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이민걸,곽호,박주영,김세종,이정복 ( Min Geol Lee,Ho Kwahck,Joo Young Park,Se Jong Kim,Jung Bock Lee ) 대한피부과학회 1991 대한피부과학회지 Vol.29 No.4
N/A Circulating immune Complex in Syphilis Min Geol Lee, M.D., Ho Kwahck, M.D., Joo Young Park, M.D.*, Se Jong Kim, M.D.*, Jung Bock Lee, M.D. Departments of Dermatology, Microbiology* Yonsei University College of Medicine, Seoul, Korea In this study, the author tried to clarify the relationships between the clinical stages of untreated syphilis and the positive rates of circalating immune complex(CIC). Additionally, the study looks at the duration of CIC conversion to negative in the treated previously positive patient by means of solid phase CIq enzyme assay(CIq EA), solid phase anti-CIq enzyme assay (anti-Ciq EA), and platelet aggregation test(PAT)to get the following results. The results are as follows : 1. Among the 132 untreated patients, 36 patients(27.3%) were CIC positive in at least one of the three tests performed, and in the negative groups, two out of 50(4.0%) were CIC positive. 2. The positive rates beginning with the highest were as follows : secondary syphilis, early latent syphilis, late latent syphilis, and primary syphilis. 3. Among the seven CIq EA positive patients before treatment, two had negative conversion in the first week after treatment. Among the remaining five, one remained positive after three weeks and four after three months. 4. Among the six anti-CIq EA positive patients before treatment, there were three negative conversions after two weeks, one after three months ; the remaining two stayed positive. 5. The one PAT positive patient showed negative coversion after one week of treatment.
조기 매독환자에서 Penicillin 치료전과 치료후의 Treponerma pallidum에 특이한 IM 항체의 변화
이민걸,Ferdinand Muller (Min Geol Lee) 대한피부과학회 1985 대한피부과학회지 Vol.23 No.6
1기 매독과 2기 매독 그리고 조기 잠복 매독환자 142명에서 페니실린 치료 전과 치료 후, 매독균에 특이한 IgM항체의 변화를 정량적으로 관찰하였다. 치료 전 이들 환자의 IgM항체는 매독의 임상기와 상관없이 1:20~≥1,280이었다. 페니실린 치료 후 IgM항체는 1기 매독환자 모두에서 9개월이내에 완전 소실되었고, 2기 매독환자의 25%와 조기 잠복매독 환자의 35%에서는 9개월 이후까지 지속되었으나 이들 환자에서도 치료후 19개월까지 IgM항체가 소실되었다. 그리고 이러한 매독균에 특이한 IgM항체의 생성과 치료후의 소실에 관여하는 면역학적 기전에 관하여도 살펴보고자 한다. N/A
Focus 2-5 (FS 2-5) : Skin manifestations of other AIDs
이민걸 ( Min Geol Lee ) 대한피부과학회 2015 대한피부과학회 학술발표대회집 Vol.67 No.1
Monogenic autoinflammatory syndromes (MAISs) are caused by innate immune system dysregulation leading to aberrant inflammasome activation and episodes of fever and involvement of skin, serous membranes, eyes, joints, gastrointestinal tract, and nervous system, predominantly with a childhood onset. To date, the autoinflammatory diseases can be grouped based on clinical findings: 1. the three classic hereditary “periodic fever syndromes”, familial Mediterranean fever (FMF); TNF receptor associated periodic syndrome (TRAPS); and mevalonate kinase deficiency/hyperimmunoglobulinemia D and periodic fever syndrome (HIDS); 2. the cryopyrin associated periodic syndromes (CAPS), comprising familial cold autoinflammatory syndrome (FCAS), Muckle-Wells syndrome (MWS) and neonatal-onset multisystem inflammatory disease (NOMID) or CINCA, and; 3. pediatric granulomatous arthritis (PGA); 4. disorders presenting with skin pustules, including deficiency of interleukin 1 receptor antagonist (DIRA); Majeed syndrome; pyogenic arthritis, pyoderma gangrenosum and acne (PAPA) syndrome; deficiency of interleukin 36 receptor antagonist (DITRA); CARD14 mediated psoriasis (CAMPS), and early-onset inflammatory bowel diseases (EO-IBD); 5. inflammatory disorders caused by mutations in proteasome components, the proteasome associated autoinflammatory syndromes (PRAAS) and 6. very rare conditions presenting with autoinflammation and immunodeficiency. The purpose of this lecture is to describe the main genetic, clinical, and therapeutic aspects of several MAISs not as famous as PAPA (Pyogenic Arthritis, Pyoderma gangrenosum, Acne) in the field of dermatology, with the ultimate goal of increasing awareness of autoinflammation among dermatologists. This lecture will mainly cover 1. DIRA (deficiency in IL-1 receptor antagonist / MIM 612852) 2. TRAPS (TNF-α-associated periodic syndrome / MIM 191190) 3. HIDS (hyperimmunoglobulinemia D syndrome / MIM 260920) 4. Cryopyrinopathies: CAPS (Cryopyrin-associated periodic syndrome): 1) familial cold urticaria: FCAS (MIM 120100) 2) MWS (MIM 191900) 3) NOMID (MIM 607115).
