최창원 교수
Chang Won Choi
서울대학교 · 의학
연구실 소개
최창원 교수의 연구실은 천연약용식물과 자연유래 물질의 생리활성 및 약리적 기전을 중심으로 연구를 진행하고 있습니다. 특히 아슈와간다, 산기소르바 등 식물에서 유래한 폴리페놀 및 플라보노이드 성분의 항산화 및 항염증 작용, 그리고 미생생물에 대한 항균 활성에 초점을 맞추고 있으며, 이는 주로 피부질환 치료 및 대사질환 예방에 응용되고 있습니다. 또한 세균 빈자리(백신 후보 물질) 및 바이러스-숙주 단백질 상호작용 메커니즘에 대한 기초 연구를 병행하여, 신약 개발 및 생물학적 방어 기전 규명에도 기여하고 있습니다.
연구 현황
연구 성과 추이
표시된 성과는 수집된 데이터 기준으로 산출되며, 일부 차이가 있을 수 있습니다.
주요 논문
15IL-6 in TA at birth can be used as a predictor of BPD in combination with the presence of PDA.
A nationwide survey was conducted to determine the incidence of bronchopulmonary dysplasia (BPD) in Korea and the intercenter differences in survival and BPD rates among preterm infants. Questionnaires were sent to all registered neonatal intensive care units (NICUs). The questionnaires inquired about the survival and BPD rates of very low birth weight (VLBW, < 1,500 g) infants who had been admitted to each NICU from 2007 to 2008. BPD was defined as requiring oxygen at 36 weeks' postmenstrual ag
Exposure to early postnatal systemic LPS induces BPD, an arrest in alveolarization, in neonatal rats. Preceding exposure to i.a. LPS protects the lungs against BPD triggered by postnatal systemic inflammation.
Chorioamnionitis was a risk factor for atypical CLD in addition to short GA and high MAP during the early postnatal period, and poor response to surfactant was a risk factor for classical CLD in addition to short GA and being male. Therefore, CLD is considered to have type-specific risk factors.
Fetal lung development normally occurs in a hypoxic environment. Hypoxia-inducible factor (HIF)-1α is robustly induced under hypoxia and transactivates many genes that are essential for fetal development. Most preterm infants are prematurely exposed to hyperoxia, which can halt hypoxia-driven lung maturation. We were to investigate whether the HIF-1α inducer, deferoxamine (DFX) can improve alveolarization in a rat model of bronchopulmonary dysplasia (BPD). A rat model of BPD was produced by intr
Although CLD without RDS was still less common than CLD with RDS, it comprised over a third of all cases of CLD in our study. Clinical characteristics and chronic oxygen requirement pattern of CLD without RDS seems to be less severe than those of CLD with RDS. Our data suggest that CLD without RDS may be developed by causes other than initial acute lung injury. Chorioamnionitis may be one of antecedents of CLD without RDS.
The Korean Neonatal Network (KNN), a nationwide prospective registry of very-low-birth-weight (VLBW, < 1,500 g at birth) infants, was launched in April 2013. Data management (DM) and site-visit monitoring (SVM) were crucial in ensuring the quality of the data collected from 55 participating hospitals across the country on 116 clinical variables. We describe the processes and results of DM and SVM performed during the establishment stage of the registry. The DM procedure included automated proof
Maternal chorioamnionitis has been associated with abnormal lung development. We examined the effect of maternal chorioamnionitis on the expression of transforming growth factor-beta1 (TGF-beta1) in the lungs of preterm infants. A total of 63 preterm (<or=34 weeks) infants who were intubated in the delivery room were prospectively enrolled. Their placentas were examined for the presence of chorioamnionitis. Bronchoalveolar lavage (BAL) fluid and cells were obtained shortly after birth. TGF-beta1
Length at birth was inversely associated with an increased risk of BPD or death in VLBW infants born earlier than 32 weeks of gestation.
Recent progress in neonatal medicine has enabled survival of many extremely low-birth-weight infants. Prenatal steroids, surfactants, and non-invasive ventilation have helped reduce the incidence of the classical form of bronchopulmonary dysplasia characterized by marked fibrosis and emphysema. However, a new form of bronchopulmonary dysplasia marked by arrest of alveolarization remains a complication in the postnatal course of extremely low-birth-weight infants. To better understand this challe
Chorioamnionitis is an inflammation in the fetal membranes or placenta. When chorioamnionitis develops, fetal lungs are exposed to inflammatory cytokines and mediators via amniotic fluid. Because inflammation plays a pivotal role in the development of bronchopulmonary dysplasia (BPD), a chronic lung disease of prematurity, fetal lung inflammation induced by chorioamnionitis has been considered to be one of the major pathogenetic factors for BPD. Although there have been a number of studies that
Maternal chorioamnionitis has been associated with abnormal lung development. We examined the effect of maternal chorioamnionitis on the expression of transforming growth factor-beta1 (TGF-β1) in the lungs of preterm infants. A total of 63 preterm (≤34 weeks) infants who were intubated in the delivery room were prospectively enrolled. Their placentas were examined for the presence of chorioamnionitis. Bronchoalveolar lavage (BAL) fluid and cells were obtained shortly after birth. TGF-β1 was meas
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