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      • Alkylhalide가 Mouse의 LDH isozyme 분포에 미치는 영향 : Cellulose Acetate Electrophoresis Method

        권미경,김영옥,박은주,이동화,이명미,이문희,이양자 曉星女子大學校 藥學大學 學生會 1988 曉星藥誌 Vol.4 No.-

        The effect of Carbontetrachloride administration on Lactatedehydrogenase isozyme patterns were analyzed by cellulose acetate electrophoresis for the brain, heart, kidney, lung, liver and mouse muscle. Each other tissue was found to have a characteristic distribution of these isozymes. At normal condition, aerobic tissue such as brain, heart, kidney, and lung were found to have all five isozymes from LDH_1 to LDH_5, while anaerobic tissues such as liver and muscle were found to have superiorly LDH_5 The toxicity of Carbontetrachloride administration was most prominence in the liver, and lung toxicity was occured also.

      • KCI등재

        Garcinia mangostana Suppresses Triacylglycerol Synthesis in Hepatocytes and Enterocytes

        Mun-Ock Kim,Su Ui Lee,Eun-Bin Kwon,Dong-Oh Moon,오은솔,Yu Na Song,Ji-Yoon Park,Hyung Won Ryu,김두영,Young-Won Chin,HyunSunLee 한국식품영양과학회 2023 Journal of medicinal food Vol.26 No.10

        Regulation of diacylglycerol acyltransferase (DGAT) and pancreatic lipase (PL) activities is important in thetreatment of triacylglycerol (TG)-related metabolic diseases. Garcinia mangostana, also known as mangosteen, is a traditionalmedicine ingredient used in the treatment of inflammation in Southeast Asia. In this study, The ethanolic extract of G. mangostana peel inhibited human recombinant DGAT1 and DGAT2, and PL enzyme activities in vitro. The inhibitoryactivity of DGAT1 and DGAT2 enzymes of four representative bioactive substances in mangosteen was confirmed. Inaddition, G. mangostana was confirmed to suppress the serum TG levels in C57 mice by inhibiting the absorption andsynthesis of TG in the gastrointestinal tract. Through this study, it was revealed that G. mangostana extract could be useful forthe prevention and amelioration of TG-related metabolic diseases such as obesity and fatty liver.

      • KCI등재

        Aqueous extract of Agaricus blazei induces human leukemiacells apoptosis via a reactive oxygen species and caspase-dependent mitochondrial pathway

        Mun-Ock Kim,Dong-Oh Moon,Jin-Woo Jeong,Cheng-Yun Jin,Gi-Young Kim,Jae-Dong Lee 한국버섯학회 2008 한국버섯학회지 Vol.6 No.2

        Agaricus blazei is well known as a traditional medicinal mushroom and it has been shown to exhibit immunostimulatory and anti-cancer activity. However, the cellular and molecular mechanism of apoptosis of cancer cells is poorly understood. In this study, we have investigated whether A. blazei extract (ABE) exerts anti-proliferative and apoptotic effects on human leukemia THP-1 cells. It was found that ABE induced a time- and dose-dependent increase in leukemia cells apoptosis through caspase-3 activation and PARP cleavage. Activation of caspase- 9 induced by ABE suggested that ABE-induced signaling was mediated through a mitochondrial death pathway. In addition, we observed an elevation of ROS and a consequent loss of mitochondrial membrane potential, further suggesting that ABE-induced death signaling was mediated through a mitochondrial oxygen stress pathway. The antioxidant Nacetylcysteine, however, opposed ABE-mediated mitochondrial dysfunction, caspase activation, and apoptosis, supporting the role of ROS in the apoptotic process. We conclude that ABE induces apoptosisin human leukemia cells through a reactive oxygen species and caspase-dependent mitochondrial pathway.

      • SCISCIESCOPUS

        Discovery of a novel class of diacylglycerol acyltransferase 2 inhibitors with a 1H-pyrrolo[2,3-b]pyridine core.

