촉매-크래킹에 의한 나프타로부터 경질 올레핀 제조기술

박용기,전종열,한상윤,김정리,이철위 한국화학공학회 2003 Korean Chemical Engineering Research(HWAHAK KONGHA Vol.41 No.5

세계적으로 에틸렌 생산공장에서 배출되는 이산화탄소의 양은 매년 141백만 톤에 이르며, 석유화학산업에서 소비되는 전체 에너지 중 약 40%는 나프타 스팀크래킹에 사용된다. 이로인한 지구 온난화를 막기 위하여 에너지 효율 증대를 통하여 이산화탄소 배출양을 최소화할 수 있는 나프타 크래킹 기술개발이 시급하다. 또한 천연가스로부터 얻어지는 에틸렌의 양이 점점 증가하기 때문에 프로필렌/에틸렌 비를 증대하기 위한 연구가 필요한 실정이다. 그러므로 에틸렌과 프로필렌 수요를 맞추기 위한 thermal cracking의 대안으로 촉매를 이용한 크래킹기술이 시도되고 있다. 본 논문에서는 나프타로부터 에틸렌, 프로필렌 등과 같은 경질 올레핀 제조에 관하여 지난 수 년간 공개된 특허와 실용화 가능한 공정 기술을 소개하고자 한다. In the whole world, the amount of CO₂ emission from the ethylene plant is about 141 million tons per year, and currently about 40% of the energy in petrochemical industry is used for steam cracking of naphtha. So, global warming issues have stimulated the development of new cracking process of naphtha which can minimize CO₂ emission through the increase of energy efficiency. Also there is an effort to increase the ratio of propylene/ethylene in naphtha cracking since the natural gas cracker which can produce ethylene preferentially increases more and more. Therefore, catalytic cracking of naphtha has been studied as an alternative of thermal cracking to balance ethylene and propylene demand and to reduce CO₂ emission. This paper will review the various routes which have been investigated and applied over the past years, hut will focus particularly on the recently patented and commercially demonstrated processes for the production of lower olefins from naphtha.

Cone-beam CT를 이용한 골격성 III급 부정교합자의 하악골 후퇴술 후 상기도 변화에 관한 연구

김나리,김용일,박수병,황대석 대한치과교정학회 2010 대한치과교정학회지 Vol.40 No.3

악교정 수술은 안면골격형태 뿐만 아니라 상기도 공간에도 영향을 준다. 본 연구는 골격성 III급 부정교합자 중 하악골 후퇴술을 시행 받은 환자를 대상으로 상기도 공간의 부피변화를 관찰하기 위하여 시행되었다. 기존의 연구들이 측모두부방사선사진을 중심으로 시행하였으나 본 연구에서는 3차원 cone-beam computed tomography (CBCT)를 이용하여 영상을 재구성한 뒤 분석하였다. 연구 대상은 하악골 후퇴술을 시행 받은 20명(남성 12, 여성 8)이었으며, 술 전 평균 1.8주(Baseline), 술 후 평균 2.3개월(T1) 그리고 술 후 평균 1년(T2) 시기에 CBCT를 촬영하였다. 상기도 공간은 기준평면에 따라 비인두, 구인두, 하인두로 나누어 계측하고 Baseline, T1, T2를 각각 비교하였다. 결과로 술후 2.3개월(T1)시기에 상기도 공간은 상당히 감소하였으며 (p < 0.001), 술 후 1년 후(T2)에도 감소된 양은 증가하지 않았다. 구인두는 상기도 공간 중 가장 많은 감소폭을 보였다. 이러한 결과로 하악골후퇴술은 상기도 공간을 장·단기간동안 감소하는 것으로 나타났다. Objective: Lateral cephalometric radiographs have been the main form of resource for assessing two dimensional anteroposterior airway changes. The purpose of this study was to evaluate the three dimensional volumetric change in the upper airway space in Class III malocclusion patients who underwent mandibular setback surgery. Methods: Three dimensional cone-beam computed tomographs (CBCT) and their three dimensional reconstruction images were analyzed. The samples consisted of 20 adult patients (12 males and 8 females) who were diagnosed as skeletal Class III and underwent mandibular setback surgery. CBCTs were taken at 3 stages - Baseline (1.8 weeks before surgery), T1 (2.3 months after surgery), and T2 (1 year after surgery). Pharyngeal airway was separated according to the reference planes and reconstructed into the nasopharynx, the oropharynx and the hypopharynx. Measurements at Baseline, T1, and T2 were compared between groups. Results: The result showed the volume of the pharyngeal airway decreased significantly 2.3 months after surgery (p < 0.001) and the diminished airway did not recover after 1 year post-surgery. The oropharynx was the most decreased area. Conclusions: These findings suggest that mandibular setback surgery causes both short-term and long-term decrease in the upper airway space.

