increased sebum, such as acne vulgaris.

- 119 -

Posters

P-27

Increased Expression of hypoxia-glycolysis-acidosis sequence related

proteins: An important role in keloid pathogenesis

Zhenlong Zheng, Junjie Piao, Hye Rang On, Kee Yang Chung, Mi Ryung Roh



Keloids represent a prolonged inflammatory fibrotic state with areas that display distinctive

histological features characterized by an abundant extracellular matrix stroma, a local infiltration

of inflammatory cells, and a milieu of enriched cytokines. Over-expression of hypoxia-inducible

factor-1α (HIF-1 ) was frequently found in keloid and was known as involved in extracellularα

matrix remodeling. HIF-1 over-expression can promote over-expression of glucose transporterα

(Glut) family and carbonic anhydrase 9 (CA9) due to aerobic glycolysis. The aim of this study

was to investigate the influence of aerobic glycolysis in keloids. The hypoxia-glycolysis-acidosis

related proteins such as HIF-1 , Glut-2 and CA9 expression were comparatively investigated inα

48 keloid tissues and 8 normal skin tissues using immunohistochemistry. All three protein expres-

sions were significantly increased in keloid fibroblast compared to fibroblast in normal skin tissues.

In addition, in keloid tissues, CA9 over-expression was significantly related to proliferating activity

of keloid fibroblast and collagen synthesis of keloid tissues. Nevertheless, proliferating activity,

collagen synthesis, motility and invasiveness were significantly decreased in CA9 knockdown group

than control group in cultured keloid fibroblast. In conclusion, aerobic glycolysis plays an

important role in keloid pathogenesis and CA9, as an end point of hypoxia-glycolysis-acidosis

sequence, may be a therapeutic target for keloid.

- 120 -


P-28

Decreased Tissue and Serum Expression of Galectin-7 in Patients with

Hypertrophic Scars

Sung Bin Cho1, Jun-Sub Kim

2, Zhenlong Zheng

1, Min Ju Choi

1, Ihn Geun Choi

3,

Hong Shik Oh4 And Keun Jae Ahn3,4

1Department of Dermatology and Cutaneous Biology Research Institute, Yonsei University College of

Medicine, Seoul, Korea2Department of Biotechnology, Korea National University of Transportation, Chungju, Korea,3Specialization Research Center, Hallym University Burn Institute, Hangang Sacred Heart Hospital,

Hallym University, Seoul, Korea4Department of Science Education, Jeju National University, Jeju, Korea

Hypertrophic scars (HS) result from an imbalance between collagen biosynthesis and matrix

degradation during wound healing. To compare the protein profiles of skin tissue obtained from

patients with HS to those of healthy controls, a proteomics approach was taken to compare the

protein profiles of tissue obtained from subjects with and without HS. Serum levels of identified

proteins were quantified by specific enzyme-linked immunosorbent assay (ELISA) in 27 HS patients

and 15 healthy controls. Tissue protein expression was subsequently evaluated using immunohisto-

chemical staining on HS tissue and on serially-obtained control tissue during wound healing.

Galectin-7 expression was decreased in HS tissues relative to control skin and was significantly

decreased in the serum of HS patients compared to healthy controls. Weaker galectin-7 immuno-

reactivity was detected along the cytoplasmic membrane of basal and suprabasal cells in HS

samples. In addition, galectin-7 was stained in the extracellular space of the upper papillary dermis

in HS tissues. Ablative laser treatment used to induce wound healing of healthy control tissue

demonstrated marked galectin-7 expression at the cytoplasmic membrane on days 3, 5, 14, and

21. Pronounced galectin-7 staining at the upper papillary dermis was detected at days 1, 3, and

10. Our data demonstrate that HS is associated with decreased tissue and serum levels of galectin-

7. These results suggest that the differences in galectin-7 expression and sub- and extracellular

distribution may be crucially involved in the pathogenic process of HS.

Key words: hypertrophic scar, galectin-7, proteomics, wound healing

- 121 -

Posters

P-29

Investigation on animal models for acne vulgaris

Sang Lim Kim, Jin Sub Lee, Yoon Hyuk Choi, Yong Hyun Jang, Hyun Ho Son, Mi Yeung Sohn,

Seok-Jong Lee, Do Won Kim, Weon Ju Lee

Department of Dermatology, Kyungpook National University School of Medicine

There exists various animal models of acnegenesis, such as the Mexican hairless dog, the Rhino

mouse, and the rabbit ear assay. Acnegenic components, such as keratinization, androgen and

sebum, have been investigated with animal models. In this study, acnegenenic components, P. acnes

and liphopolysaccharide (LPS), were examined on the ear and back of mouse.

Ear thickness, morphological and histopatholgical examination, gene and protein expression

were investigated after injection of P. acnes and LPS each on the ear and back of mouse. For human

model, human hair follicle transplantation was conducted to the mouse. We could see the difference

of ear thickness between treated site and control site. We could find that mouse ear was more

prominent inflammation than its back. In addition, inflammatory infiltrate was prominent in the

treated ear compared with control ear. PCR analysis showed the expression of IL-1ß, IL-6 and

TLR-2 was increased in the treated ear according to their concentration. Immunohistochemistry

also supported an increase of their protein expression. Human hair follicles were successfully

transplanted into the mouse back.