        Kim, Mun Ock,Lee, Suui,Choi, Kwangman,Lee, Sangku,Kim, Hyeongki,Kang, Hyunju,Choi, Miri,Kwon, Eun Bin,Kang, Myung Ji,Kim, Sunhong,Lee, Hyun-Jun,Lee, Hyun Sun,Kwak, Young-Shin,Cho, Sungchan Pharmaceutical Society of Japan 2014 Biological & pharmaceutical bulletin Vol.37 No.10

        <P>Diacylglycerol acyltransferase 2 (DGAT2), which catalyzes the final step in triacylglycerol (TG) synthesis, is a key enzyme associated with hepatic steatosis and insulin resistance. Here, using an in vitro screen of 20000 molecules, we identified a class of compounds with a substituted 1H-pyrrolo[2,3-b]pyridine core which proved to be potent and selective inhibitors of human DGAT2. Of these compounds, H2-003 and -005 exhibited a considerable reduction in TG biosynthesis in HepG2 hepatic cells and 3T3-L1 preadipose cells. These compounds exert DGAT2-specific-inhibitory activity, which was further confirmed in DGAT2- or DGAT1-overexpressing HEK293 cells. In addition, these compounds almost completely abolished lipid droplet formation in 3T3-L1 cells when co-treated with a DGAT1 inhibitor, which was not attained using either a DGAT2 or DGAT1 inhibitor alone. Collectively, we identified two DGAT2 inhibitors, H2-003 and -005. These compounds will aid in DGAT2-related lipid metabolism research as well as in therapeutic development for the treatment of metabolic diseases associated with excessive TG.</P>

      • SCISCIESCOPUS

        Gartanin induces autophagy through JNK activation which extenuates caspase-dependent apoptosis

        KIM, MUN-OCK,LEE, HYUN-SUN,CHIN, YOUNG-WON,MOON, DONG-OH,AHN, JONG-SEOG Spandidos Publications 2015 ONCOLOGY REPORTS Vol.34 No.1

        <P>Hepatocellular carcinoma (HCC) is the third leading cause of cancer-related death worldwide. Development of novel agents to eradicate liver cancer cells is required for treatment of HCC. Gartanin, a xanthone-type compound isolated from mangosteen, is known to possess potent antioxidant, anti-inflammatory, antifungal and antineoplastic properties. In the present study, we investigated the cytotoxic effect of gartanin on HCC and explored the cell death mechanism. We showed that gartanin induced both the extrinsic and intrinsic apoptotic pathways, which were interconnected by caspase-8, -9 and -3 activation. We also provided convincing evidence that gartanin induced autophagy in various cancer cells, as demonstrated by acridine orange staining of intracellular acidic vesicles, the degradation of p62, the conversion of LC3-I to LC3-II and GFP-LC3 punctate fluorescence. Additionally, gartanin induced the formation of typical autophagosomes and autolysosomes and enhanced the degradation rate of intracellular granule(s), including mitochondria. Notably, gartanin-mediated apoptotic cell death was further potentiated by pretreatment with autophagy inhibitors (3-methyladenine and bafilomycin A1) or small interfering RNAs against the autophagic genes (Atg5). These findings suggested that gartanin-mediated autophagic response protected against eventual cell death induced by gartanin. Moreover, gartanin treatment led to phosphorylation/activation of JNK and JNK-dependent phosphorylation of Bcl-2. Importantly, JNK inhibitor (SP600125) inhibited autophagy yet promoted gartanin-induced apoptosis, indicating a key requirement of the JNK-Bcl-2 pathway in the activation of autophagy by gartanin. Taken together, our data suggested that the JNK-Bcl-2 pathway was the critical regulator of gartanin-induced protective autophagy and a potential drug target for chemotherapeutic combination.</P>

      • SCIESCOPUS

        β-Ionone Enhances TRAIL-Induced Apoptosis in Hepatocellular Carcinoma Cells through Sp1-Dependent Upregulation of DR5 and Downregulation of NF-κB Activity

        Kim, Mun-Ock,Moon, Dong-Oh,Kang, Chang-Hee,Kwon, Taeg Kyu,Choi, Yung Hyun,Kim, Gi-Young American Association for Cancer Research 2010 Molecular Cancer Therapeutics Vol.9 No.4