中國國有企業의 民營化改革에 관한 硏究

최장호,박영일 단국대학교 1999 論文集 Vol.34 No.-

Under the System of Chinese Socialism, the position and the role of state enterprises is very important in Chinese national economy. However, state enterprises were getting worse. The lack of efficiency and accumulated deficit caused the loss of government subsidies each year. Therefore, need of reform in state enterprises is evident. The reform with various new policies has begun from 1978 by planning and implementation. Chinese private enterprises has been taking rapid growth. But it still shows many problems. From these empirical studies, many problems of the privatization of state enterprises were found. Those are government interference, ownership structure, conditions of competitions between companies, financial difficulty and so on. As a conclusion, some solutions and future directions for more effective privatization of state enterprises were suggested. The reform of state enterprises in china may be the precedent of the reform of Korea's public enterprises.

4주간의 육미지황탕 투여가 최대하운동시 근대 5종 선수들의 혈액성분 및 혈액가스성분 변화에 미치는 영향

오재근,최용어,서인원,조준용,유루리 韓國體育大學校 1997 論文集 Vol.20 No.-

The purpose of this study was to estimate the changes of blood components and blood gases on submaximal exercise after Yuk-mi-ji-Whang-tang administration during 4 weeks. Ten modern pentathlon athletes participated as subjects of this study. The result and conclusion of this study is as follows; The changes of blood components on pre-, post-sumaximal exercise and during recovery time was not significant difference in Yuk-mi-ji-whang-tang administration group except for WBC(p<.05.). But comparative observation of blood gases levels such as pH, PCO₂, PO₂, HCO₃, O₂SAT, O₂CT was showed a tendency of being lower acidity, higher PO₂, lower PCO₂on pre-, post-sumaximal exercise and during recovery time in Hyang-sa-pyung-yi-san than in Yuk-mi-ji-whang-tang administration group.

MCC 950 ameliorates house dust mite-induced asthma through the regulation of ASC oligomerization and NEK7-NLRP3 binding in NLRP3 inflammasome assembly

( Yong Chul Lee ),( Jae Seok Jeong ),( So Ri Kim ),( Hae Jin Park ),( Kyeong Hwa Park ),( Navin Ray ),( Yeong Hun Choe ),( Seung Yong Park ) 대한결핵 및 호흡기학회 2018 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.126 No.-