P. acnes and LPS were proved to be main acnegenic factors in the developing acne animal model.

In the near future, animal model reflecting human acne may be established using a human hair

transplanted mouse.

- 122 -


P-30

Utility of eosinophil cationic protein levels in early diagnosis of intrinsic atopic

dermatitis

Song Youn Park, MD1, Sohee Oh, PhD

2, EunJi Kim, MD

1, So Young Yoon, MD

1,

Hyun Sun Park, MD1, Hyun-Sun Yoon, MD, PhD1, Soyun Cho MD, PhD1

1Department of Dermatology, 2Department of Biostatistics, Seoul National University Boramae Hospital,

Seoul, Korea

Background: Intrinsic type atopic dermatitis (ADi) is atopic dermatitis (AD) with low serum IgE

and no allergen-specific IgE. There have been few laboratory markers to diagnose or evaluate

the severity of ADi. Recently several reports have been published showing that eosinophil

cationic protein (ECP) correlates with clinical severity of atopic dermatitis; however, report

are scarce and controversial regarding the age-related changes and diagnostic utility of ECP

in AD.

Objectives: We aimed to compare the clinical and laboratory parameters between ADi and extrinsic

atopic dermatitis (ADe) and to assess the usefulness of ECP in diagnosing AD including ADi.

Methods: A retrospective chart review was done on 178 patients 0~42 years of age diagnosed with

atopic dermatitis. All patients were checked for total IgE, ECP and allergen-specific IgE with

a thorough review of their medical history.

Results: Mean age of subjects with ADi and ADe was 5.2 ± 7.1 and 10.3 ± 10.9 (p=0. 014), respec-

tively. ADi had milder disease compared to ADe and less family history. ECP was elevated

in both AD phenotypes. It was lower in ADi group (23.9 ± 17.0) than in ADe (56.2 ± 107.9)

but not significantly (p=0.10). There was a positive correlation between age and total IgE

(r=0.504, p< 0.0001), and between severity and total IgE (p=0.01). ADi patients under age two

had significant negative correlation of ECP with age (r=-0.785, p=0.001).

Conclusion: ECP can be considered an early marker of AD especially in very young children. High

ECP value can assist in the diagnosis of ADi in infants.

Key words: atopic dermatitis, eosinophil cationic protein, intrinsic atopic dermatitis

- 123 -

Posters

P-31

Clinical manifestations and skin barrier properties of Korean male patients

with X-linked recessive ichthyosis diagnosed by FISH analysis to detect STS

deletion

Noo Ri Lee, Bo-Kyung Kim, Na Young Yoon, Minyoung Jung, Eung Ho Choi

Department of Dermatology, Yonsei University Wonju College of Medicine, Wonju, Korea

X-linked recessive ichthyosis (RXLI) is an inherited ichthyosis characterized by generalized

dryness and scales, and is caused by deficiency of steroid sulfatase (STS) which results in an

accumulation of cholesterol sulfate in the intercorneocyte lipids. The STS gene is located on the

distal tip of the short arm of X chromosome, locus Xp22.3. RXLI must be differentiated from

ichthyosis vulgaris (IV) showing very similar clinical manifestations.

We evaluated clinical manifestations and skin barrier function of 11 Korean male RXLI patients,

who were diagnosed by fluorescence in situ hybridization (FISH) and array analysis. Their ages

ranged from 8 to 39 years old (mean=19.8). The onset age of ichthyosis of 3 patients were ‘from

birth’, 3 patients were ‘between 2 to 12 months old’, and 5 patients were ‘after 1 year old’. In

the progress of skin lesions, 6 patients showed ‘no changes’, 2 patients showed ‘aggravation’ and

3 patients showed ‘improvement’ of the skin lesion. All of the patients had uninvolved ‘flexural

skin of extremities’, which was quite different with previous reports, and 7 patients also showed

uninvolved ‘face’. As the past history of atopic diseases, 4 patients had ‘atopic dermatitis’, 3

patients ‘allergic rhinitis’ and 1 patient ‘asthma and allergic rhinitis’. Among them, 5 patients had

atopic symptoms in the past year. Three patients had family history of atopic dermatitis. Four

patients showed elevated serum IgE level. Histopathology of ichthyosis lesions showed normal

or slightly increased granular layers in all patients. In the functional study on skin barrier, all

patients showed significantly lower stratum corneum hydration compared to normal controls, but

no difference in basal transepidermal water loss (TEWL). Skin surface pH was increased in the

ichthyosis lesion compared to the uninvolved skin.

We believe that this is the first report on RXLI patients in Korea diagnosed by FISH and array

analysis as the most definite diagnosis. Here we have found the novel features of RXLI that it

usually does not involve the flexures of extremities, frequently correlate with atopic diseases like

IV, and does not accompany changes in basal TEWL.

Keyword: X-linked recessive ichthyosis, atopic diseases, skin barrier, FISH

- 125 -


대한피부연구학회 회칙

제 1장 총 칙

제 조 명칭 본 학회는 대한피부연구학회 라1 ( ) (The Korean Society of Investigative Dermatology)

칭한다.

제 조 목적 본 학회는 피부과학의 기초 및 임상 연구를 촉진하여 피부과학 발전에 기여함을2 ( )

목적으로 한다.

