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Eum, Won Sik,Shin, Min Jea,Lee, Chi Hern,Yeo, Hyeon Ji,Yeo, Eun Ji,Choi, Yeon Joo,Kwon, Hyun Jung,Kim, Duk-Soo,Kwon, Oh Shin,Lee, Keun Wook,Han, Kyu Hyung,Park, Jinseu,Kim, Dae Won,Choi, Soo Young Elsevier 2019 Biochimie Vol.156 No.-
<P><B>Abstract</B></P> <P>Parkinson's disease (PD), a neurodegenerative disorder, is characterized by a loss of dopaminergic neurons in the substantia nigra (SN) of the brain and it is well known that the pathogenesis of PD is related to a number of risk factors including oxidative stress. Antioxidant 1 (ATOX1) protein plays a crucial role in various diseases as an antioxidant and chaperone. In this study, we determined whether Tat-ATOX1 could protect against 1-methyl-4-phenylpyridinium ion (MPP<SUP>+</SUP>)-induced SH-SY5Y cell death and in a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced animal model of PD. In the MPP<SUP>+</SUP> exposed SH-SY5Y cells, Tat-ATOX1 markedly inhibited cell death and toxicities. In addition, Tat-ATOX1 markedly suppressed the activation of Akt and mitogen activated protein kinases (MAPKs) as well as cleavage of caspase-3 and Bax expression levels. In a MPTP-induced animal model, Tat-ATOX1 transduced into brain and protected dopaminergic neuronal cell loss. Taken together, Tat-ATOX1 inhibits dopaminergic neuronal death through the suppression of MAPKs and apoptotic signal pathways. Thus, Tat-ATOX1 represents a potential therapeutic protein drug candidate for PD.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Tat-ATOX1 transduces into SH-SY5Y cells and inhibited MPP<SUP>+</SUP>-induced cell death. </LI> <LI> Tat-ATOX1 suppressed the activation of Akt and MAPKs in MPP<SUP>+</SUP> exposed SH-SY5Y cells. </LI> <LI> Tat-ATOX1 inhibited dopaminergic neuronal cell loss in MPTP-induced animal model. </LI> <LI> Tat-ATOX1 represent a potential therapeutic agent for PD. </LI> </UL> </P>
문한별(Moon, Han Byoul),엄진주(Eum, Jin Joo) 우리문학회 2015 우리文學硏究 Vol.0 No.47
대만과 조선은 일제에 의해 오랜 기간 강제 점령을 당했으며 검열 제도를 통하여 강도 높은 사상 탄압을 받아야만 했다. 본고는 일제강점기 대만과 조선이 받은 사상검열에 대하여 고찰하기 위해 근대적 대중 매체인 영화를 중심으로 논의를 진행하였다. 영화는 출판 매체에 비해 늦은 1920년대에 들어 본격적으로 총독부의 검열 대상이 되었으며, 식민지 각국의 상황은 서로 다른 성격을 보이고 있었다. 일제는 대만과 조선의 영화에 대해 1920년대 초반부터 각 지방별로 검열을 진행하다가 1926년에 비로소 통일된 법령을 만들어 탄압을 심화시켰다. 검열의 진행은 유사했으나 실제 내용은 식민지별로 큰 차이를 보이는데, 조선의 경우 대만보다 1. 5배 이상의 검열료와 처벌규정이 적용되었으며, 이에 따라 조선의 영화 관련 종사자들은 검열료 인하 운동 등을 통하여 대만과의 차별적 대우에 대해 강하게 저항하였다. 또한 대만은 느슨한 검열 제도 덕에 영화를 대체할 수 있는 전통적인 공연 장르들이 조선에 비해 상당 부분 존치할 수 있었으나, 조선은 강한 탄압에 의해 전통 공연들은 일찍 붕괴되었고 그 결과 영화라는 새로운 대중 매체에 대중들의 관심이 집중될 수밖에 없었다. 대만과 조선 영화에 대한 차별적 탄압은 결국 일제강점기 말에 이르러 조선 공연 예술과 산업의 전반적인 몰락을 가져오고 말았다. Taiwan and Korea suffered repression by the Japanese occupation forced for a long period of time, received intense ideological oppression by the censorship. This paper conducted a discussion with a focus on the film as a modern mass media in order to investigate the ideological censorship against Taiwan and Korea in the Japanese occupation. The film became the target of censorship in earnest by Government General in the 1920s, colonial situation of each country showed a different personality. Japan was proceeding to censorship in each region about the movies of Taiwan and Korea from the early 1920s, strengthened the crackdown by creating for the first time a unified legislation in 1926. Progress of the censorship was similar, but the actual content was a big difference in each colony. In the case of Korea, 1.5 times more censorship fee and strong punishment than Taiwan were applied. Accordingly, film workers in Korea were strongly resisted through such censorship fee-cuts movement against discriminatory treatment. In Taiwan unlike Korea, traditional performing genre that can replace a film could a large portion remained due to the loose censorship. In contrast, Korea’s traditional performances collapsed in the early by the strong repression, it led to results that the attention of the public was focused on the new mass medium of film. Discriminatory repression of the film in Taiwan and Korea by the end of Japanese colonial rule was eventually resulted in the overall collapse of the performing arts and industry in Korea.
