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Upregulation of receptor tyrosine kinase-like orphan receptor 2 in idiopathic pulmonary fibrosis
( Ji-hye Son ),( Jong-uk Lee ),( Susie Chin ),( Eun-suk Go ),( Jai-seong Park ),( Hwa-kyun Shin ),( Hun Soo Chang ),( Jong-sook Park ),( Choon-sik Park ) 대한내과학회 2021 The Korean Journal of Internal Medicine Vol.36 No.4
Background/Aims: Receptor tyrosine kinase-like orphan receptor 2 (ROR2) is a major regulator of Wnt signaling, which is involved in fibroblast dysfunction. Because its role has not been evaluated in idiopathic pulmonary fibrosis (IPF), we examined the clinical implications of ROR2 expression. Methods: ROR2 mRNA expression was measured using reverse transcription polymerase chain reaction in lung tissue-derived fibroblasts from IPF patients (n = 14) and from controls (n = 10). ROR2 protein was measured using enzyme-linked immunosorbent assay in primary fibroblasts from IPF patients (n = 14) and controls (n = 10), and in bronchoalveolar lavage (BAL) fluids obtained from normal controls (NC; n = 30). IPF patients (n = 84), and other patients with interstitial lung diseases, including nonspecific interstitial pneumonia (NSIP; n = 10), hypersensitivity pneumonitis (HP; n = 10), and sarcoidosis (n = 10). Results: ROR2 mRNA and protein levels were significantly higher in IPF fibroblasts than in controls (p = 0.003, p = 0.0017, respectively). ROR2 protein levels in BAL fluids from patients with IPF were significantly higher than in those from NC (p < 0.001), and from patients with NSIP (p = 0.006), HP (p = 0.004), or sarcoidosis (p = 0.004). Receiver operating characteristic curves showed a clear difference between IPF and NC in ROR2 protein level (area under the curve, 0.890; confidence interval, 0.829 to 0.950; p < 0.001). ROR2 protein levels were significantly higher in GAP stage III than in GAP stages I and II (p = 0.016). Conclusions: ROR2 may be related to the development of IPF, and its protein level may be a useful and severity-dependent candidate marker for IPF.
Cytoplasmic and nuclear leptin expression in lacrimal gland tumours: a pilot study
Kim, Yong Joon,Kim, Young Shin,Chin, Susie,Yoon, Jin Sook,Lee, Sang Yeul,Kim, Chang Yeom,Jang, Sun Young BMJ Publishing Group Ltd 2015 British journal of ophthalmology Vol.99 No.9
<P><B>Purpose</B></P><P>To investigate leptin expression and distribution in the tissue of lacrimal gland epithelial tumours, and leptin concentration in the tears secreted by these tumours.</P><P><B>Methods</B></P><P>Clinical records and microscopic slides of six pleomorphic adenoma (PA), three adenoid cystic carcinoma (ACC), and one chronic sclerosing dacryoadenitis (CSD) cases were reviewed. Normal-appearing gland tissue adjacent to tumours from patients with PA served as controls. Tissue leptin expression and distribution were assessed using leptin immunohistochemistry staining. Preoperative and postoperative leptin concentrations in tears were measured in the tumour-affected eye in two patients with PA, two with ACC and one with CSD, and in the contralateral eye in one patient with ACC and one with CSD.</P><P><B>Results</B></P><P>Moderate cytoplasmic staining was observed in all tumour-adjacent morphologically normal tissue, PA, ACC and CSD tissues. ACC tissues revealed moderate nuclear staining in tumour cells, whereas other tissues did not reveal leptin nuclear staining (p=0.012). Leptin in tears was not detected in the eyes of patients with PA preoperatively and postoperatively. However, leptin was detected in tears of patients with ACC and CSD preoperatively, and its concentration markedly decreased at 1 month postoperatively. Leptin was not detected in any sample from the contralateral eyes of patients for which such samples were available.</P><P><B>Conclusions</B></P><P>The leptin concentration in tears was greater in patients with ACC than in those with PA. Leptin nuclear staining was only observed in the ACC tissue. Further investigations should be conducted to identify the cause and significance of these findings.</P>
Exogenous Tryptophan Aggravates Experimental Lung Fibrosis Through Activation of AKT-mTORC1 Pathway
( Ki Sung Song ),( Jisu Hong ),( Ae-rin Baek ),( Susie Chin ),( An Soo Jang ),( Do Jin Kim ),( Sung Woo Park ) 대한결핵 및 호흡기학회 2021 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.129 No.-
Background Using the metabolomic approach, we previously reported that lung tryptophan levels were significantly increased in IPF. However, the role of tryptophan in IPF pathogenesis remains unclear. we investigated whether regulation of tryptophan modulates the severity of lung fibrosis and to find its possible mechanism. Methods We measured the expression of main extracellular matrix components in MRC-5 cells with or without tryptophan. IPF primary fibroblasts were used to perform proliferation assay and measurement of tryptophan hydroxylase (TPH-1). Exogenous tryptophan was administrated in the bleomycin (BLM) exposed mice. Results In IPF lung lysates and fibroblast, TPH-1 protein levels were significantly increased than controls. Treatment of tryptophan increased collagen, fibronectin, and a-SMA expressions in MRC5 cells. Tryptophan dramatically augments fibroblast proliferation. Treatment of tryptophan activates AKT-mTOR C1 pathway molecules in IPF fibroblast. Exogenous tryptophan promotes BLM-induced lung damage and fibrosis in mice. Conclusions These findings suggest that overproduction of tryptophan may contribute to the IPF pathogenesis and regulation of the tryptophan pathway may have therapeutic potential in preventing lung fibrosis. This study was supported by National research foundation of Korea grant 2019R1A2C1006351.
