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      • KCI등재

        급성과 만성 피부 이식편 대 숙주질환의 소견이 동반된 중첩증후군

        천민석 ( Min Seok Cheon ),이영복 ( Young Bok Lee ),김정은 ( Jung Eun Kim ),조백기 ( Baik Kee Cho ),박현정 ( Hyun Jeong Park ) 대한피부과학회 2011 大韓皮膚科學會誌 Vol.49 No.2

        Graft-versus-host disease (GVHD) has been divided into acute GVHD and chronic GVHD on the basis of 100 days post-transplantation. Recently, the National Institutes of Health in the USA proposed new consensus criteria for chronic GVHD; 1) classic chronic GVHD, presenting with diagnostic features of only chronic GVHD without characteristics of acute GVHD and 2) an overlap syndrome in which there are distinctive manifestations of chronic GVHD together with features of acute GVHD, irrespective of the period after transplantation. Herein we report a case of overlap syndrome that developed in a 15 year-old male who had undergone unrelated peripheral blood stem cell transplantation 4 years earlier. (Korean J Dermatol 2011; 49(2):198~201)

      • Effects of Extracellular $Ca^{++}$ on PKC or cAMP-stimulated Increases in LH Release and $LH{\beta}$ Subunit mRNA Levels in Rat Anterior Pituitary Cells

        박덕배,김창미,천민석,유경자,Park, Deok-Bae,Kim, Chang-Mee,Cheon, Min-Seok,Ryu, Kyung-Za The Korean Society of Pharmacology 1996 대한약리학잡지 Vol.32 No.3

        We examined the effects of EGTA and verapamil on phorbol ester-and forskolin-stimulated LH releases and $LH{\beta}$ subunit mRNA levels in order to verify the role of extracellular $Ca^{++}$ on PKC- or cAMP-induced increases in LH release and $LH{\beta}$ subunit mRNA levels in cultured anterior pituitary cells of rat. Forskolin-stimulated $LH{\beta}$ subunit mRNA levels as well as LH release were all suppressed by prevention of $Ca^{++}$ mobilization from extracellular environment, after the treatment of EGTA as a $Ca^{++}$ chelator or verapamil as a $Ca^{++}$ channel blocker. PMA-stimulated $LH{\beta}$ subunit mRNA levels were also suppressed by the treatment of EGTA and verapamil, while PMA-induced LH release was not affected. From the present study, it is, therefore, suggested that PKC activation and cAMP elevation all stimulate $LH{\beta}$ subunit mRNA levels and these are extracellular $Ca^{++}$-dependent. However, LH releases by PKC activation and cAMP increase seem to be different each other. LH release by PKC activation is thought to be independent of extracellular $Ca^{++}$. On the other hand, cAMP stimulated-LH release is thought to be dependent on the entry of extracellular $Ca^{++}$. 흰쥐 뇌하수체 전엽배양세포에서 PKC나 cAMP에 의한 LH 분비와 $LH{\beta}$subunit mRNA 증가과정에서 세포외 $Ca^{++}$의 역할을 검증하기 위하여 phorbol ester와 forskolin에 의해 촉진된 LH 분비와 $LH{\beta}$ subunit mRNA 수준에 미치는 EGTA와 verapamil의 영향을 조사하였다. Forskolin에 의해 촉진된 LH 분비와 $LH{\beta}$ subunit mRNA 수준은 $Ca^{++}$ chelator인 EGTA나 $Ca^{++}$ 채널차단제인 verapamil의 처리로 세포외부로부터 $Ca^{++}$의 이동을 억제시켰을때 모두 감소하였다. PMA에 의해 유도된 LH 분비는 EGTA와 verapamil 처리에 의해 영향을 받지 않았으나 PMA에 의해 촉진된 $LH{\beta}$ subunit mRNA는 억제되었다. 따라서 본 연구에 의하면 PKC 활성화나 세포내 cAMP 농도 증가는 $LH{\beta}$ subunit mRNA 수준을 증가시키며 이러한 과정은 세포외 $Ca^{++}$ 의존적인 것으로 생각된다. 그러나 PKC 활성화나 cAMP 증가에 의한 세포외 $Ca^{++}$의 역할이 서로 다른 양상을 보인다. PKC 활성화에 의한 LH 분비는 세포외 $Ca^{++}$에 비의존적이나 cAMP에 의해 촉진된 LH 분비는 세포외 $Ca^{++}$ 유입의 영향을 받는 것으로 사료된다.

      • SCOPUSKCI등재

        제주지역에서 발생한 중증열성혈소판감소증후군 4예

        허상택 ( Sang Taek Heo ),천민석 ( Min Seok Cheon ),김재왕 ( Jae Wang Kim ) 대한피부과학회 2014 대한피부과학회지 Vol.52 No.3

        Severe fever with thrombocytopenia syndrome (SFTS) is an emerging infectious disease caused by a novel SFTS bunyavirus (SFTSV), a member of the genus Phlebovirus in the family Bunyaviridae. SFTSV is believed to be transmitted by Haemaphysalis longicornis. Common symptoms of SFTS include high fever, vomiting, diarrhea, thrombocytopenia, leukocytopenia, and multi-organ failure with an average case-fatality rate of 12∼30%. In 2009, SFTS was firstly reported in China. In 2013, 27 cases of SFTS were documented in Korea, and 6 cases were confirmed on Jeju Island. Although the pathogenesis and transmission mode of SFTS remain unclear, SFTS is now considered endemic in East Asia. Accordingly, SFTS needs to be differentiated from scrub typhus, leptospirosis, and hemorrhagic fever with renal syndrome. We here report 4 cases of SFTS preceded by a tick bite, which were in need of a differential diagnosis of scrub typhus. (Korean J Dermatol 2014;52(3):173∼177)

