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      • A Case of Breast abscess due to Mycobacterium fortuitum

        ( Kwi Hyun Bae ),( Eun Sung Choi ),( Seong Yeol Ryu ) 대한내과학회 2011 대한내과학회 추계학술대회 Vol.2011 No.1

        The rapidly growing nontuberculous mycobacteria, Mycobacterium fortuitum are of increasing clinical importance. The ubiquitous M. fortuitum has been isolated from water, soil and dust. M.fortuitum usually causes skin or soft-tissue infections through direct inoculation occurring in surgery or penetrating trauma but may infect a wide variety of tissues including the lungs, lymph nodes, bones, joints and meninges. We believe this is the first report of breast abscess due to M. fortuitum, which presented in an immunocompetent woman in Korea after nipple piercing. A 26-year-old female presented with a 5-month history of a tender Rt. breast lump that was gradually increasing in size after nipple piercing. Ultrasound examination showed a poorly marginated lesion with areas of cavitation. Open biopsy with debridement found solid and necrotic tissue without purulence. Histologic examination confirmed granulomatous inflammation. Culture grew Mycobacterium fortuitum. The Rt breast abscess were improved by antibiotic therapy with doxycycline and moxifloxacin for 6 month. When breast abscess is recurrent and bacterial cultures are sterile, mycobacterial infection should be considered, particularly when there is a history of previous nipple piercing procedures.

      • KCI등재후보

        Relationship between Circulating FGF21 Concentrations and the Severity of Coronary Artery Damage in Subjects with Cardiovascular Disease

        박성돈,Kwi-Hyun Bae,Yeon-Kyung Choi,Jae-Han Jeon,Jung-Beom Seo,Namkyun Kim,Chang-Yeon Kim,김성우,Won Kee Lee,Jung-Guk Kim,In Kyu Lee,Jang Hoon Lee,박근규 한국지질동맥경화학회 2018 지질·동맥경화학회지 Vol.7 No.1

        Objective: Fibroblast growth factor (FGF) 21 is a recently established therapeutic target for treating metabolic syndromes, which include potential precursors to cardiovascular disease, suggesting a link between FGF21 and atherosclerosis. However, the association between serum FGF21 concentrations and coronary artery disease remain controversial. The aim of this study is to evaluate the association between circulating FGF21 concentrations and coronary artery lesions and clinical severity. Methods: We enrolled 137 subjects who underwent coronary angiography, due to suspected acute coronary syndrome (ACS), from December 2009 to July 2012. Serum FGF21 levels were measured. Coronary artery lesions and clinical severities of the subjects were evaluated using the SYNergy between percutaneous coronary intervention with (paclitaxel-eluting) TAXus stent and cardiac surgery (SYNTAX) and Global Registry of Acute Coronary Events (GRACE) scoring system, respectively. Results: After adjusting for established cardiovascular disease risk factors, including age, body mass index, total cholesterol, and low-density lipoprotein cholesterol, patients with coronary artery lesions (n=112 men) had significantly higher levels of FGF21 than individuals without such lesions (n=25; men) (377.1±20.1 pg/mL vs. 267.1±43.5 pg/mL; p=0.026). However, no correlations were found between serum levels of FGF21 and either the calculated STNTAX score (r=0.117; p=0.176) or GRACE risk score, which is a risk prediction tool applicable for ACS subjects (r=0.113; p=0.193). Conclusion: Although serum levels of FGF21 were higher in individuals with coronary lesions than in those without such lesions, FGF21 levels were not associated with angiographic severity.

      • Effect of nanotubular-micro-roughened titanium surface on cell response <i>in vitro</i> and osseointegration <i>in vivo</i>

        Yun, Kwi-Dug,Yang, Yunzhi,Lim, Hyun-Pil,Oh, Gye-Jeong,Koh, Jeong-Tae,Bae, In-Ho,Kim, Jaehyung,Lee, Kwang-Min,Park, Sang-Won Elsevier 2010 Materials science & engineering. C, Materials for Vol.30 No.1

        <P><B>Abstract</B></P><P>This study was to evaluate wettability, cell response, and osseointegration of nanotubular titanium (Ti) surface by anodic oxidation. Commercially pure Ti discs were treated by polishing, sandblasting, and anodizing. These surfaces were characterized by scanning electron microscopy and contact angle measurement. MC3T3-E1 osteoblast cell was used to evaluate cell response <I>in vitro</I>. The cell morphology, cell viability, and alkaline phosphatase (ALP) specific activity were assessed. The Ti implants of 2.0mm diameter and 5.0mm long treated by anodizing and sandblasting/anodizing were inserted into the tibia of rats. After 3weeks, the histology of the Ti–bone interface was examined. SEM observations showed that the anodizing and sandblasting/anodizing created the nanotubular surface and graded nanotubular-micro-roughened surfaces, respectively. The anodizing and sandblasting/anodizing significantly improved the hydrophilicity of Ti. The significant greatest cell spreading and ALP specific activity were observed on the graded nanotubular-micro-roughened surfaces treated by sandblasting/anodizing. The <I>in vivo</I> study shows that newly formed bone was intimately in contact with the nanotubular surfaces without adverse immune response. This study has suggested that the graded nanotubular-micro-roughened surface of Ti treated with sandblasting/anodizing is very promising in implantology due to improved hydrophilicity, favorable cell response, and excellent osseointegration.</P>