제 조 사업 사업 본 학회는 제 조의 목적 달성을 위하여 다음과 같은 사업을 수행한다3 ( ) ( ) 2 .

학술대회 및 강연회 개최1.

학회보 및 학회지의 발행2.

국내 국외의 관계 학술 단체와의 교류 및 제휴3. ,

기타 본 학회 목적 달성에 필요한 사업4.

제2장 회 원

제 조 자격 본 학회의 회원은 피부과학의 연구에 종사하거나 피부과학 연구에 관심을 가지고4 ( )

본 학회의 취지에 찬동하는 자로서 소정의 입회 수속을 밟고 상임이사회의 심의

및 추천을 받은 후 이사회의 의결을 거친 자로 한다.

제 조 구분 본 학회의 회원은 다음과 같이 구분한다5 ( ) .

정 회 원 피부과학 또는 관련분야의 연구자로서 본 학회 목적에 찬동하는 자로 한다1. : .

국외회원 외국에서 피부과학 또는 관련분야에 종사하는 자로서 본 학회 목적에 찬동하는2. :

자는 국외회원이 될 수 있다.

명예회원 피부과학 연구 업적이 탁월하고 본 학회 발전에 공헌이 지대한 자는 명예회원3. :

이 될 수 있다.

단체회원 본 학회의 목적에 찬동하는 연구소는 단체회원이 될 수 있다4. : .

제 조 의무 회원은 본 학회의 회칙 제규정 및 결의사항을 준수하여야 하고 정회원 국외회원6 ( ) , , ,

및 단체회원은 회비 및 기타의 부담금을 납부할 의무가 있다.

제 조 권리 모든 회원은 본 학회에서 발간하는 학회지를 배부 받을 권리가 있으며 정회원은7 ( )

선거권 피선거권 및 기타 소정의 의결권을 가진다, .

제 조 제명 본 학회의 의무를 준수하지 않거나 본 학회의 명예를 훼손하거나 정당한 이유없이8 ( ) , ,

년 이상 회비를 납부하지 않은 회원은 이사회의 의결을 거쳐 총회의 인준을 받아3

제명할 수 있다.

제3장 임 원

제 조 구성 본 학회는 회장 명 차기회장 명 이사장9 ( ) (President) 1 , (President-elect) 1 , (Chairman)

명 이사 명 내외 감사 명의 임원을 둔다1 , (Board of Directors) 20 , (Auditors) 2 .

- 126 -


제 조 선임10 ( )

회장과 차기회장은 전임회장단의 추천 후 총회에서 인준한다1. .

감사는 총회에서 선출한다2. .

이사장은 이사회에서 투표로 선출하여 총회의 인준을 받는다3. .

이사 및 상임이사는 이사장이 선임하고 총회의 인준을 받는다4. .

제 조 임기 임원의 임기는 년으로 하며 연임할 수 있다 단 회장의 임기는 년으로 한다11 ( ) 2 . , 1 .

회장 및 이사장은 연임할 수 없다 이사의 임기는 년으로 하고 매년 분의 씩. 3 3 1

보선 교체한다 전임자의 유고로 인해 보선된 임원의 임기는 전임자의 잔여 임기.

간으로 한다.

제 조 직무12 ( )

회장은 본 학회를 대표하여 업무를 총괄하고 총회의 의장이 된다1. .

차기회장은 회장 유고 시 그 직무를 대행하여 현 회장의 임기 후 회장작을 맡는다2. .

이사장은 이사회의 업무를 총괄하고 이사회 및 상임이사회의 의장이 된다3. .

이사는 이사회의 구성원이 되며 본 학회 운 의 주요한 사항을 심의한다4. .

상임이사는 이사회 및 상임이사회의 구성원이 되며 본 학회의 제반 업무를 집행한다5. .

상임이사의 제반 업무를 보좌하기 위하여 간사를 둘 수 있다 간사는 이사회 및 상임이사6. .

회에 참석할 수 있다.

감사는 본 학회의 재산 상황과 사업과 관련된 사항을 감사하고 이를 총회에 보고한다7. .

제4장 회 의

제 조 구분 본 학회에는 총회 이사회 상임이사회를 둔다13 ( ) , , .

제 조 총회14 ( )

정기총회는 년 회 회장이 소집한다 단 정회원 분의 이상의 요구나 이사회의 요청이1. 1 . , 5 1

있으면 임시총회를 소집하여야 한다.

총회는 정회원의 분의 출석으로 성립하고 재적인원 과반수로 의결한다 단 총회가2. 3 1 . ,

성립되지 않을 때는 총회에 참가 등록한 정회원의 분의 출석으로 성립하고 재적인원3 1

과반수로 의결한다.

총회는 다음과 같은 사항을 의결한다3. .

회장 차기회장 감사 선출(1) , ,

이사장 이사 상임이사 인준(2) , ,

예산과 결산(3)

회칙 개정의 인준(4)

기타 이사회에서 제출한 사항(5)

제 조 이사회15 ( )

이사회는 이사장 이사와 상임이사로 구성하고 회장단 감사 및 간사가 참석할 수 있다1. , .

이사회는 이사 과반수 출석으로 성립하고 재적인원 과반수로 의결한다2. .

