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FBG 센서를 활용한 고강도 콘크리트 구조물의 계측 및 모니터링에 관한 연구
장일열,주웅비 금오공과대학교 2008 論文集 Vol.29 No.-
Fiber Bragg grating (FBG) sensors have already been the focus for structural health monitoring due to their distinguished advantage. However, due to bare optical fiber's fragility, bare FBG without encapsulation is not properly applied in practical infrastructures directly. So the encapsulation techniques to make encapsulated FBG sensor show very important in pushing forward the application of FBGs in structural health monitoring. In this paper, based on the FBG's strain and temperature sensing principles, monitoring techniques for steel sleeve packaged FBG sensors are brought forward.
Jang, Woong Bi,Park, Ji Hye,Ji, Seung Taek,Lee, Na Kyung,Kim, Da Yeon,Kim, Yeon Ju,Jung, Seok Yun,Kang, Songhwa,Lamichane, Shreekrishna,Lamichane, Babita Dahal,Ha, Jongseong,Yun, Jisoo,Moon, Hyung Ryo Hindawi 2018 Oxidative medicine and cellular longevity Vol.2018 No.-
<P>Diabetic cardiomyopathy (DCM) is tightly linked to heart disorders and dysfunction or death of the cardiomyocytes including resident cardiac progenitor cells (CPCs) in diabetic patients. In order to restore loss of function of resident or transplanted CPCs, much research has focused on novel therapeutic strategies including the discovery of novel function-modulating factors such as reactive oxygen species (ROS) scavengers. Here, we developed and defined a novel antioxidant, MHY-1684, for enhancing the angiogenic potential of CPCs against ROS-related DCM. Short-term treatment with MHY-1684 restored ROS-induced CPC cell death. Importantly, MHY-1684 decreased hyperglycemia-induced mitochondrial ROS generation and attenuated hyperglycemia-induced mitochondrial fragmentation. We observed that the activation process of both Drp1 (phosphorylation at the site of Ser616) and Fis-1 is drastically attenuated when exposed to high concentrations of D-glucose with MHY-1684. Interestingly, phosphorylation of Drp1 at the site of Ser637, which is an inhibitory signal for mitochondrial fusion, is restored by MHY-1684 treatment, suggesting that this antioxidant may affect the activation and inhibition of mitochondrial dynamics-related signaling and mitochondrial function in response to ROS stress. In conclusion, our finding of the novel compound, MHY-1684, as an ROS scavenger, might provide an effective therapeutic strategy for CPC-based therapy against diabetic cardiomyopathy.</P>
음향을 이용한 추자도 바다목장 해역의 계절별 어군의 분포 조사
장지웅(Ji-Woong JANG),오선영(Sun-Young OH),민은비(Eun-Bi MIN),황두진(Doo-Jin HWANG) 전남대학교 어업기술연구소 2020 어업기술연구소보고지 Vol.13 No.1
The purpose of this research is to investigate the distribution of seasonal fish schools in Chujado Marine Ranch Area. Acoustic surveys were conducted three times in May, August, and November 2019. The results of the survey were a low fish density in May and November while the highest density was recorded in August. In May and November, there were no fish schools, and small number of individual fish appeared. In August, a large fish schools was formed throughout the depths of the surveyed sea. The water temperature was the highest in August compared to May and November. It was found that the fish schools changes according to the time of day or night, the seasonal environment, water temperature, and the submarine topography. Regular and systematic investigation is necessary to construct a marine ranch suitable for the target sea area.
Oleuropein induces apoptosis in colorectal tumor spheres via mitochondrial fission
김다연,Park Sangmi,윤지수,Jang Woong Bi,비누스,Van Le Thi Hong,Giang Ly Thanh Truong,최재우,Lim Hye ji,권상모 대한독성 유전단백체 학회 2023 Molecular & cellular toxicology Vol.19 No.2
Background 5-Fluorouracil (5-FU) has been used as a standard chemotherapeutic agent for colorectal cancer (CRC). However, chemo-resistant cancer cells can survive under chemotherapeutic regimens, resulting in cancer recurrence. Thus, a novel approach is required to overcome chemo-resistance in CRC. Objective Recently, oleuropein (OLP), an extract derived from olive leaves, has shown anticancer eff ects and induces apoptosis in cancer cells; however, the role of OLP in 5-FU-resistant cells remains to be elucidated. Therefore, we have assessed the anticancer eff ect of OLP on tumor spheres and 5-FU-resistant cells, but also synergistic eff ect in combination of OLP and 5-FU. Results Our fi ndings revealed that OLP had a marked suppressive eff ect on tumor sphere formation capacity. Annexin V-PI staining data showed that OLP-induced apoptosis occurred in a dose-dependent manner. Mitochondrial fragmentation and mitochondrial superoxide production were observed following treatment with OLP. OLP treatment drastically suppressed the metastatic potential, including cell migration ability and anchorage-independent growth capability. In addition, combination treatment with 5-FU and OLP revealed a synergistic eff ect on cell viability in DLD-1 cells and 5-FU-resistant cells. Conclusion These fi ndings showed the suppressive eff ects of OLP against the colorectal tumor spheres and 5-FU-resistant cells. In addition, these results off er the new insights into novel therapeutic strategies for combining 5-FU and OLP in patients with chemo-resistant CRC.