      • 흰쥐 뇌하수체 전엽세포에서 PKC나 cAMP에 의한 LH 분비 및 LHβ Subunit mRNA 증가에 미치는 Ca<sup>++</sup>의 영향

        박덕배(Deok-bae Park),김창미(Chang-mee Kim),천민석(Min-seok Cheon),유경자(Kyung-za Ryu) 대한약리학회 1996 대한약리학잡지 Vol.32 No.3

        흰쥐 뇌하수체 전엽배양세포에서 PKC나 cAMP에 의한 LH 분비와 LHβsubunit mRNA 증가과정에서 세포외 Ca<sup>++</sup>의 역할을 검증하기 위하여 phorbol ester와 forskolin에 의해 촉진된 LH 분비와 LHβ subunit mRNA 수준에 미치는 EGTA와 verapamil의 영향을 조사하였다. Forskolin에 의해 촉진된 LH 분비와 LHβ subunit mRNA 수준은 Ca<sup>++</sup> chelator인 EGTA나 Ca<sup>++</sup> 채널차단제인 verapamil의 처리로 세포외부로부터 Ca<sup>++</sup>의 이동을 억제시켰을때 모두 감소하였다. PMA에 의해 유도된 LH 분비는 EGTA와 verapamil 처리에 의해 영향을 받지 않았으나 PMA에 의해 촉진된 LHβ subunit mRNA는 억제되었다. 따라서 본 연구에 의하면 PKC 활성화나 세포내 cAMP 농도 증가는 LHβ subunit mRNA 수준을 증가시키며 이러한 과정은 세포외 Ca<sup>++</sup> 의존적인 것으로 생각된다. 그러나 PKC 활성화나 cAMP 증가에 의한 세포외 Ca<sup>++</sup>의 역할이 서로 다른 양상을 보인다. PKC 활성화에 의한 LH 분비는 세포외 Ca<sup>++</sup>에 비의존적이나 cAMP에 의해 촉진된 LH 분비는 세포외 Ca<sup>++</sup> 유입의 영향을 받는 것으로 사료된다. We examined the effects of EGTA and verapamil on phorbol ester-and forskolin-stimulated LH releases and LHβ subunit mRNA levels in order to verify the role of extracellular Ca<sup>++</sup> on PKC- or cAMP-induced increases in LH release and LHβ subunit mRNA levels in cultured anterior pituitary cells of rat. Forskolin-stimulated LHβ subunit mRNA levels as well as LH release were all suppressed by prevention of Ca<sup>++</sup> mobilization from extracellular environment, after the treatment of EGTA as a Ca<sup>++</sup> chelator or verapamil as a Ca<sup>++</sup> channel blocker. PMA-stimulated LHβ subunit mRNA levels were also suppressed by the treatment of EGTA and verapamil, while PMA-induced LH release was not affected. From the present study, it is, therefore, suggested that PKC activation and cAMP elevation all stimulate LHβ subunit mRNA levels and these are extracellular Ca<sup>++</sup>-dependent. However, LH releases by PKC activation and cAMP increase seem to be different each other. LH release by PKC activation is thought to be independent of extracellular Ca<sup>++</sup>. On the other hand, cAMP stimulated-LH release is thought to be dependent on the entry of extracellular Ca<sup>++</sup>.

      • SCOPUSKCI등재

        흰쥐뇌하수체 배양세포에서 FSH 유전자 발현 및 FSH 분비 조절

        박덕배,유경자,박용빈,감경윤,천민석 대한내분비학회 2000 Endocrinology and metabolism Vol.15 No.2

        Background : FSH is a heterodimeric glycoprotein and is composed of αand β subunits. αsubunit is common to FSH and LH, while an unique β subunit determines the biological specificity of each hormone. The synthesis of β subunit is the primary rate-limiting step in the synthesis of each hormone. Although FSH plays a pivotal role in folliculogenesis and ovulation, very little studies have been performed on the regulation of FSH β gene expression. Therefore, the present study attempted to examine the effect of GnRH or activin on the expression of FSH β mRNA as well as FSH release and signaling pathway involved in their actions. Methods : The primary cultures of rat anterior pituitary were used for this study. To determine FSH β mRNA levels, northern blotting method was used. The concentration of FSH in the culture medium was evaluated by using a specific radioimmunoassay for rat FSH. Results : PMA, an activator of PKC, increased FSH β mRNA levels and FSH release, whereas forskolin, an activator of adenlase, showed no effect. The application of GnRH augmented FSH release, but not FSH β mRNA levels. However, the administration of activin increased FSH β mRNA levels as well as FSH release. Staurosporine, an inhibitor of PKC, suppressed activin-induced increment of FSH β mRNA levels and FSH release. Conclusion : The present study demonstrated that activin rather than GnRH is a major regulator for FSH β mRNA expression, and suggest that PKC-dependent pathway is also involved in the action of activin on the expression of FSH β mRNA and FSH release(J Kor Soc Endocrinol 15:179-189, 2000).

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