정기이사회는 년 회 이사장이 소집한다 단 임시 이사회는 이사장이 수시로 소집할 수3. 2 . ,

있으며 이사 분의 이상의 요구가 있을 때 소집하여야 한다, 3 1 .

이사회는 본 학회의 운 에 필요한 제반 사항을 심의 의결 또는 인준한다4. , .

- 127 -


제 조 상임이사회16 ( )

1. 상임이사회는 이사장 총무이사 학술이사 간행이사 재무이사 정보이사 및 약간 명의 무, , , , ,

임소 이사로 구성하며 본 학회의 운 에 필요한 제반 사항을 심의하고 업무를 집행한다.

각 상임이사는 다음과 같이 회무를 분담한다2. .

총무이사 본 회의 관리 회무 및 회원 상호간의 친목 등에 관한 업무 총괄1) : ,

학술이사 학술대회 및 학술 등에 관한 업무2) :

간행이사 학회보 학회지 및 기타 간행 등에 관한 업무3) : ,

재무이사 재정 및 회계 등에 관한 업무4) :

정보이사 정보 통신 및 홈페이지 관리와 운 에 관한 업무5) : ,

각 상임이사는 정회원 약간명씩으로 구성된 운 위원회 학술위원회 간행위원회 재무위3. , , ,

원회 정보위원회를 구성할 수 있다, .

제5장 재 정

제 조 재원 본 학회의 재원은 회비 입회비 찬조금 및 기타 수익금으로 한다17 ( ) , , .

제 조 회계 연도 본 학회의 회계 연도는 매년 정기총회에서 다음 정기총회일까지로 한다18 ( ) .

제 조 감사 본 학회의 수지결산은 감사의 감사를 거쳐 차기 정기총회에 보고한다19 ( ) .

제6장 부 칙

제 조 본 회칙의 개정은 이사회의 심의를 거쳐 총회의 인준을 받아야 한다20 .

제 조 본 회칙에 규정되지 않은 세칙은 일반 관례에 준한다21 .

제 조22

본 회칙은 공포일 년 월 일부터 시행한다1. (1991 3 23 ) .

본 회칙은 년 월 일부터 개정 시행한다2. 1992 3 21 .







- 128 -


대한피부연구학회 연혁

1991. 2. 2 발기인대회

강남성모병원에서 발기인 인이 참석50

1991. 3. 23 창립총회 및 제 차 학술대회1 르네상스호텔( )

특강연자 : Sadao Imamura (Kyoto Univ.)

박상대 서울대 자연과학대( )

일반연제 편10

제 대 회장단 취임1

회장 김 표 이사장 이정복: , :

1991. 11. 23 제 차 심포지엄1

주제 발표 연제: Interleukin, : 6

강남성모병원

1992. 3. 21 제 차 학술대회2 르네상스호텔( )

특강연자: Jouni Uitto (Thomas Jefferson Univ.)

교육강연 연제 심포지엄 광피부과학 연제 심포지엄 연제2 , 6 , PCR 6 ,

포스터 연제19

제 차 총회에서 회칙개정2

평의원제를 폐지하고 이사장 상임이사제도를 신설,

1992. 11. 7 제 차 심포지엄2 가톨릭의대 대학원 강의실( )

주제 피부세포배양 발표 연제: , : 6

가톨릭의대 대학원 강의실 여명 참석130

대한피부연구학회보 창간

1993. 3. 20 제 차 학술대회3 르네상스호텔( )

특강연자 : Irvin H. Epstein (USCF)

교육강연 연제 구연 연제 포스터 연제6 , 13 , 14

제 대 회장단 취임2

회장 이유신 이사장 윤재일: , :

1993. 11. 6 제 차 심포지엄3 가톨릭의대 대학원 강의실( )

주제 분자생물학 발표 연제: , : 9

국외 초청연자 : Peter Steinert (NIH)

정수일 (NIH)

1994. 3. 19 제 차 학술대회4 소피텔 앰버서더호텔( )

특강연자 : K. Nishioka (Tokyo Medical and Dental Univ.)


1994. 11. 5 제 차 심포지엄4 가톨릭의대 마리아홀( )

주제 광의학 발표 연제: , : 8

대한피부연구학회지 창간호 발간

1995. 3. 18 제 차 학술대회5 쉐라톤 워커힐호텔( )

특강연자 : Roger Allen (University Hospital Nottingham)


- 129 -


제 대 회장단취임3

회장 허원 이사장 노병인: , :

1995. 11. 25 제 차 심포지엄5 가톨릭의대 마리아홀( )

주제 발표 연제: Apoptosis, : 5

국외 초청연자 대학: Kouichi Ikai (Kyoto )

1996. 3. 16 제 차 학술대회6 서울중앙병원( )

특강연자 : Motomu Manabe (Juntendo Univ.)

교육강연 연제 구연 연제 심포지엄 유전질환 연제 포스터 연제4 , 14 , ( ) 6 , 8

1996. 11. 23 제 차 심포지엄 호텔롯데6 ( )

주제 노화와 광노화 발표 연제: , : 13

국외 초청연자 : John J. Voorhees (Univ. of Michigan)

Masamitsu Ichihash (Kobe Univ.)