( He Yun Choi ),( Ji Hye Park ),( Woong Bi Jang ),( Seung Taek Ji ),( Seok Yun Jung ),( Da Yeon Kim ),( Songhwa Kang ),( Yeon Ju Kim ),( Jisoo Yun ),( Jae Ho Kim ),( Sang Hong Baek ),( Sang Mo Kwon ) 한국응용약물학회 2016 Biomolecules & Therapeutics(구 응용약물학회지) Vol.24 No.4
Cardiovascular disease is the most common cause of death in diabetic patients. Hyperglycemia is the primary characteristic of diabetes and is associated with many complications. The role of hyperglycemia in the dysfunction of human cardiac progenitor cells that can regenerate damaged cardiac tissue has been investigated, but the exact mechanism underlying this association is not clear. Thus, we examined whether hyperglycemia could regulate mitochondrial dynamics and lead to cardiac progenitor cell dysfunction, and whether blocking glucose uptake could rescue this dysfunction. High glucose in cardiac progenitor cells results in reduced cell viability and decreased expression of cell cycle-related molecules, including CDK2 and cyclin E. A tube formation assay revealed that hyperglycemia led to a significant decrease in the tube-forming ability of cardiac progenitor cells. Fluorescent labeling of cardiac progenitor cell mitochondria revealed that hyperglycemia alters mitochondrial dynamics and increases expression of fission-related proteins, including Fis1 and Drp1. Moreover, we showed that specific blockage of GLUT1 improved cell viability, tube formation, and regulation of mitochondrial dynamics in cardiac progenitor cells. To our knowledge, this study is the first to demonstrate that high glucose leads to cardiac progenitor cell dysfunction through an increase in mitochondrial fission, and that a GLUT1 blocker can rescue cardiac progenitor cell dysfunction and downregulation of mitochondrial fission. Combined therapy with cardiac progenitor cells and a GLUT1 blocker may provide a novel strategy for cardiac progenitor cell therapy in cardiovascular disease patients with diabetes.
Choi, He Yun,Park, Ji Hye,Jang, Woong Bi,Ji, Seung Taek,Jung, Seok Yun,Kim, Da Yeon,Kang, Songhwa,Kim, Yeon Ju,Yun, Jisoo,Kim, Jae Ho,Baek, Sang Hong,Kwon, Sang-Mo The Korean Society of Applied Pharmacology 2016 Biomolecules & Therapeutics(구 응용약물학회지) Vol.24 No.4
Cardiovascular disease is the most common cause of death in diabetic patients. Hyperglycemia is the primary characteristic of diabetes and is associated with many complications. The role of hyperglycemia in the dysfunction of human cardiac progenitor cells that can regenerate damaged cardiac tissue has been investigated, but the exact mechanism underlying this association is not clear. Thus, we examined whether hyperglycemia could regulate mitochondrial dynamics and lead to cardiac progenitor cell dysfunction, and whether blocking glucose uptake could rescue this dysfunction. High glucose in cardiac progenitor cells results in reduced cell viability and decreased expression of cell cycle-related molecules, including CDK2 and cyclin E. A tube formation assay revealed that hyperglycemia led to a significant decrease in the tube-forming ability of cardiac progenitor cells. Fluorescent labeling of cardiac progenitor cell mitochondria revealed that hyperglycemia alters mitochondrial dynamics and increases expression of fission-related proteins, including Fis1 and Drp1. Moreover, we showed that specific blockage of GLUT1 improved cell viability, tube formation, and regulation of mitochondrial dynamics in cardiac progenitor cells. To our knowledge, this study is the first to demonstrate that high glucose leads to cardiac progenitor cell dysfunction through an increase in mitochondrial fission, and that a GLUT1 blocker can rescue cardiac progenitor cell dysfunction and downregulation of mitochondrial fission. Combined therapy with cardiac progenitor cells and a GLUT1 blocker may provide a novel strategy for cardiac progenitor cell therapy in cardiovascular disease patients with diabetes.
Park, Ji Hye,Choi, Sung Hyun,Kim, Hyungtae,Ji, Seung Taek,Jang, Woong Bi,Kim, Jae Ho,Baek, Sang Hong,Kwon, Sang Mo MDPI 2016 INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES Vol.17 No.10
<P>Doxorubicin (DOXO) is widely used to treat solid tumors. However, its clinical use is limited by side effects including serious cardiotoxicity due to cardiomyocyte damage. Resident cardiac progenitor cells (hCPCs) act as key regulators of homeostasis in myocardial cells. However, little is known about the function of hCPCs in DOXO-induced cardiotoxicity. In this study, we found that DOXO-mediated hCPC toxicity is closely related to calcium-related autophagy signaling and was significantly attenuated by blocking mTOR signaling in human hCPCs. DOXO induced hCPC apoptosis with reduction of SMP30 (regucalcin) and autophagosome marker LC3, as well as remarkable induction of the autophagy-related markers, Beclin-1, APG7, and P62/SQSTM1 and induction of calcium-related molecules, CaM (Calmodulin) and CaMKII (Calmodulin kinase II). The results of an LC3 puncta assay further indicated that DOXO reduced autophagosome formation via accumulation of cytosolic Ca<SUP>2+</SUP>. Additionally, DOXO significantly induced mTOR expression in hCPCs, and inhibition of mTOR signaling by rapamycin, a specific inhibitor, rescued DOXO-mediated autophagosome depletion in hCPCs with significant reduction of DOXO-mediated cytosolic Ca<SUP>2+</SUP> accumulation in hCPCs, and restored SMP30 and mTOR expression. Thus, DOXO-mediated hCPC toxicity is linked to Ca<SUP>2+</SUP>-related autophagy signaling, and inhibition of mTOR signaling may provide a cardio-protective effect against DOXO-mediated hCPC toxicity.</P>