http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
이상엽 외 중앙대학교 의과대학 의학연구소 2004 中央醫大誌 Vol.29 No.1·2
The blood pressure (BP) response is a valuable predictor of coronary heart disease (CHD). However, little is known about the blood pressure responses, especially pulse pressure, mean arterial pressure during exercise. The purpose of this study was to evaluate the clinical significance of the blood pressure responses during exercise for prediciting CHD. The blood pressure responses during treadmill exercise test were measured in 82 patients who underwent coronary angiography. 58 patients had the coronary artery disease and 24 persons had normal coronary artery. The results were as follows: 1) During resting stage, the systolic blood pressure (SBP), diastolic blood pressure (DBP), pulse pressure (PP), mean arterial pressure (MAP) had no significant difference between patients with CHD and normal subjects (p>0.05). 2) During peak exercise, DBP (72 mmHg) in patients with CHD was significantly lower than in normal subjects (83 mmHg, p=0.004) and MAP (96 mmHg) in patients with CHD was significantly lower than in normal subjects (106 mmHg, p=0.02). SBP and PP were not significantly different between patients with CHD and normal subjects (p>0.05). 3) During recovery stage, the BP responses had no significant difference between patients with CHD and normal subjects (p>0.05). DBP during peak exercise was the most important factor of predicting CHD (p<0.0001). These results indicate that DBP and MAP during peak exercise was significantly lower in the patient with coronary artery disease. DBP and MAP during peak exercise seem to be a valuable predictor of the ischemic heart disease.
Lee, Sung Yong,Kang, Eun Joo,Hur, Gyu Young,Jung, Ki Hwan,Jung, Hye Cheol,Lee, Sang Yeub,Kim, Je Hyeong,Shin, Chol,In, Kwang Ho,Kang, Kyung Ho,Yoo, Se Hwa,Shim, Jae Jeong American Physiological Society 2006 American Journal of Physiology: Lung cellular and Vol.291 No.1
<P>The main etiologic factor for chronic bronchitis is cigarette smoke. Exposure to cigarette smoke is reported to induce goblet cell hyperplasia and mucus production. Mucin synthesis in airways has been reported to be regulated by the EGFR system. Peroxisome proliferator-activated receptor-gamma (PPAR-gamma) is a member of the ligand-activated nuclear receptor superfamily. PPAR-gamma is implicated in anti-inflammatory responses, but mechanisms underlying these varied roles remain ill-defined. Recently, reports have shown that upregulation of phosphatase and tensin homolog deleted on chromosome 10 (PTEN) might be one of the mechanisms through which PPAR-gamma agonists exert their anti-inflammatory actions. However, no data are available on the role of PPAR-gamma in smoke-induced mucin production. In this study, we investigated the effect of PPAR-gamma agonist (rosiglitazone) on smoke-induced mucin production in NCI-H292 cells. Exposure to cigarette smoke causes a significant decrease in PTEN expression and increases dose-dependent EGFR-specific tyrosine phosphorylation, resulting in MUC5AC mucin production in NCI-H292 cells. PPAR-gamma agonists or specific inhibitors of phosphoinositide 3-kinase exert inhibition of cigarette smoke-induced mucin production, with the upregulation of PTEN signaling and downregulation of Akt expression. This study demonstrates that PPAR-gamma agonist functions as a regulator of epithelial cell inflammation that may result in reduction of mucin-producing cells in airway epithelium.</P>
2 Cases of a Benign Pulmonary Metastasizing Leiomyoma
Lee, Eun Joo,Jeong, Hye Cheol,Lee, Sung Yong,Kim, Je Hyeong,Lee, Sang Yeub,Shin, Chol,Shim, Jae Jeong,In, Kwang Ho,Kang, Kyung Ho,Yoo, Se Hwa,Lee, Sang Hoon,Kim, Han-Kyeom,Oh, Yu Whan The Korean Academy of Tuberculosis and Respiratory 2009 Tuberculosis and Respiratory Diseases Vol.67 No.6
A benign pulmonary metastasizing leiomyoma is a recognized clinical entity that has been infrequently reported in the medical literature. We report two cases of a benign pulmonary metastasizing leiomyoma. A 35-year-old woman who underwent myomectomy and a cesarean section approximately 6 years earlier visited our hospital for further evaluation of incidentally revealed multiple lung nodules. A diagnostic percutaneuous biopsy was performed. Finally she was diagnosed with a benign metastasizing leiomyoma. The patient then received LH-RH and has been followed up since. The other 44-year-old woman presented after an initial radiology evaluation revealed the presence of multiple, small-sized lung nodules. She underwent a right middle lung wedge resection to confirm the diagnosis. Finally she diagnosed with a benign metastasizing leiomyoma. The multiple lung nodules have been followed up closely.