1997. 3. 4 대한피부연구학회가 대한의학회 준회원으로 인준받음

1997. 3. 15 제 차 학술대회7 서울중앙병원( )

특강연자 : C. E. Orfanos (Free Univ.)

심포지엄 모발 특강연자 : S. Arase (Tokushima Univ.) /

R. Tsuboi (Juntendo Univ.) / A. G. Messenger (Royal Hallamshire

김정철 경북대Hospital) / ( )

구연 연제 포스터 연제14 , 10


회장 이성낙 이사장 방동식: , :

1997. 11. 15 제 차 심포지엄7 가톨릭의대 의과학연구원( )

주제 피부과학 연구에서 새로운 연구장비의 활용 발표 연제: , : 7

국외 초청연자 (SID sponsored lecturer) : David A. Norris (Univ. of Colorado)

Warren W. Piette (Univ. of Iowa)

1998. 3. 14 제 차 학술대회8 가톨릭의대 의과학연구원( )

특강연자 : Kazuhiko Takehara (Kanazawa Univ.)

교육강연 연제 자유연제 연제 포스터 연제3 , 15 , 20

심포지엄 연제Wound healing, 5

1998. 9. 24 제 차 심포지엄8

주제 : Bullous dermatoses

특강연자 : Grant J. Anhalt (Johns Hopkins Univ.)

발표 연제: 5

1999. 3. 13 제 차 학술대회9 서울대학교병원 임상의학연구소( )

특강연자 : Alfred T. Lane (Standford Univ.) / 이광훈 연세의대( ) /

Russell P. Hall (Duke Univ.)

자유연제 연제 포스터 연제18 , 21

심포지엄 피부질환 연구를 위한 동물실험기법 연제, 5

제 회 우암학술상 시상 이광훈 연세의대1 : ( )


회장 고재경 이사장 은희철: , :

대한피부연구학회지 년 회 발행4

- 130 -


년부터 년 회에서 회로 발행함1999 2 4

2000. 3. 17 제 차 학술대회10 서울대학교병원 임상의학연구소( )

특강연자: Luis Diaz (North Carolina Univ.)

Irene Leigh (St.Bartholomew's and Royal London School)

Yasuo Kitjma (Gifu Univ.)

자유연제 연제 포스터 연제 심포지엄 자가면역질환 연제18 , 14 , 7

피부생물학 연수교육 강의12

제 회 우암학술상 시상 조광현 서울의대2 : ( )

2001. 3. 17 제 차 학술대회11

특강연자: 고베 대학 일본Masamitsu Ichihashi ( , )

Ralf Paus (Hamburg Uni., Germany)

자유연제 연제 포스터 연제 심포지엄 피부생물학 연수교육 강의16 , 24 , 12

제 회 우암학술상 시상 김도원 경북의대3 : ( )


회장 이정복 이사장 이광훈: , :

2002. 3. 15 제 차 학술대회12 가톨릭대학교 의과대학 의과학 연구원( )

특강연자: Mark Udey (NIH NCI), Kunihiko Tamaki (Tokyo Uni.)/

Thomas Luger (Westfaelische Wilhelms Uni.),

Setsuya Aiba (Tohoku Uni.)

자유연제 연제 포스터 연제 심포지엄 연제15 , 27 , Dendritic Cell, 7


제 회 우암학술상 시상 김수찬 연세의대4 : ( )

2003. 3. 28 제 차 학술대회13 강남성모병원 의과학연구원( )

특강연자: 미국 의과대학 피부과 교수Michael J. Detmar, M.D. / Harvard

미국 원장Stephen I. Katz, MD, Ph.D. / NIAMS NIH

독일 대학 피부과 교수Enno Christophers, M.D./ Kiel

자유연제 연제 포스터 연제 심포지엄 연제 피부생물학 연수교육 강의18 , 35 , 6 , 8

제 회 우암학술상 시상 서성준 중앙의대5 : ( )

2004. 3. 26 제 차 학술대회14 서울아산병원 동관 층 대강당( 6 )

특강연자 미국 의과대학 피부과 교수: Thomas S. Kupper, M.D. / Harvard

미국Joost J. Oppenheim, M.D. / NIH Laboratory of Molecular

Immunoregulation

자유연제 연제 포스터연제 연제 심포지엄 연제 피부생물학 연수교육 강의20 , 26 , 6 , 8

제 회 우암학술상 시상 김태윤 가톨릭의대6 : ( )

2005. 3. 25 제 차 학술대회15 서울아산병원 동관 층 대강당( 6 )

특강연자 일본: Akira Ito, Ph.D. / Department of Biochemistry and Molecular

교수Biology, Tokyo University of Pharmacy and Life Science

미국 의대 병리학 교수James Varani, Ph.D. / University of Michigan

자유연제 연제 포스터연제 연제 심포지엄 연제19 , 28 , Extracellular matrix, 7


제 회 우암학술상 시상 이민걸 연세의대6 : ( )

2006. 3. 24 제 차 학술대회16 서울대학교병원 임상의학연구소 층 강당( 1 )

