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Biochemical and Biological Progress in the Studies of Keratinization and Dyskeratosis
Hideoki, Ogawa,Kenji, Takamori,Makoto, Negi,Yoshiike, Takashi 대한피부과학회 1985 大韓皮膚科學會誌 Vol.23 No.4
Recent topics of biochemical and biological progress in keratinization and dyskeratosis were reviewed and discussed. The main topics were as follows: (1) what is keratin (2) Differentiation of keratinocytes (keratinization), (3) Components of horny substances and their derivation, (4) Keratin filament and keratohyaline granule, (5) Synthesis of horny cell membrane (disulfide bonds, e- (T-glutamyl) lysine bonds), (6) Biochernical analysis of dyskeratosis (harlequin fetus, ichthyosis vulgaris, X-linked ichthyosis, lamellar ichthyosis, bullous congenital ichthyosiform erythroderma, psoriasis vulgaris, Dariers disease, M:enke's syndrome, Netherton's disease, Richner-Hanhart syndrome). These findings should lead to a more cornplete understanding of the pathologic events that occur in the process of keratinization and more rational therapy for many disorders in keratinization.
( Kunihiro Hayakawa ),( Keigo Ikeda ),( Maki Fujishiro ),( Yuko Yoshida ),( Takuya Hirai ),( Hiroshi Tsushima ),( Tomoko Miyashita ),( Shinji Morimoto ),( Yasushi Suga ),( Kenji Takamori ),( Hideoki O 대한피부과학회 2018 Annals of Dermatology Vol.30 No.1
Background: Connective tissue growth factor (CTGF) is a multifunctional cellular protein and playing a role as a central mediator in tissue remodeling and fibrosis. The physiological function of CTGF in psoriasis is unknown. Objective: The purpose of this study was to investigate the function of CTGF in psoriasis using the established imiquimod (IMQ)- induced psoriasis murine model and psoriasis patients. Methods: Anti-CTGF monoclonal antibody was applied to IMQ induced psoriasis mice and those skin were clinically, pathologically and immunologically analyzed. Additionally, CTGF expression was analyzes using skin samples and plasma from psoriasis patients. Results: CTGF expression was observed in the dermis from both IMQ-induced psoriatic mice and psoriasis patients. CTGF inhibition using an anti-CTGF antibody slightly worsened IMQ-induced dermatitis. In addition, the increase of CTGF showed tendency to suppress the psoriatic dermatitis through inhibition of suprabasal cells proliferation and macrophage infiltration in the skin. CTGF was also detected significantly higher in plasma from psoriasis patients comparing with healthy control. Conclusion: Our findings suggest that CTGF could contribute to the healing rather than the worsening of psoriasis skin lesions. (Ann Dermatol 30(1) 47∼53, 2018)