Clinical Results of Drug-Coated Balloon Treatment in a Large-Scale Multicenter Korean Registry Study
Sang Yeub Lee,Yun-Kyeong Cho,Sang-Wook Kim,Young-Joon Hong,Bon-Kwon Koo,Jang-Whan Bae,Seung-Hwan Lee,Tae Hyun Yang,Hun Sik Park,Si Wan Choi,Do-Sun Lim,Soo-Joong Kim,Young Hoon Jeong,Hyun-Jong Lee,Kwan 대한심장학회 2022 Korean Circulation Journal Vol.52 No.6
Background and Objectives: The aim of this study was to demonstrate the efficacy and safety of treatment with drug-coated balloon (DCB) in a large real-world population. Methods: Patients treated with DCBs were included in a multicenter observational registry that enrolled patients from 18 hospitals in Korea between January 2009 and December 2017. The primary outcome was target lesion failure (TLF) defined as a composite of cardiovascular death, target vessel myocardial infarction, and clinically indicated target lesion revascularization at 12 months. Results: The study included 2,509 patients with 2,666 DCB-treated coronary artery lesions (1,688 [63.3%] with in-stent restenosis [ISR] lesions vs. 978 [36.7%] with de novo lesions). The mean age with standard deviation was 65.7±11.3 years; 65.7% of the patients were men. At 12 months, the primary outcome, TLF, occurred in 179 (6.7%), 151 (8.9%), 28 (2.9%) patients among the total, ISR, and de novo lesion populations, respectively. A history of hypertension, diabetes, acute coronary syndrome, previous coronary artery bypass graft, reduced left ventricular ejection fraction, B2C lesion and ISR lesion were independent predictors of 12 months TLF in the overall study population. Conclusions: This large multicenter DCB registry study revealed the favorable clinical outcome of DCB treatment in real-world practice in patient with ISR lesion as well as small de novo coronary lesion.
The inhibitory effects of rebamipide on cigarette smoke-induced airway mucin production
Lee, Sung Yong,Kang, Eun Joo,Hur, Gyu Young,Jung, Ki Hwan,Jung, Hye Cheol,Lee, Sang Yeub,Kim, Je Hyeong,Shin, Chol,In, Kwang Ho,Kang, Kyung Ho,Yoo, Se Hwa,Shim, Jae Jeong Elsevier 2006 Respiratory medicine Vol.100 No.3
<P><B>Summary</B></P><P>Cigarette smoke may be the main cause of chronic bronchitis. Exposure of cigarette smoke induces the recruitment of inflammatory cells in the airway epithelium, and release of the tumor necrosis factor <I>α</I> (TNF<I>α</I>) from airways. Previous reports have shown that cigarette smoke induces goblet cell metaplasia by activating an epidermal growth factor receptor (EGFR) cascade, and that this results in mucin production. Rebamipide (2-(4-chlorobenzoylamino)-3-[2(1H)-quinolinon-4-yl] propionic acid, OPC-12759) directly inhibits the production of superoxide (O<SUB>2</SUB><SUP>−</SUP>) and inhibits proinflammatory cytokines (such as TNF<I>α</I> and IL-8). In the present study, we aimed to analyze the inhibitory effects of rebamipide on TNF<I>α</I> and EGFR activation after cigarette smoke treatment in vitro and in vivo.</P><P>NCl-H292 cells and Sprague-Dawley rats were used for in vitro and in vivo studies. In vitro studies, cigarette smoke solution was found to increase TNF<I>α</I> secretion, and EGFR-specific tyrosine phosphorylation, and to elevate MUC5AC production. These effects were inhibited dose-dependently by pretreatment with rebamipide (MUC5AC protein levels were inhibited from 44% to 17%, P<0.05). In vivo studies, cigarette smoke was found to cause inflammatory cell recruitment and to increase the secretion of TNF<I>α</I> in bronchoalveolar lavage (BAL) fluids (from 198±78 to 2270±158pg/ml, P<0.01). Moreover, the pretreatment of rats with rebamipide inhibited goblet cell metaplasia and TNF<I>α</I> secretion, dose-dependently (from 2270±158 to 1377±112pg/ml, P<0.05).</P><P>In conclusion, the exposure of airway epithelium to cigarette smoke-induced TNF<I>α</I> production, neutrophil recruitment, activated EGFR, and caused MUC5AC mucin synthesis. Moreover, rebamipide was found to prevent this cigarette smoke-induced TNF<I>α</I> release, and mucin production.</P>
Lee, Seung Hyeun,Kim, Sung-Woo,Lee, Sehyun,Kim, EunSub,Kim, Duck-Joong,Park, Sohyun,Lee, Eun Joo,Lee, Sang Yeub,Lee, Ji Sung,Lim, Chae Seung,Kim, Won-Ki,In, Kwang Ho Elsevier 2014 Chest Vol.146 No.5
<P>NBS LabChip G2-3 is a novel, ultrafast, chip-type portable real-time polymerase chain reaction (PCR) system. We evaluated the clinical usefulness of this system in detecting pulmonary TB and assessed its diagnostic performance compared with a conventional tube-type PCR system.</P>