NLRP3 inflammasome, consisting of NLRP3, the adaptor protein ASC, and the protease caspase-1, is responsible for the production of active forms of IL-1β and IL-18. In this process, oligomerization of ASC is a key step in assembly/activation of inflammasome and, recently, NEK7, a serine and threonine kinase, has been also reported as an essential activator of the NLRP3 inflammasome. MCC 950 is a small-molecule inhibitor of NLRP3 inflammasome, however, molecular action mechanism of MCC 950 is not fully understood. We investigated the therapeutic effects of the MCC 950 and its action mechanism in house dust mite (HDM)-induced allergic lung inflammation, particularly focusing on the NLRP3 inflammasome assembly process involving ASC and NEK7. Respiratory HDM exposure into mice led to the significant increases of pulmonary NLRP3, caspase-1, and IL-1β. Furthermore, levels of ASC oligomers were elevated in lung tissues of HDM-exposed mice and we observed the cytoplasmic co-localization of immunofluorescence intensities of NLRP3 and NEK7 in bronchoalveolar lavage (BAL) cells. Notably, treatment with MCC 950 significantly reduced the HDM-induced increases of ASC oligomerization and NLRP3-NEK7 colocalization in the lung of mice, and that ameliorated the HDM-induced increases of airway inflammatory cells infiltration, airway hyper-reactivity, and pulmonary TH2 cytokines. These results suggest that MCC 950 may have potential for treating HDM-induced allergic asthma partly through the regulation of HDM-induced ASC oligomerization and NEK7-NLRP3 binding in NLRP3 inflammasome assembly.

Free Paper Presentation : OS-76 ; Endoplasmic Reticulum Stress Is Implicated in the Development of Allergic Airway Remodeling via the Induction of VEGF Expression

( Yong Chul Lee ),( So Ri Kim ),( Yun Hee Ko ),( Yang Keun Rhee ),( Heung Bum Lee ),( Seoung Ju Park ),( Yeong Hun Choe ),( Seung Yong Park ) 대한결핵 및 호흡기학회 2014 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.118 No.-

Background: Vascular endothelial growth factor (VEGF) is a key player in the tissue fibrosis, especially airway disorders. Recent studides have demonstrated that endoplasmic reticulum (ER) stress has been reported to be implicated in various chronic pulmonary disorders such as chronic obstructive pulmonary disorder (COPD), bronchial asthma, and pulmonary fibrosis. However, little is known concerning the role of ER stress in the pathogenesis of bronchial asthma, particularly airway remodeling. Methods: We used a long-term exposure murine model of allergic airway disease to evaluate the effect of 4-PBA, an ER stress regulator, on hyperresponsiveness, inflammation, and remodeling of the airways. Results: This study with the chronic model of allergic airway disease revealed the typical pathophysiological features; increased the expression of ER stress markers and the protein levels of unfolded-protein response (UPR)-related markers in lung tissues, increased numbers of airway inflammatory cells, increased plasma exudation, airway hyperresponsiveness, and increased levels of Th2 cytokines, TGF-β1, and VEGF. In addition, the mice chronically exposed to ovalbumin (OVA) developed features of airway remodeling, including thickening of the peribronchial smooth muscle layer, subepithelial collagen deposition, and increased airway mucus production. Administration of 4-PBA reduced the pathophysiological symptoms of asthma including airway remodeling, plasma exudation, Th2 cytokines, TGF-β1, and VEGF in lungs as well as the increased expression of ER stress markers and the protein levels of UPR-related markers after OVA inhalation. Conclusions: These results indicate that inhibition of ER stress may attenuate chronic antigen-induced airway inflammation, hyperresponsiveness, and airway remodeling through the regulation of VEGF.

Free Paper Presentation : OS-75 ; NLRP3 Inflammasome Is Regulated by Phosphoinositide 3-Kinase δ Isoform in Aspergillus Fumigatus-induced Severe Allergic Inflammation of Mice

( Yong Chul Lee ),( So Ri Kim ),( Yun Hee Ko ),( Soon Ha Kim ),( Yang Keun Rhee ),( Heung Bum Lee ),( Seoung Ju Park ),( Yeong Hun Choe ),( Seung Yong Park ) 대한결핵 및 호흡기학회 2014 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.118 No.-