- 131 -


특강연자: 미국Jackie Bickenbach, Ph.D./ Anatomy & Cell Biology,

Dermatology, Molecular Biology, The University of Iowa

일본Emi Nishimura, M.D., Ph.D./ Department of Dermatology and

Creative Research Institute Sousei, Hokkaido University Graduate

School of Medicine

자유연제 연제 포스터연제 연제 심포지엄 연제19 , 62 , Epidermal stem cell 7

연제 피부생물학 연수교육 강의6

제 회 우암학술상 시상 최지호 울산의대8 : ( )


특강연자 미국: Prof. George Cotsarelis, M.D/ Dept of Dermatology, University

of Pennsylvania School of Medicine

일본Prof. Kotaro Yoshimura, M.D./ Department of Plastic Surgery,

University of Tokyo School of Medicine

자유연제 연제19

포스터연제 연제36

심포지엄 연제Stem cell 5

제 회 우암학술상 시상 이증훈9 : 충남의대( )


특강연자: 프랑스Alain Mauviel Ph.D/ Research Director 2nd class,DR2, INSERM

일본Prof. Hiroshi Shimizu M.D./ Dept of Dermatology Hokkaido

University Graduated School of Medicine

자유연제 연제 포스터연제 연제 연제10 , 40 , 1st KSID-JSID Joint Symposium 6

제 회 우암학술상 시상 이원수 원주의대10 : ( )

2009. 3. 19~ 21 제 차 학술대회19 서울대학교병원 임상의학연구소 층 강당( 1 )

특강연자 : Tan Suat Hoon (National Skin Center, SIN)

Richard Clark (The State Univ. of New York Stony Brook, USA)

John McGrath (King's College, St. Thomas's Hospital, London, GBR)

Dong Youn Lee (Sungkyunkwan Univ., KOR)

Yohanes Widodo (Gadjah Mada Univ., INA)

Amrinder Jit Kanwar (Postgraduate Institute of Medical Education

and Research-Chandigarh, IND)

Li-Fang Wang (National Taiwan Univ. Hospital, TPE)

Phan Hong Hai (Hospital of Dermato-Venereology, Ho Chi Minh City, VIE)

Zhou Chen (Peking Univ. People's Hospital, CHN)

Belen Dofitas (St. Luke's Medical Center, PHI)

자유연제 연제 포스터연제 연제 연제10 , 40 , Symposium I: Aging 4 ,

연제Symposium II: Animal Models in Dermatologic research 3 ,

제 회 우암학술상 시상 박경찬 서울의대11 : ( )

2009. 10.31~11. 1 제 회1 Research CAMP

Cutaneous Biology(Epidermis, Dermis, Adipose Tissue, Skin Appendage),

Skin Diseases (FMF, Acne, vitiligo, Atopic dermatitis, Psoriasis, etc)

2010. 4. 2~3 제 차 학술대회 서울대학교병원 임상의학연구소 층 강당20 ( 1 )

- 132 -


특강연자 : Shigetoshi Sano (Kochi Univ. Japan)

Chun-CDi HE (China Medical Univ., China)

Hironobu Ihn (Kumamoto Univ., Japan)

자유연제 연제 포스터구연 연제 포스터연제 연제 연제8 , 6 , 40 , SymposiumI: EMT 3

연제Plenary Lecture 2

제 회 우암학술상 시상 유욱 연세의대12 : ( )

2010. 8.27~28 제 회2 Research CAMP

Melanogenesis & Pigmentary disorders, Inflammation & Autoimmunity

2011. 3. 25~26 제 차 학술대회 서울대학교병원 임상의학연구소 층 강당21 ( 1 )

특강연자 : Sonja Ständer (Münster Univ, Germany)

Kenji Takamori (Juntendo Univ, Japan)

Hideya Ando (Doshisha Univ, Japan)

Shiou-Hwa Jee (National Taiwan Univ, Taiwan)

자유연제 연제 포스터구연 연제 포스터연제 연제 연제6 , 6 , 31 , Symposium I: Itch 3 ,

연제 연제Symposium II: Melanogenesis 3 , Plenary Lecture 2

제 회 우암학술상 시상 이석종 경북대13 : ( )

2012. 3. 23~24 제 차 학술대회 가톨릭의대 성마리아홀22 ( )

특강연자 : Chung-Hsing Chang (Kaohsiung, Taiwan)

Manabu Ohyama (Tokyo, Japan)

Jürgen Schauber (Munich, Germany)

Alain Mauviel (Orsay, France)

Tomotaka Mabuchi (Kanagawa, Japan)

Liangdan Sun (Anhui, China)

자유연제 연제 포스터연제 연제포스터구연 연제9 , 36 ( 7 ), Symposium I: Angiogenesis

연제3 , 연제 연제Symposium II: Hair 3 , Plenary Lecture 1

제 회 우암학술상 시상 김창덕14 : 충남의대( )

2012. 10. 26~27 제 회 추계심포지움 및 부산대학교병원4 KSID Research Camp 2012 ( )

Mesenchymal Stem Cells, Dendritic Cells, Research Communication

2013. 3. 22~23 제 차 학술대회 가톨릭의대 성마리아홀23 ( )

특강연자 : Keiji Iwatsuki (Okayama University, Japan)

Sam Hwang (Medical College of Wisconsin, USA)

Kenji Kabashima (Kyoto University, Japan)

Yoshiki Tokura (Hamamatsu University, Japan)

Masayuki Amagai (Keio University, Japan)

Chikako Nighigori (Kobe University, Japan)

Shigaku Ikeda (Juntendo University, Japan)

Jianzhong Zhang (Peking University, China)

자유연제 연제 포스터연제 연제포스터구연 연제 연제5 , 36 ( 5 ), Invited Lectures 1~6: 15

제 회 우암학술상 시상15 : 최응호 연세원주의대( )

제목 : 대한피부연구학회 평생회원 안내 및 회비 납부안내의 말씀

1. 대한피부연구학회에 대한 귀 회원님의 관심과 성원에 감사드립니다.

