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SangJin Kim,SeongWoo Nam,WonChul Yang,JinChul Kim,JaeHee Kim,SangSoo Kim 제어로봇시스템학회 2008 제어로봇시스템학회 국제학술대회 논문집 Vol.2008 No.10
Utilities in advanced power markets realized the importance of power value-added services, and they have studied power value-added services and the infrastructure for the services. In Korea, we also know the importance of power value-added services but R&D for the services is not vitalized. As time goes by, the importance of the services will be increased because the services are caused by the change of power market and this change will continue. Because this power value-added service market is the Blue ocean which is undeveloped yet, it has potentialities to penetrate world market which these services are not introduced. In this paper, we will introduce how to develop the value added-service BM(Business Model) and its system for Korea power market through analyzing international power market change, the effect of this change for Korea power market and present state of Korea power value-added service environment.
흉부 영상에서 간질성 폐질환 검출을 위한 컴퓨터지원진단 시스템 연구
김진철(Jinchul Kim),송종태(Jongtae Song),이우주(Wuju Lee),이배호(Baeho Lee) 한국정보과학회 2003 한국정보과학회 학술발표논문집 Vol.30 No.1B
간질성 폐질환(Interstitial lung disease) 컴퓨터지원진단(Computer Aided Diagnosis: CAD)시스템은 방사선의사들이 흉부 X-ray영상에서 석회화와 섬유화를 탐지하고자 적용하였다. 진단 중에 발생할 수 있는 오진율을 줄이고 간질성 폐질환이 존재하는 폐야에서 이상유무를 판단하여 검출을 표시하도록 하였다. 본 논문에서는 디지털 흉부영상에서의 간질성 폐질환을 검출하기 위해 폐 텍스처(texture)의 물리적 척도를 측정하기 위한 방법을 제안한다. 2차원의 푸리에 변환으로부터 얻어지는 파워스펙트럼(power spectrum) 분석에 기반을 두는 방법으로 각각의 ROI(Region Of Interest)에서 구한 평균제곱자승오차(Root Mean Square: RMS)와 파워스펙트럼의 첫 번째 모멘트(Moment)는 폐 텍스처의 밀도변동의 크기(magnitude)와 섬세함(fineness)을 나타낸다. 실험결과 다양한 간질성폐질환을 가진 비정상 폐 텍스처의 RMS와 첫 번째 모멘트는 정상 폐 텍스처의 RMS와 첫 번째 모멘트와는 차이가 있었다. 디지털 흉부영상으로부터 계산되어진 정량화된 텍스처의 척도는 방사선의사의 간질성 폐질환을 진단함에 효율적인 질환 탐지를 가능하게 하였으며 진단율을 향상시킬 수 있었다.
Mi-jee Kim,Jinchul Kim,Jin-su Im,Inho Kang,Jeong Keun Ahn 생화학분자생물학회 2021 BMB Reports Vol.54 No.12
Hepatitis B virus (HBV) infection is a major cause of hepatocellularcarcinoma (HCC), which is a highly aggressive cancer. HBV X protein (HBx), one of four HBV gene products, playspivotal roles in the development and metastasis of HCC. It hasbeen reported that HBx induces liver cancer cell migration andreorganizes actin cytoskeleton, however the molecular basisfor actin cytoskeleton reorganization remains obscure. In thisstudy, we for the first time report that HBx promotes actinpolymerization and liver cancer cell migration by regulatingcalcium modulated protein, calmodulin (CaM). HBx physicallyinteracts with CaM to control the level of phosphorylated cofilin,an actin depolymerizing factor. Mechanistically, HBx interactswith CaM, liberates Hsp90 from its inhibitory partner CaM,and increases the activity of Hsp90, thus activating LIMK1/cofilinpathway. Interestingly, the interaction between HBx and CaMis calcium-dependent and requires the CaM binding motif onHBx. These results indicate that HBx modulates CaM whichplays a regulatory role in Hsp90/LIMK1/cofilin pathway of actinreorganization, suggesting a new mechanism of HBV-inducedHCC metastasis specifically derived by HBx.
( Inho Kang ),( Ji Ae Kim ),( Jinchul Kim ),( Ju Hyeon Lee ),( Mi-jee Kim ),( Jeong Keun Ahn ) 생화학분자생물학회 2022 BMB Reports Vol.55 No.5
Hepatocellular carcinoma (HCC), a primary type of liver cancer, is one of the leading causes of cancer related deaths worldwide. HCC patients have poor prognosis due to intrahepatic and extrahepatic metastasis. Hepatitis B virus (HBV) infection is one of the major causes of various liver diseases including HCC. Among HBV gene products, HBV X protein (HBx) plays an important role in the development and metastasis of HCC. However, the mechanism of HCC metastasis induced by HBx has not been elucidated yet. In this study, for the first time, we report that HBx interacts with the suppressor of cytokine signaling 1 (SOCS1) which negatively controls NF-κB by degrading p65, a subunit of NF-κB. NF-κB activates the transcription of factors associated with epithelial-mesenchymal transition (EMT), a crucial cellular process associated with invasiveness and migration of cancer cells. Here, we report that HBx physically binds to SOCS1, subsequently prevents the ubiquitination of p65, activates the transcription of EMT transcription factors and enhance cell migration and invasiveness, suggesting a new mechanism of HBV-associated HCC metastasis. [BMB Reports 2022; 55(5): 220-225]
Compound K improves skin barrier function by increasing SPINK5 expression
Park, No-June,Bong, Sim-Kyu,Lee, Sullim,Jung, Yujung,Jegal, Hyun,Kim, Jinchul,Kim, Si-Kwan,Kim, Yong Kee,Kim, Su-Nam The Korean Society of Ginseng 2020 Journal of Ginseng Research Vol.44 No.6
Background: The skin acts as a barrier to protect organisms against harmful exogenous agents. Compound K (CK) is an active metabolite of ginsenoside Rb1, Rb2 and Rc, and researchers have focused on its skin protective efficacy. In this study, we hypothesized that increased expression of the serine protease inhibitor Kazal type-5 (SPINK5) may improve skin barrier function. Methods: We screened several ginsenosides to increase SPINK5 gene promoter activity using a transactivation assay and found that CK can increase SPINK5 expression. To investigate the protective effect of CK on the skin barrier, RT-PCR and Western blotting were performed to investigate the expression levels of SPINK5, kallikrein 5 (KLK5), KLK7 and PAR2 in UVB-irradiated HaCaT cells. Measurement of transepidermal water loss (TEWL) and histological changes associated with the skin barrier were performed in a UVB-irradiated mouse model and a 1-chloro-2,4-dinitrobenzene (DNCB)-induced atopic dermatitis-like model. Results: CK treatment increased the expression of SPINK5 and decreased the expression of its downstream genes, such as KLKs and PAR2. In the UVB-irradiated mouse model and the DNCB-induced atopic dermatitis model, CK restored increased TEWL and decreased hydration and epidermal hyperplasia. In addition, CK normalized the reduced SPINK5 expression caused by UVB or DNCB, thereby restoring the expression of the proteins involved in desquamation to a level similar to normal. Conclusions: Our data showed that CK contributes to improving skin-barrier function in UVB-irradiated and DNCB-induced atopic dermatitis-like models through SPINK5. These results suggest that therapeutic attempts with CK might be useful in treating barrier-disrupted diseases.