Background: NLRP3 inflammasome is activated by various pathophysiological stimuli and plays a cruicial role in th pathogenesis of several pulmonary disorders. Phosphoinositide 3-kinase delta (PI3K-d) signaling has been repoted to be implicated in the pathogenesis of allergic airway inflammation. However, it is still not known about the role of PI3K-d in relation to activation of the NLRP3 inflammasome in airway inflammation. Methods: In this study, we focused on an association of NLRP3 inflammasome activation with PI3K-d signaling in Aspergillus fumigatus- induced allergic lung inflammation. Using Aspergillus fumigatus-exposed in vivo and in vitro experimental systems, we have investigated the role of PI3K-d in the regulation of NLRP3 inflammasome activation in the pathogenesis of fungus-induced allergic lung inflammation. Results: The protein expression of NLRP3, caspase-1, and IL-1β in lungs was significantly increased after Aspergillus fumigatus challenge in Aspergillus fumigatus-sensitized and -challenged mice. Protein expression of NLRP3 and caspase-1 was also remarkably elevated in Aspergillus fumigatus-stimulated cultured tracheal epithelial cells. But, administration of PI3K-d inhibitor significantly reduced the increases of the protein levels of NLRP3, caspase-1, and IL-1β in the lung. And, blockade of PI3K-d signaling using PI3K-d inhibitor or PI3K-d specific siRNA also markedly reduced increased protein expression of NLRP3 and caspase-1 in Aspergillus fumigatus-stimulated cultured tracheal epithelial cells. Furthermore, inhibition of PI3K-d improved various pathophysiologic features in Aspergillus fumigatus-induced allergic lung inflammation. Lastly, neutralization of IL-1β substantially reduced airway inflammation and hyperresponsiveness in The Aspergillus fumigatus-sensitized and -challenged mice. Conclusions: These findings suggest that PI3K-d signaling influences Aspergillus fumigatus-induced allergic lung inflammation via the regulation of NLRP3 inflammasome activation.

Free Paper Presentation : OS-83 ; Activation of Phosphoinositide 3-Kinase δ Pathway Contributes to Aspergillus Fumigatus-Induced Severe Allergic Asthmatic Inflammation via the Regulation of ER Stress in Mice

( Yong Chul Lee ),( So Ri Kim ),( Yun Hee Ko ),( Soon Ha Kim ),( Yang Keun Rhee ),( Heung Bum Lee ),( Seoung Ju Park ),( Yeong Hun Choe ),( Seung Yong Park ),( Jae Seok Jeong ) 대한결핵 및 호흡기학회 2014 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.118 No.-

Background: Phosphoinositide 3-kinase (PI3K)-d signaling and endoplasmic reticulum (ER) stress are critically involved in various inflammatory processes. However, there is no information concerning their interrelationship in allergic inflammation. Methods: In this study, we aimed to elucidate an association of ER stress with PI3K-d signaling in fungus-induced allergic lung inflammation. Using Aspergillus fumigatus-exposed in vivo and in vitro experimental systems, we have investigated the role of PI3K-d in the regulation of ER stress in the pathogenesis of allergic lung inflammation. Results: The Aspergillus fumigatus-sensitized and -challenged mice showed that the expression of ER stress markers and the protein levels of unfolded protein response (UPR)-related markers in lung tissues were significantly increased after Aspergillus fumigatus challenge. Protein expression of ER stress markers was also remarkably elevated in Aspergillus fumigatus- stimulated cultured tracheal epithelial cells. However, administration of PI3K-d inhibitor significantly reduced the increases in ER stress markers and UPR-related proteins in the lung. And, blockade of PI3K-d signaling using PI3K-d inhibitor or PI3K-d specific siRNA also markedly reduced the expression of ER stress markers in Aspergillus fumigatus-stimulated cultured tracheal epithelial cells. Furthermore, inhibition of PI3K-d or ER stress improved various pathophysiologic features in Aspergillus fumigatus-induced allergic lung inflammation. Conclusions: These findings suggest that PI3K-d signaling is implicated in Aspergillus fumigatus-induced allergic lung inflammation through the modulation of ER stress.