Ju Seong Gyeong,Yoon Yu Sung,Cha Jang Gyu,Chin Susie 대한자기공명의과학회 2023 Investigative Magnetic Resonance Imaging Vol.27 No.3
Xanthogranulomatous osteomyelitis is a rare, chronic inflammatory disease characterized by infiltrating lipidized histiocytes, lymphocytes, and plasma cells. Xanthogranulomatous osteomyelitis commonly presents as a mass-like lesion on imaging and may be mistaken for a tumor. Here, we describe an unusual manifestation of xanthogranulomatous osteomyelitis with imaging findings resembling those of Brodie’s abscess, posing a diagnostic challenge in a child. Additionally, we suggest a potential correlation between xanthogranulomatous osteomyelitis and a history of prior trauma.
Astrocyte elevated gene-1 overexpression in hepatocellular carcinoma
Hae Il Jung,Taesung Ahn,Sang Ho Bae,Jun Chul Chung,Hyungjoo Kim,Susie Chin,Dongjun Jeong,Hyon Doek Cho,Moon Soo Lee,Hyung Chul Kim,Chang Ho Kim,Moo-Jun Baek 대한외과학회 2015 Annals of Surgical Treatment and Research(ASRT) Vol.88 No.2
Purpose: Astrocyte elevated gene-1 (AEG-1) plays important roles in tumorigenesis such as proliferation, invasion, metastasis, angiogenesis, and chemoresistance. We examined the expression of AEG-1 in patients with hepatocellular carcinoma (HCC). Methods: Eighty-five samples were collected from patients with HCC who underwent surgery and were histopathologically confirmed to have HCC. Two independent pathologists, experienced in evaluating immunohistochemistry and blinded to the clinical outcomes of the patients, reviewed all samples. They determined AEG-1 expression semiquantitatively by assessing the percentage of positively stained immunoreactive cells and staining intensity. Clinicopathological data were analyzed in association with prognosis. Results: The association was estimated by univariate and multivariate analyses with Cox regression. Tumor size (hazard ratio [HR], 2.285; 95% confidence interval [CI], 1.175?4.447; P = 0.015), microvascular invasion (HR, 6.754; 95% CI, 1.631?27.965; P = 0.008), and AEG-1 expression (HR, 4.756; 95% CI, 1.697?13.329; P = 0.003) were independent prognostic factors for overall survival. Those for disease-free survival rate were tumor size (HR, 2.245; 95% CI, 1.282?3.933; P = 0.005) and AEG-1 expression (HR, 1.916; 95% CI, 1.035?3.545; P = 0.038). The cumulative 5-year survival and recurrence rates were 89.2% and 50.0% in the low-expressing group and 24.5% and 82.4% in the high-expressing group, respectively. Conclusion: The results suggest that AEG-1 overexpression could serve as a valuable prognostic marker in patients with HCC.
Establishment of Particulate Matter Induced Acute Lung Inflammation Model in Mice
( Jisu Hong ),( Ki Sung Song ),( Hye-sun Shin ),( Jong-sang Youn ),( Ki-joon Jeon ),( Susie Chin ),( Sung Woo Park ),( Sung Hwan Jeong ) 대한결핵 및 호흡기학회 2021 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.129 No.-
Background Particulate matter (PM) is one of the main causes of the development and progression of lung diseases. Animal experiments have been attempted to investigate the effect of PM on human lung diseases. However, various Methods of PM delivery into lungs as shown in published reports cannot reflect the actual exposure of PM in humans. In this study, we want to establish mouse model of PM exposure using a whole-body inhalation system that is similar to humans exposed to PM. Then, we evaluated the damage of lung following inhalation of various doses of PM. Methods Low grade (50), middle (150), and high grade (300 μg/m3) concentrations of road dust were inhaled to C57 BL/6J mice for 8h/ day during 7 days. At D8, the mice were sacrificed then bronchoalveolar lavage (BAL)Fluids and lung tissues were prepared for analyzing cell & diff count, H & E stain, and cytokine assay. Results Total cell count and macrophage in BAL fluid were significantly increased at 150 and 300 μg/m3 treated group than controls. The percentage of foamy macrophage was significantly increased by treatment of road dust in a dose-dependent manner. Histologic findings from 300 mg/m3 group mice revealed dust contained alveolar macrophages, peribranchial dust deposition with subtle fibrosis, and bronchial epithelial regenerative hyperplasia. The levels of TNF-α in BAL fluids were increased by treatment of road dust. Conclusions We established a PM-induced lung inflammation model that is close to human exposure. Further studies including longer exposure duration will be needed to establish a chronic lung injury model. We suggest that our exposure system is suitable to apply to lung fibrosis, asthma, and emphysema model for studying the effect of PM in the diseases. This research was funded by Korea Environmental Industry & Technology Institute.