Lee, Taek Joon,Chang, Cha-Wen,Hahm, Suk Gyu,Kim, Kyungtae,Park, Samdae,Kim, Dong Min,Kim, Jinchul,Kwon, Won-Sang,Liou, Guey-Sheng,Ree, Moonhor IOP Pub 2009 Nanotechnology Vol.20 No.13
<P>We have fabricated electrically programmable memory devices with thermally and dimensionally stable poly(<I>N</I>-(<I>N</I>′,<I>N</I>′-diphenyl-<I>N</I>′-1,4-phenyl)-<I>N</I>,<I>N</I>-4,4′-diphenylene hexafluoroisopropylidene-diphthalimide) (6F-2TPA PI) films and investigated their switching characteristics and reliability. 6F-2TPA PI films were found to reveal a conductivity of 1.0 × 10<SUP>−13</SUP>–1.0 × 10<SUP>−14</SUP> S cm<SUP>−1</SUP>. The 6F-2TPA PI films exhibit versatile memory characteristics that depend on the film thickness. All the PI films are initially present in the OFF state. The PI films with a thickness of >15 to <100 nm exhibit excellent write-once-read-many-times (WORM) (i.e. fuse-type) memory characteristics with and without polarity depending on the thickness. The WORM memory devices are electrically stable, even in air ambient, for a very long time. The devices’ ON/OFF current ratio is high, up to 10<SUP>10</SUP>. Therefore, these WORM memory devices can provide an efficient, low-cost means of permanent data storage. On the other hand, the 100 nm thick PI films exhibit excellent dynamic random access memory (DRAM) characteristics with polarity. The ON/OFF current ratio of the DRAM devices is as high as 10<SUP>11</SUP>. The observed electrical switching behaviors were found to be governed by trap-limited space-charge-limited conduction and local filament formation and further dependent on the differences between the highest occupied molecular orbital and the lowest unoccupied molecular orbital energy levels of the PI film and the work functions of the top and bottom electrodes as well as the PI film thickness. In summary, the excellent memory properties of 6F-2TPA PI make it a promising candidate material for the low-cost mass production of high density and very stable digital nonvolatile WORM and volatile DRAM memory devices. </P>
Jang Ju-hong,Lee Jeong Woong,Cho Min Ji,Hwang Byungtae,Kwon Min-Gi,Kim Dong-Hwan,Lee Nam-Kyung,Lee Jangwook,Park Young-Jun,Yang Yong Ryoul,Kim Jinchul,Kim Yong-Hoon,An Tae Hyeon,오경진,Bae Kwang-Hee,Park 생화학분자생물학회 2022 Experimental and molecular medicine Vol.54 No.-
Obesity is a growing global epidemic that can cause serious adverse health consequences, including insulin resistance (IR) and nonalcoholic fatty liver disease (NAFLD). Obesity development can be attributed to energy imbalance and metabolic inflexibility. Here, we demonstrated that lack of Kelch-like protein 3 (KLHL3) mitigated the development of obesity, IR, and NAFLD by increasing energy expenditure. KLHL3 mutations in humans cause Gordon’s hypertension syndrome; however, the role of KLHL3 in obesity was previously unknown. We examined differences in obesity-related parameters between control and Klhl3−/− mice. A significant decrease in body weight concomitant with fat mass loss and improved IR and NAFLD were observed in Klhl3−/− mice fed a high-fat (HF) diet and aged. KLHL3 deficiency inhibited obesity, IR, and NAFLD by increasing energy expenditure with augmentation of O2 consumption and CO2 production. Delivering dominant-negative (DN) Klhl3 using adeno-associated virus into mice, thereby dominantly expressing DN-KLHL3 in the liver, ameliorated diet-induced obesity, IR, and NAFLD. Finally, adenoviral overexpression of DN-KLHL3, but not wild-type KLHL3, in hepatocytes revealed an energetic phenotype with an increase in the oxygen consumption rate. The present findings demonstrate a novel function of KLHL3 mutation in extrarenal tissues, such as the liver, and may provide a therapeutic target against obesity and obesity-related diseases.