Effects of antihistamines on mast cells and basophils
이민걸 ( Min Geol Lee ) 대한피부과학회 2013 대한피부과학회 학술발표대회집 Vol.65 No.2
Mast cells and basophils are functionally and developmentally similar cells which are generally associated with allergic immune responses. These cells have several things in common. They contain basophilic plasma granules and show metachromatic staining pattern when stained with aniline dyes. They both express SCF receptor and FcεRI on their membrane. They can release histamine and other mediators when stimulated. However, they also have many differences in their functional and phenotypical aspects. Mast cells and basophils are known to have various functions and their functions are still being discovered. Majority of their functions are done by preformed or produced mediators. Among them, histamine is most widely known and the functions are most investigated. The classical roles of histamine are allergic reaction, gastric acid secretion and neurotransmitter. Four histamine receptors are known and H1, H2 and H4 receptors are expressed by mast cells and basophils. H1 receptor is strongly associated with allergy and pruritus, therefore, antihistamine against H1 receptor is the most commonly used medication targeting histamine receptor in Dermatology. Antihistamines are most widely used drugs to treat various cutaneous diseases including urticarial and eczema. Besides their well-known classical action suppressing histamine, additional functions have been recognized and appreciated recently. Antihistamines also have additional effects on mast cells and basophils. They are known to inhibit the release of mediators by mast cells and basophils. They also suppress the production of inflammatory cytokines. Antihistamine inhibits CD107a (marker of mast cell degranulation) expression on human mast cells after stimulation. It also inhibits histamine release by human mast cells and basophils after stimulation. Other mediators, such as tryptase, leukotriene 4 and prostaglandin D2 release are also suppressed by antihistamine. The proposed mechanism of inhibiting the release of mediators is that antihistamine impairs the increase of intracellular Ca2+ following cell activation which results in reduced release of mediators. Antihistamine also inhibits interleukin-4, 6, 8 secretions by mast cells and basophils. TNF-α and GM-CSF secretions were also inhibited by antihistamine. Inhibition of NF-κB signaling is suggested as a mechanism of cytokine suppression. Additional roles of antihistamine on mast cells and basophils have been discovered. However there are many things still we do not know. Therefore it needs to be investigated in near future and its clinical relevance should also be addressed to widen our knowledge about the effect of antihistamine on mast cells and basophils.
이민걸(Min Geol Lee),이원수(Won Soo Lee),전수일(Soo Il Chun),한충섭(Choong Seop Hahn) 대한피부과학회 1988 대한피부과학회지 Vol.26 No.1
We reported a case of subcutaneous mass in a 22-year-old lady having unusual histopathologic findings mixed with both features of pilomatricoma and epidermal cyst and the meanings of these peculiar findings were discussed.
전자현미경으로 바이러스 입자를 관찰한 재발성 대상 포진으로 추정되는 2예
이민걸(Min Geol Lee),이은소(Eun So Lee),남인환(In Whan Nam),이성낙(Sung Nack Lee) 대한피부과학회 1987 대한피부과학회지 Vol.25 No.4
Herpes zoster is known to recur only rarely. However reports on the recurrence rates by various authors ranges from 0.l% to 8%. We have experienced 2 cases of recurrent herpes zoster in a 63-year-old female and a 62-year-old male who presented with typical clinical features and previous history of herpes zoster. They were suffering from breast cancer and Hodgkin's disease, respectively. By employing negative and positive staining methods of electron microscopy, typical herpes viral particles were demonstrated from the vesicular fluid.