NecroX Compounds Attenuate Pulmonary Fibrosis through The Modulation of ER Stress-associated Inflammatory Responses

( Yong Chul Lee ),( So Ri Kim ),( Kyung Bae Lee ),( Hae Jin Park ),( Soon Ha Kim ),( Yang Keun Rhee ),( Heung Bum Lee ),( Seoung Ju Park ),( Yeong Hun Choe ),( Seung Yong Park ) 대한결핵 및 호흡기학회 2015 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.120 No.0

Mitochondrial oxidative damage has been recognized as being involved in many diseases and in the aging process. Fibrotic changes appear as sequelae to insults by a diverse group of infectious, environmental, and therapeutic exposures. To date, bloemycin-inhaled animal model represents as a relatively well established experimental tool for pulmonary fibrosis. In this study, we aimed to investgate the role of mitochondrial ROS in the pathogenesis of bleomycin-induced pulmonary fibrosis and the related mechanisms. These results showed the increased the generation of mitochondrial ROS in inflammatory cells and lung tissues, increased numbers of airway inflammatory cells, increased levels of pro-inflammatory cytokines and TGF-β1, the increased expression of ER stress markers, and increased nuclear translocation of NF-κB in bleomycin-inhaled mice. In addition, the bleomycin-inhaled mice developed features of pulmonary fibrosis, including thickening of the peribronchial smooth muscle layer, subepithelial collagen deposition, and increased ECM production. Administration of NecroX compounds reduced the pathophysiological symptoms of pulmonary fibrosis, increased NF-κB activation, and TGF-β1 in lungs as well as the increased generation of mitochondrial ROS and increases of ER stress in lung after bleomycin inhalation. These results indicate that reduction of mitochondrial ROS may attenuate pulmonary fibrotic changes through the regulation of ER stress and NF-κB pathway, providing the therapeutic potential of NecroX compounds as an anti-fibrotic agent.

Free Paper Presentation : OS-10 ; Mitochondrial ROS Contribute to PHMG-Induced Pulmonary Fibrosis of Mice

( Yong Chul Lee ),( So Ri Kim ),( Dong Im Kim ),( Soon Ha Kim ),( Yang Keun Rhee ),( Heung Bum Lee ),( Seoung Ju Park ),( Yeong Hun Choe ),( Seung Yong Park ) 대한결핵 및 호흡기학회 2014 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.118 No.-

Background: Overproduction of reactive oxygen species (ROS), most frequently either by excessive stimulation of nicotinamide adenine dinucleotide phosphate reduced (NADPH) by cytokines or by the mitochondrial electron transport chain and xanthine oxidase, results in oxidative stress. Oxidative stress is a deleterious process that leads to damage to lung and consequently various disease states. Recently, inhaled form of polyhexamethylene biguanide (PHMG) has been turned out the cause of the fatal lung injury in Korea. However, to date, the inhaled form of these chemicals has been shortly evaluated for the linkage with oxidative stress, especially mitochondrial ROS. Methods: Using PHMG-inhaled mice and a newly developled mitochondrial ROS inhibitor, we evaluated the role of mitochondrial ROS in the pathogenesis of PHMG-induced pulmonary fibrosis. Results: In this study, we have found that the PHMG-inhaled mice showed the similar pathologic features of pulmonary fibrosis with acute inflammation; increased the generation of moitochondrial ROS in lung tissues and inflammatory cells, increased numbers of airway inflammatory cells, increased collagen accumulation, smooth muscle hyperplasia, and increased levels of pro-inflammatory cytokines, TGF-β1, Smad 3 expression, and nuclear translocation of NF-κB. The administration of NecroX-5 and -7 significantrly reduced the levels of mitochondrial ROS, attenuates the pathologic changes, and decreased the increased levels NF-κB activity, the numbers of airway inflammatory cells, pro-inflammatory cytokines, collagen accumulation, the smooth muscle actin expression, TGF-β1, and Smad 3 expression. Conclusions: These results indicate that mitochondrial ROS play a critical role in the pathogenesis of PHMG-inhaled lung injury via the modulation of NF-κB pathway as well as pro-fibrotic cytokines.