      • KCI등재

        독일 의료보험제도 변화과정에서의 공공성에 관한 연구

        배귀희 ( Kwi-hee Bae ),이건형 ( Keon-hyung Lee ),여영현 ( Young-hyun Yeo ) 중앙대학교 국가정책연구소 2016 국가정책연구 Vol.30 No.4

        현재 독일의 의료보험의 기본적인 틀은 1883년 비스마르크 시절 도입된 공적의료보험 제도(SHI; Social Health Insurance)이고 독일에서 가장 오래된 사회보험제도로 많은 환경 변화속에서 지속적인 개혁이 이루어졌다. 이러한 환경변속에서 거의 대부분의 선진국들에서 발견되어지는 현상이지만 독일의 의료비 지출 증가가 GDP 증가보다 빠르게 증가하고 있고 의료비 비용 증가도 지속적으로 나타나고 있다. 본 연구의 목적은 독일 의료보험 개혁의 원인, 과정 및 의료보험 개혁의 과정에서 나타난 특성들을 살펴보고 이러한 개혁 과정에서 의료보험의 독일 의료보험의 공공성의 변화 등을 살펴보는 것이다. 독일 의료보험에서 비용을 억제하고 통제하려는 목적으로 1980년대부터 독일의 의료보험 제도의 개혁이 시작되었고 이후부터 의료보험 재정의 안정화를 위한 자기부담금과 같은 의료보험의 수입 부문과 의료공급자인 의사들을 위한 인센티브 구조를 변화시키려는 다양한 노력들이 제도화 되었다. 이러한 과정에서도 독일의 의료공공성은 2013년 기준으로 높은 공공성을 유지하는 것으로 나타났다. The basic frame of healthcare system in Germany has been social health insurance since the Bismarch era. Reducing healthcare cost has become an critical issue for advanced countries. The purpose of this study is to examine change of publicness of substantial German healthcare reform. In order to contain cost of healthcare in Germany, many attempts to stabilize healthcare finance have institutionalized by reforming revenue structures of healthcare and changing incentive structures of physicians. Our study demonstrate that the publicness of healthcare reform process has been maintained with high levels.

      • KCI등재

        증례 : 감염 ; 후천성면역결핍증 환자의 칸디다 헤르페스, 거대세포바이러스 식도염 1예

        김현아 ( Hyun Ah Kim ),배귀현 ( Kwi Hyun Bae ),류성열 ( Seong Yeol Ryu ) 대한내과학회 2009 대한내과학회지 Vol.77 No.2

        AIDS 환자의 증가뿐만 아니라, 치료법의 획기적인 개선으로 인해 더 이상 AIDS는 죽음의 병이 아닌 고혈압, 당뇨병처럼 만성 질환이 되어 기회감염의 조기 진단과 치료에 관심이 증대되고 있다. HIV 감염 환자에서 발생하는 각종 기회감염질환 중 식도를 포함한 위장관계 감염질환이 40% 정도 동반될 정도로 흔한 합병증이며, 예후 결정의 중요한 인자로 알려져 있다. HIV 감염 환자에서 식도 증상을 일으키는 가장 흔한 원인은 칸디다, 거대세포바이러스, 단순헤르페스바이러스 등에 의한 감염성 식도염이며, 드물게 AIDS 감염자 같은 면역 저하자에서 칸디다 식도염에 바이러스에 의한 식도염이 동반된다. 외국문헌에 칸디다 식도염에 거대세포바이러스, 헤르페스바이러스에 의한 식도염이 병발된 보고가 있으나 국내에는 아직까지 보고된 바 없는데, 이에 저자는 국내에서 처음으로 칸디다 식도염에 헤르페스, 거대세포바이러스에 의한 식도염이 병발한 1예를 경험하였기에 문헌 고찰과 함께 보고하는 바이다. Since the first case of human immunodeficiency virus (HIV) infection was reported in Korea in 1985, the number of HIV patients has risen steadily and reached 5,323 in December 2007. Consequently, multiple opportunistic infections have become a significant clinical problem. Diseases of the gastrointestinal tract are among the most frequent complications of acquired immunodeficiency syndrome (AIDS) and cause morbidity in patients with HIV infection. Opportunistic infections are the leading cause of esophageal complaints. Candida albicans is the most frequently identified cause of esophageal symptoms, followed by herpes simplex virus (HSV) and cytomegalovirus (CMV) infections. Esophageal candidiasis often occurs concurrently with other infectious esophageal disorders. Simultaneous esophageal infection with HSV, CMV, and Candida spp. is rare. We report a case of combined HSV, CMV, and candidal esophagitis in an AIDS patient. He was treated with highly active antiretroviral therapy (HAART) and the appropriate antiviral and antifungal agents. (Korean J Med 77:255-260, 2009)