        <P>beta-Ionone (ION), an end-ring analogue of beta-carotenoid, has been known to inhibit tumor cell growth and induce apoptosis in various types of cancer cells. Nevertheless, its apoptosis-related molecular mechanisms remain unclear. Here, we first investigated the molecular mechanisms by which ION sensitizes cancer cells to the therapeutic potential of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL). Notably, treatment with subtoxic concentrations of ION and TRAIL effectively inhibited cell viability in the hepatocellular carcinoma cell line Hep3B and other cancer cell lines such as colon carcinoma cell line HCT116 and leukemia cell line U937. Combined treatment with ION and TRAIL was also more effective in inducing DR5 expression, caspase activities, and apoptosis than treatment with either agent alone. ION-mediated sensitization to TRAIL was efficiently reduced by treatment with a chimeric blocking antibody or small interfering RNA specific for DR5. Electrophoretic mobility shift assay and a chromatin immunoprecipitation assay confirmed that ION treatment upregulates the binding of transcription factor Sp1 to its putative site within the DR5 promoter region, suggesting that Sp1 is an ION-responsive transcription factor. In addition, ION significantly increased hepatocellular carcinoma cell sensitivity to TRAIL by abrogating TRAIL-induced NF-kappaB activation and decreasing the expression of antiapoptotic proteins such as XIAP and IAP-1/2. Taken together, these data suggest that ION is a useful agent for TRAIL-based cancer treatments. Mol Cancer Ther; 9(4); 833-43. (c)2010 AACR.</P>

      • KCI등재
      • KCI등재

        삼차신경통에 대한 사이버나이프 방사선수술의 조기 치료 효과

        문성권(Seong Kwon Mun),최병옥(Byung Ock Choi),최일봉(Ihl Bohng Choi),강영남(Young Nam Kang),장지선(Ji Sun Jang),강기문(Ki Mun Kang) 대한방사선종양학회 2006 Radiation Oncology Journal Vol.24 No.2

        목 적: 삼차신경통 환자에서 사이버나이프 방사선수술이 효과적이며 안전한 치료방법인지 알아보고자 하였다. 대상 및 방법: 2004년 3월부터 2005년 5월까지 수술 후 실패하였거나 수술이 부적합한 삼차신경통 환자 26명을 대상으로 사이버나이프 방사선수술을 시행하여 후향적 분석을 하였다. 치료 표적은 삼차신경근 진입구역으로부터 3 mm 떨어진 지점의 삼차신경 최고 근위부를 제외한 6 mm 길이의 삼차신경 부위를 설정하고, 그 부위에 80% 등선량 곡선에 단일 조사로 총방사선량은 60∼64 Gy를 조사하였다(중앙선량: 64 Gy). 결 과: 추적관찰기간은 3∼15개월이었다(중앙추적관찰기간 : 9개월). 대상환자 26명에서 사이버나이프 방사선 수술 후 24시간 이내에 50% (13/26)에서 통증 완화를 관찰하였으며. 7일 이내에 조기 통증 완화를 보였던 환자는 96.2% (25/26)이었다. 치료 실패는 7.7% (2/26)에서 나타났으며 통증 개선 실패와 통증 재발이 각각 1명에서 관찰되었다. 치료 부작용으로 안면감각 감퇴가 11.5% (3/26)에서 관찰되었다. 결 론: 삼차신경통 환자를 대상으로 사이버나이프 방사선수술을 시행한 예비 결과로 비교적 안전하며, 효과적인 치료임을 확인하였다. Purpose: We evaluated whether Cyberknife radiosurgery is an effective and safe method of therapy for medically intractable trigeminal neuralgia (TN). Materials and Methods: We retrospectively analyzed the outcome of 26 patients, who failed to surgery or were not suitable candidates for invasive intervention and were treated by Cyberknife radiosurgery between March 2004 and May 2005. Radiosurgery doses of 60∼64 Gy were delivered to the 80% isodose line prescribed to an 6 mm length of the nerve, sparing the most proximal 3 mm away from the trigeminal nerve root entry zone (median dose: 64 Gy). Results: Follow-up period was 3∼15 months (median follow-up period: 9 months) Preliminary results from a cohort of 26 patients undergoing Cyberknife radiosurgery for TN showed that pain relief was achieved in 50% (13/26) of patients within the first 24 hrs after treatment. At last follow-up, 96.2% (25/26) of patients reported early pain relief within 7 days. Treatment failure developed in 2 of 26. Poor response occurred in one patient and relapse was observed in the other patient. 3 patients had hypoesthesia (11.5%), which was the only complication observed with any of our patients. Conclusion: With these results, authors assumed that Cyberknife radiosurgery for TN could be one of safe and effective therapeutic methods.