2. 본 대한피부연구학회는 피부과학의 기초 및 임상연구를 촉진하여 우리나라 피부과학의 기초 연

구분야 발전에 기여함을 목적으로 1991년 창립 후 피부과의사뿐만 아니라 관련분야의 과학자와

연구자가 함께 참여하는 모임으로 피부질환의 연구, 피부과 관련분야 학술대회, 강연회 및 연구

자캠프 개최, 학회보 및 학술지의 발행은 물론 향후에도 각종 피부건강 증진을 위한 각종 다양

한 사업을 전개코자 노력하고 있습니다.

3. 회원님을 비롯한 목적을 같이하시는 분들의 성원에 힘있어 학회 창립부터 현재까지 많은 회원

들이 가입하셨고, 활동을 하고 계시지만, 가입 후 연회비 수취가 제대로 이루어지지 않으면서,

본학회의 재정 및 회원관리에 어려움이 있어 왔습니다. 하여 안정적인 학회 재정 운영 및 회원

관리를 목적으로 2008년부터 연회비제도 외에 평생회비(30만원)제도를 신설한 바 있습니다.

4. 따라서 금번에 기존에 매번 연회비를 내고 계신 회원님들께 평생회원으로 전환하시도록 적극

권유드리는 바이며, 학회의 안정적 운영을 위해 평생회비 납부에 적극 동참하여 주실 것을 부

탁드립니다.

물론, 종전대로 연회비(년 3만원) 납부도 가능합니다.

5. 평생회비(30만원) 및 연회비(년3만원) 입금은 아래 계좌를 참조하시기 바랍니다.

입금계좌 : KB국민은행 210701-04-309136 예금주 : 이경호(대한피부연구학회)

첨부된 평생회원 등록양식을 아래 Email로 보내주시면 됩니다.

또한 학회 홈페이지(www.ksid.com)에서 회원가입을 하시면 평생회원으로 여러 가지 다양하고

유익한 정보 등을 전달받으실 수 있습니다.

문의 및 접수 : 대한피부연구학회 재무이사 이경호

E-MAIL : [email protected]

