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임지민(Ji-Min Lilm),양선제(Seon-Je Yang),국태용(Tae-Yong Kuc),박종구(Jong-Koo Park),고낙용(Nak-Yong Ko),문용선(Young-Seon Moon) 대한전자공학회 2016 대한전자공학회 학술대회 Vol.2016 No.6
In this paper, we propose a simple and effective path following controller for USV(Unmanned Surface Vehicle). The proposed controller consists of path planner, coordinator, velocity profile generator, and velocity-thruster converter. Simulation results demonstrate the effectiveness of the proposed path following controller
외과계 진료과별 수혈 결정 혈색소 비교 및 수혈 적정성 분석
양미나,임지향,김훈석,이종미,정진,최승준 대한수혈학회 2018 大韓輸血學會誌 Vol.29 No.2
Background: Red blood cell (RBC) transfusion is an essential practice during surgery to accommodate for bleeding. As such, there are efforts being made to allow for a safe and appropriate transfusion due to shortages of blood components and to minimize transfusion-related adverse reactions. However, a conventional transfusion decision with relatively high hemoglobin (Hb) threshold is still performed in clinical setting. In this study, we investigated the threshold of Hblevel and appropriateness of RBC transfusion in patients receiving perioperative RBC transfusion in surgical departments. Methods: We investigated the pre-transfusion Hb level of 1,379 patients (2,170 episodes) receiving perioperative RBC transfusion in five surgical departments, including cardiothoracic surgery (CS), general surgery (GS), neurosurgery (NS), obstetrics and gynecology (OBGY), and orthopedics (OS), between June 2017 and March 2018. The appropriateness of transfusion was evaluated with two criteria: 1) pretransfusion Hb level ≤10 g/dL and 2) posttransfusion Hb level ≤10 g/dL. Results: The median pretransfusion Hb level was 8.5 g/dL (interquartile range 7.7∼9.4); that of each department was as follows: 8.6 g/dL (7.9∼9.2) in CS, 7.9 g/dL (7.3∼8.6) in GS, 9.1 g/dL (8.5∼9.8) in NS, 8.5 g/dL (7.7∼9.8) in OBGY, and 8.7 g/dL (7.9∼9.7) in OS. With a criteria of pretransfusion of Hb level ≤10 g/dL, 85.4% of total episodes were appropriate. With criteria of post-transfusion of Hb level ≤10 g/dL, 44.7% were appropriate. Conclusion: This study presents a fundamental data observing the trend of RBC transfusion in a single institution. A significant proportion of inappropriate RBC transfusion are still being conducted in surgical setting. Continuous and effective education of clinicians and implementation of monitoring systems to assess the appropriateness of RBC transfusion may be necessary.
Antitumor Effect of KX-01 through Inhibiting Src Family Kinases and Mitosis
김선경,민아름,이경훈,양예원,김태용,임지민,박소정,남현진,김정은,송상현,한세원,오도연,김지현,김태유,David Hangauer,Johnson Yiu-Nam Lau,임경옥,이동순,방영주,임석아 대한암학회 2017 Cancer Research and Treatment Vol.49 No.3
Purpose KX-01 is a novel dual inhibitor of Src and tubulin. Unlike previous Src inhibitors that failed to show clinical benefit during treatment of breast cancer, KX-01 can potentially overcome the therapeutic limitations of current Src inhibitors through inhibition of both Src and tubulin. The present study further evaluates the activity and mechanism of KX-01 in vitro and in vivo. Materials and Methods The antitumor effect of KX-01 in triple negative breast cancer (TNBC) cell lines was determined by MTT assay. Wound healing and immunofluorescence assays were performed to evaluate the action mechanisms of KX-01. Changes in the cell cycle and molecular changes induced by KX-01 were also evaluated. A MDA-MB-231 mouse xenograft model was used to demonstrate the in vivo effects. Results KX-01 effectively inhibited the growth of breast cancer cell lines. The expression of phospho- Src and proliferative-signaling molecules were down-regulated in KX-01–sensitive TNBC cell lines. In addition, migration inhibition was observed by wound healing assay. KX-01– induced G2/M cell cycle arrest and increased the aneuploid cell population in KX-01–sensitive cell lines. Multi-nucleated cells were significantly increased after KX-01 treatment. Furthermore, KX-01 effectively delayed tumor growth in a MDA-MB-231 mouse xenograft model. Conclusion KX-01 effectively inhibited cell growth and migration of TNBC cells. Moreover, this study demonstrated that KX-01 showed antitumor effects through the inhibition of Src signaling and the induction of mitotic catastrophe. The antitumor effects of KX-01 were also demonstrated in vivo using a mouse xenograft model.
이미소,이경훈,민아름,김정은,김성영,장혜민,임지민,김소현,하동현,정원재,서경진,양예원,김태용,오도연,방영주,임석아 대한암학회 2019 Cancer Research and Treatment Vol.51 No.2
Purpose Pim kinases are highly conserved serine/threonine kinases, and different expression patterns of each isoform (Pim-1, Pim-2, and Pim-3) have been observed in various types of human cancers, including gastric cancer. AZD1208 is a potent and selective inhibitor that affects all three isoforms of Pim. We investigated the effects of AZD1208 as a single agent and in combination with an Akt inhibitor in gastric cancer cells. Materials and Methods The antitumor activity of AZD1208 with/without an Akt inhibitor was evaluated in a large panel of gastric cancer cell lines through growth inhibition assays. The underlying mechanism was also examined by western blotting, immunofluorescence assay, and cell cycle analysis. Results AZD1208 treatment decreased gastric cancer cell proliferation rates and induced autophagy only in long-term culture systems. Light chain 3B (LC3B), a marker of autophagy, was increased in sensitive cells in a dose-dependent manner with AZD1208 treatment, which suggested that the growth inhibition effect of AZD1208 was achieved through autophagy, not apoptosis. Moreover, we found that cells damaged by Pim inhibition were repaired by activation of the DNA damage repair pathway, which promoted cell survival and led the cells to become resistant to AZD1208. We also confirmed that the combination of an Akt inhibitor with AZD1208 produced a highly synergistic effect in gastric cancer cell lines. Conclusion Treatment with AZD1208 alone induced considerable cell death through autophagy in gastric cancer cells. Moreover, the combination of AZD1208 with an Akt inhibitor showed synergistic antitumor effects through regulation of the DNA damage repair pathway.