      • Vortex fluctuation of grain-aligned HgBa₂Ca₂Cu₃O8+6

        Bae, Myoung-Kwang Choi, M.S. Mun, Mi-Ock Lee, Sergey Lee, Sung-Ik Lee, W.C. 숙명여자대학교 자연과학연구소 1994 자연과학논문집 Vol.- No.5

        We have measured the reversible magnetization M(H,T) for grain-aligned HgBa₂Ca₂Cu₃O8+6. Our data exhibit a clear vortex fluctuation about 6K below the superconducting onset temperature. The derived in-plane magnetic penetration depth ab(0) is 1700Å which is similar to those of other high-Tc superconductors. In addition, the zero-temperature GL coherence length (0) is 22 ±5Å, which implies GL parameter k=77 ±13. This k is much greater than that of HgBa₂Ca₂Cu₃O8+6, but similar to that of zYBa₂Cu₃O7,

      • Atializumab, a humanized anti-aminoacyl-tRNA synthetase-interacting multifunctional protein-1 (AIMP1) antibody significantly improves nephritis in (NZB/NZW) F1 mice

        Mun, Chin Hee,Kim, Jin-Ock,Ahn, Sung Soo,Yoon, Taejun,Kim, Su Jeong,Ko, Eunhee,Noh, Hee-Dong,Park, Yong-Beom,Jung, Hak-Jun,Kim, Tae Sung,Lee, Sang-Won,Park, Sang Gyu Elsevier 2019 Biomaterials Vol.220 No.-

        <P><B>Abstract</B></P> <P>Aminoacyl-tRNA synthetase (ARS)-interacting multifunctional protein 1 (AIMP1) enhances the expression of proinflammatory cytokines. In our previous study, we have shown that serum AIMP1 in patients with SLE was significantly higher than that of healthy controls. To address whether neutralization of AIMP1 could ameliorate nephritis in lupus-prone mice, we generated atializumab, a humanized antibody against AIMP1 and investigated its therapeutic efficacy. ELISA showed that serum AIMP1 at 23 weeks old was significantly higher than that at 13 weeks old in lupus-prone mice. Therefore, lupus-prone mice were randomly assigned to 5 groups (vehicle, methylprednisolone and 0.5, 2, and 5 mg/kg atializumab). After treatment, disease severity was assessed using a variety of phenotypes, including proteinuria, histological damages, renal deposition of immune-complex. In addition, serum cytokines, anti-dsDNA and IgG subclasses were determined. T cell subsets were analyzed using a fluorescence-activated cell sorter. Atializumab significantly diminished proteinuria, improved glomerular and tubular damages and reduced the renal deposition of immune-complexes. Moreover, atializumab significantly decreased serum interferon (IFN)-γ, interleukin (IL)-17A, and IL-6, whereas it increased serum IL-10. Similarly, atializumab reduced the numbers of T<SUB>H</SUB>1, T<SUB>H</SUB>2 and T<SUB>H</SUB>17 cells in a dose-dependent manner, while atializumab enhanced the number of regulatory T (Treg) cells. Furthermore, atializumab decreased not only splenic plasma cells and serum anti-dsDNA but also pathogenic IgG subclasses for nephritis. It suppressed NF-κB activation by inhibiting IκBα degradation in a dose-dependent manner <I>in vitro</I>. Atializumab alleviated nephritis by inhibiting autoreactive T, B, and plasma cells and decreasing NF-κB-related proinflammatory cytokines in lupus-prone mice. These results suggest that treatment targeting AIMP1 could be a novel and highly immune-modulating therapeutic strategy in lupus nephritis.</P>

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