Tel : 032)340-7054 Fax : 032)340-2118 C.P : 010-5232-0471

대한피부연구학회 회장 조 광 현

- 134 -


평생회원KSID

회원번호 성 명 영문이름 재직기관

LM00001 훈 Jeung Hoon Lee 충남 피 과학 실

LM00002 태 진 Tae Jin Yoon 경상 피 과학 실

LM00003 진 Jin Ho Chung 울 피 과학 실

LM00004 철 Hee Chul Eun 울 피 과학 실

LM00005 양 Kee Yang Chung 연 피 과학 실

LM00006 Hee Joon Yu 한양 피 과학 실

LM00007 도 원 Do-Won Kim 경 피 과학 실

LM00008 Seok Jong Lee 경 학 학전 학원 피 과학 실

LM00009 규 한 Kyu Han Kim 울 피 과학 실

LM00010 양 원 Yang Won Lee 건 피 과학 실

LM00011 Hae Young Choi 여 학 목동병원 피 과

LM00012 상 Sang-Hyun Cho 가톨릭 모 애병원 피 과

LM00013 Eun-So Lee 아주 피 과학 실

LM00014 강 Hee Young Kang 아주 피 과학 실

LM00015 향 Seong Hyang Sohn 아주 피 과학 실

LM00016 동 Dong Youn Lee 균 삼 울병원 피 과

LM00017 경 Kyung Ho Lee 가톨 피 과학 실

LM00018 Kwang Hyun Cho 울 학 병원 피 과

LM00019 원 Chong Hyun Won 울아산병원 피 과

LM00020 연 So Yun Cho 울 학 보라매병원 피 과

LM00021 원 주 Weon Ju Lee 경 피 과학 실

LM00022 병 Byung Soo Kim 산 피 과학 실

LM00023 태 Tae Heung Kim 트라 하얀피 과 원

LM00024 Seong Jun Seo 앙 피 과학 실

LM00025 Il-Hwan Kim 고려 학 안산병원 피 과

LM00026 찬 Soo Chan Kim 연 피 과학 실

LM00027 창 덕 Chang Deok Kim 충남 학 학전 학원 피 과학 실

LM00028 태 Tae Yoon kim 가톨 피 과학 실

LM00029 립 Young Lip Park 순천향 천병원 피 과

LM00030 애 Ai-Young Lee 동 피 과학 실

LM00031 승 Seung Ho Lee 동 피 과학 실

LM00032 허 창 훈 Chang Hun Huh 울 피 과학 실

LM00033 경 찬 Kyoung Chan Park 울 피 과학 실

LM00034 양 모 Jun Mo Yang 균 삼 울병원 피 과

LM00035 찬 Kee-Chan Moon 울아산병원 피 과

LM00036 용 Yong Beom Choe 건 피 과학 실

LM00037 안 규 Kyu-Joong Ahn 건 피 과학 실

LM00038 신 Jeong Hyun Shin 하 피 과학 실

- 135 -


평생회원 등록양식KSID

성 명 영문이름

최종학위 재직기관

연 락 처 핸드폰 E-mail

수신주소

-

회원번호 성 명 영문이름 재직기관

LM00039 Gwang Seong Choi 하 피 과학 실

LM00040 상 Oh Sang Kwon 울 피 과학 실

LM00041 노 주 Joo Young Roh 가천 병원 피 과

LM00042 Myung Hwa Kim 단 피 과학 실

LM00043 Takashi Takahashi Takashi Takahashi

LM00044 Hyun Je Park 산 피 과학 실

LM00045 민 걸 Min Geol Lee 연 피 과학 실

LM00046 Ki-Ho Kim 동아 피 과학 실

LM00047 규 Whang Kyu Uang 순천 피 과학 실

LM00048 균 Moon Kyun Cho 순천 피 과학 실

LM00049 Eung Ho Choi 연 학 원주 과 학 피 과학 실

LM00050 찬 You Chan Kim 아주 피 과학 실

LM00051 훈 Kwang Hoon Lee 연 피 과학 실

LM00052 령 Hye-Ryung Choi 당 울 학 병원 피 과

LM00053 동 식 Dongsik Bang 연 피 과학 실

LM00054 진 Seong Jin Kim 전남 피 과학 실

LM00055 장 민 Jang, Min Soo 고신 학 복 병원 피 과학 실

LM00056 상 Sang Ho Oh 연 학 과 학 피 과학 실

LM00057 송 해 Hae Jun Song 고려 학 로병원 피 과

LM00058 대 Dae Suk Kim 연 학 과 학 피 과학 실

LM00059 Young Lee 충남 학 과 학 피 과학 실

LM00060 Myung Im 충남 학 과 학 피 과학 실

LM00061 Hyun-Sun Yoon 울특별시보라매병원

- 136 -


현 임 원 진년 월 현재(2013 3 )

회 장 단

회 장 조광현서울의대( )

차 기 회 장 이광훈연세의대( )

상 임 이 사

(2011. 4~2013. 3)

이 사 장 김태윤가톨릭의대( )

총 무 이 사 정기양연세의대( )

학 술 이 사 이동윤성균관의대( )

재 무 이 사 이경호가톨릭의대( )

간 행 이 사 권오상서울의대( )

정 보 이 사 최광성인하의대( )

무임소이사 이승원 생명과학(LG )

감 사

(2011. 3~2013. 3)윤태진경상의대 황규왕순천향의대( ), ( )

이 사

임기 년3

(2012. 4~2015. 3)

김규한서울의대 김기호 동아의대( ), ( ),

서성준 중앙의대 이광훈연세의대( ), ( ),

이원주 경북의대 이은소아주의대( ), ( ),

이증훈 충남의대 조소연보라매병원( ), ( ),

조재위 계명의대( )

임기 년2

(2012. 4~2014. 3)

김도원경북의대 김수찬 연세의대( ), ( ),

김일환 고려의대 노주 가천의대( ), ( ),

박석돈 원광의대 양준모성균관의대( ), ( ),

이미우 울산의대 정진호서울의대( ), ( ),

최혜 이화의대( )

임기 년1

(2012. 4~2013. 3)

강희 아주의대 노 석 한양의대( ), ( ),

박경찬 서울의대 박 립순천향의대( ), ( ),

송해준 고려의대 원 호전남의대( ), ( ),

이민걸 연세의대 이애 동국의대( ), ( )

당연직 이사 이사장 상임이사 대한피부과학회 이사장, ,

- 137 -


학 술 위 원 회

위 원 장 양준모성균관의대( )

간 사 이동윤성균관의대( )

위 원

강희 아주의대 김기호 동아의대( ), ( ),

노주 가천의대 서성준중앙의대( ), ( ),

윤상웅 서울의대 윤태진경상의대( ), ( ),

이미우 울산의대 이원주경북의대( ), ( ),

조문균 순천향의대 조소연서울의대 보라매병원( ), ( ),

조재위 계명의대 최응호연세원주의대( ), ( )

간 행 위 원 회

위 원 장 방동식연세의대( )

간 사 권오상서울의대( )

위 원

정기양연세의대 노주 가천의대( ), ( ),

이동윤 성균관의대 이원주경북의대( ), ( ),

서 준 충남의대( )

정 보 위 원 회

위 원 장 김수찬연세의대( )

간 사 최광성인하의대( )

위 원

이양원건국의대 김범준 중앙의대( ), ( ),

김철우 한림의대 김경문가톨릭의대( ), ( ),

신정현 인하의대( )

기 금 위 원 회

위 원 장 이승철전남의대( )

간 사 이경호가톨릭의대( )

위 원

김정수한양의대 오상호 연세의대( ), ( ),

손상욱 고려의대 이 충남의대( ), ( ),

김병수 부산의대 이상훈순천향대( ), ( )

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