이승환 교수
Seunghwan Lee
고려대학교 법학전문대학원 · 의학
연구실 소개
이승환 교수의 연구실은 대사질환, 신경질환, 면역반응 간의 상호작용을 중심으로 한 기초 및 임상 연구를 수행하고 있습니다. 인슐린 저항성 지표인 TyG 지수와 콜레스테롤 변동성의 임상적 의미를 규명하며 심혈관 질환의 예측 가능성을 높이고 있으며, 뇌내 인슐린 작용과 신경염증 반응의 기전을 밝혀 신경질환 및 정신질환 치료 전략을 모색하고 있습니다. 특히 자연살해세포(NK 세포)의 면역 조절 기전과 바이러스 감염에 의한 면역 반응 조절 메커니즘을 중심으로 면역학적 기전을 규명하고 있습니다.
연구 현황
연구 성과 추이
표시된 성과는 수집된 데이터 기준으로 산출되며, 일부 차이가 있을 수 있습니다.
주요 논문
15The TyG index, a simple measure reflecting insulin resistance, might be useful in identifying individuals at high risk of developing diabetes.
Aims: A high visit-to-visit variability in cholesterol levels has been suggested to be an independent predictor of major adverse cardiovascular events in patients with coronary artery disease (CAD). Because whether this notion applies to general population is not known, we aimed to investigate the associations between total cholesterol (TC) variability and the risk of all-cause mortality, myocardial infarction (MI), and stroke. Methods and results: We identified 3 656 648 subjects without a hist
Natural killer (NK) cells have the potential to deliver both direct antimicrobial effects and regulate adaptive immune responses, but NK cell yields have been reported to vary greatly during different viral infections. Activating receptors, including the Ly49H molecule recognizing mouse cytomegalovirus (MCMV), can stimulate NK cell expansion. To define Ly49H's role in supporting NK cell proliferation and maintenance under conditions of uncontrolled viral infection, experiments were performed in
Implications for the treatment of obesity, type 2 diabetes, dementia, and mood disorders are discussed in the context of brain insulin action. Intranasal insulin may have potential in the treatment of central nervous system-related metabolic disorders.
Introduction Neuropathic pain is a debilitating condition. The importance of neuroimmune interactions in neuropathic pain has been evidenced by the involvement of different immune cells in peripheral and central sensitization of pathological pain. Macrophages and microglia are the most abundant immune cells activated in injured nerves and spinal cord, respectively. Several lines of evidence showed that macrophage/microglia survival, activation, proliferation, and differentiation require the invo
NK cell expression and use of the IL-2Rα-chain (CD25), required for the high-affinity IL-2R, remain poorly understood. The studies reported in this article demonstrate that infections with murine CMV (MCMV), but not with lymphocytic choriomeningitis virus, induce CD25 on NK cells, along with high levels of IL-12 and IL-18. The cytokines act ex vivo to increase CD25 levels, and IL-12, IL-12R, and STAT4, but not the NK activating receptor Ly49H, are required for peak induction in vivo. All examine
AIMS: Nocturnal acid breakthrough has been considered an unmet need of proton-pump inhibitors. Tegoprazan, a novel potassium-competitive acid blocker, is expected to show improved properties for this unmet need. This study was aimed to compare night-time acid suppression by tegoprazan with that by vonoprazan or esomeprazole, and to explore the effect of CYP2C19 phenotypes on acid-suppressive effects. METHODS: A randomized, open-label, 3-period, 6-sequence crossover study was conducted. A single
The current study assessed the influence of the CYP2C19 genotype on the pharmacokinetics and tolerability of voriconazole after single and multiple oral doses in healthy volunteers. Six subjects for the CYP2C19 homozygous extensive metabolizer (EMs), 6 for heterozygous extensive metabolizer (HEMs), and 6 for poor metabolizer (PMs) were enrolled, and their CYP2C9, CYP3A5, and MDR1 genotypes were analyzed. After a single intravenous infusion or single and multiple oral doses of 200 mg of voriconaz
OBJECTIVE: To assess bone mineral density (BMD), serum levels of soluble receptor activator of nuclear factors-kappaB ligand (sRANKL) and osteoprotegerin (OPG) in patients with ankylosing spondylitis (AS), and to determine their relationships with disease activities. METHODS: Serum levels of sRANKL and OPG in AS were measured by sandwich enzyme-linked immunosorbent assay. The disease activities were determined using Bath Ankylosing Spondylitis Disease Activity Score Index, Bath Ankylosing Spondy
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