      • SCISCIESCOPUS

        Lactate dehydrogenase-A is indispensable for vascular smooth muscle cell proliferation and migration

        Kim, Ji-Hyun,Bae, Kwi-Hyun,Byun, Jun-Kyu,Lee, Sungwoo,Kim, Jung-Guk,Lee, In Kyu,Jung, Gwon-Soo,Lee, You Mie,Park, Keun-Gyu Academic Press 2017 Biochemical and biophysical research communication Vol. No.

        <P><B>Abstract</B></P> <P>The proliferation and migration of vascular smooth muscle cells (VSMCs) have been implicated in the pathogenesis of atherosclerosis. Increased aerobic glycolysis is a key feature of cellular phenotypes including cancer and immune cells. However, the role of aerobic glycolysis in the atherogenic phenotype of VSMCs remains largely unknown. Here, we investigated the role of lactate dehydrogenase-A (LDHA), which is a key enzyme for glycolysis, in the proliferation and migration of VSMCs. Activation of primary rat VSMCs with fetal bovine serum (FBS) or platelet-derived growth factor (PDGF) increased their proliferation and migration, glycolytic activity, and expression of LDHA. Wound healing and transwell migration assays demonstrated that small interfering RNA-mediated knockdown of LDHA and pharmacological inhibition of LDHA by oxamate both effectively inhibited VSMC proliferation and migration. Inhibition of LDHA activity by oxamate reduced PDGF-stimulated glucose uptake, lactate production, and ATP production. Taken together, this study shows that enhanced glycolysis in PDGF- or FBS-stimulated VSMCs plays an important role in their proliferation and migration and suggests that LDHA is a potential therapeutic target to prevent vessel lumen constriction during the course of atherosclerosis and restenosis.</P> <P><B>Highlights</B></P> <P> <UL> <LI> LDHA levels were upregulated in proliferative and migratory VSMCs. </LI> <LI> Inhibition of LDHA suppressed growth factor-stimulated VSMC proliferation/migration. </LI> <LI> Inhibition of LDHA reduced growth factor-stimulated glycolysis in VSMCs. </LI> <LI> Targeting LDHA has a potential to treat excessive VSMC proliferation and migration. </LI> </UL> </P>

      • SCISCIESCOPUS

        Orphan nuclear receptor Nur77 mediates fasting-induced hepatic fibroblast growth factor 21 expression.

        Min, Ae-Kyung,Bae, Kwi-Hyun,Jung, Yun-A,Choi, Yeon-Kyung,Kim, Mi-Jin,Kim, Ji-Hyun,Jeon, Jae-Han,Kim, Jung-Guk,Lee, In-Kyu,Park, Keun-Gyu The Endocrine Society 2014 Endocrinology Vol.155 No.8

        <P>The fasting-induced hepatic hormone, fibroblast growth factor 21 (FGF21), is a potential candidate for the treatment of metabolic syndromes. Although peroxisome proliferator-activated receptor (PPAR)α is known to play a major role in the induction of hepatic FGF21 expression, other fasting-induced transcription factors that induce FGF21 expression have not yet been fully studied. In the present study, we investigated whether the fasting-induced activation of the orphan nuclear receptor Nur77 increases hepatic FGF21 expression. We found that fasting induced hepatic Nur77 and FGF21 expression. Glucagon and forskolin increased Nur77 and FGF21 expression in vivo and in vitro, respectively, and adenovirus-mediated overexpression of Nur77 (Ad-Nur77) increased FGF21 expression in vitro and in vivo. Moreover, knockdown of endogenous Nur77 expression by siRNA-Nur77 abolished the effect of forskolin on FGF21 expression. The results of ChIP assays, EMSA, and mutagenesis analysis showed that Nur77 bound to the putative NBRE of the FGF21 promoter in cultured hepatocytes and fasting induced Nur77 binding to the FGF21 promoter in vivo. Knockdown of PPARα partially inhibited forskolin-induced FGF21 expression, suggesting PPARα involvement in glucagon-stimulated FGF21 expression. In addition, double knockdown of PPARα and Nur77 further diminished FGF21 expression in cultured hepatocytes. In conclusion, this study shows that Nur77 mediates fasting-induced hepatic FGF21 expression, and suggests an alternative mechanism via which hepatic FGF21 transcription is mediated under fasting conditions.</P>

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