자궁 경부암에서 골반 임파절 전이의 예측 인자로서 SCC (squamous cell carcinoma antigen) 의 가치에 대한 연구
강기주,오한진,윤만수,설미영,박창수,고형권,염상탁 대한산부인과학회 2000 Obstetrics & Gynecology Science Vol.43 No.3
목적: 자궁경부암에서 치료전 SCC와 임상적 병기, 종양의 크기, 병변의 범위와의 연관성은 이미 밝혀진 바 있고 또 항암요법이나 방사선 치료 시에 SCC치의 감소는 좋은 예후와 관계됨이 밝혀져 있다. 이에 본 연구는 침윤성 자궁경부암의 치료전 SCC치와 골반 임파절 전이, 종양의 크기, 침윤 정도와의 상관성 유무를 밝히고자 시행하였다. 연구방법: 1995년 3월부터 1998년 12월까지 삼성서울병원 산부인과에서 선행항암요법 없이 자궁경부암으로 양측 골반 임파절 절제를 포함한 양측 골반 임파절 절제를 포함한 광범위 자궁적출술을 시행받은 환자중 수술전 SCC치가 검사된 157명의 환자를 대상으로 하였다. 골반 임파절 전이 유무에 따른 치료전 SCC치 차이를 통계적 증명하기 위해 Mann-Whitney U test를 이용하였으며, 치료전 SCC치에 대한 통계적으로 유의한 독립변수를 분석하기 위해 다중회귀분석법을 이용하였다. 결과: 골반 임파절 전이가 없는 125명의 90%에 해당하는 SCC치 2.9 ng/ml를 기준으로 했을때 SCC치 2.9ng/ml 이상의 환자군 중 골반 임파절 전이가 있을 확률은 60.7%로 2.9미만에서 골반 임파절 전이 양성확률보다 5배 이상 차이를 보였다. SCC치와 종양의 크기, 침윤의 깊이, 골반 임파절 전이 유무에 대한 다중회귀분석에서는 종양의 크기(p=0.04)와 골반 임파절 전이(p=0.002)는 유의한 연관성을 보였으며 침윤의 깊이(p=0.31)는 SCC치와 통계적 유의한 연관성을 보이지 않았다. 본 연구에서는 종양의 크기보다 골반 임파절(p$lt;0.01)전이유무가 SCC치와 더 관련 있는 것으로 나타났다. 결론: 자궁경부암에서 치료전 SCC치가 2.9 ng/ml이상의 경우 골반 임파절 전이의 고위험 인자로 생각되며, 명확하게 정해진 환자군의 범위 내에서 연구가 대규모가 이루어진다면 치료전 SCC치의 기준과 그 타당성의 정도가 좀더 구체적으로 제시될 수 있을 것으로 사료된다. Objective: The clinical value of preoperative serum squamous cell carcinoma antigen(SCC) in relation to clinical stage, tumor volume, disease extent and prognosis has already reported in many papers. The aim of this study is to analyse the relationship between preoperative SCC level and pelvic lymph node metastasis. Matrials and Methods: From March 1995 to December 1998, 157 patients who examined pretreatment SCC levels before undergoing radical hysterectomy for squamous cell carcinoma of uterine cervix were included. The effect of pelvic lymph node status on the SCC level was examined by comparing 125 cases with cancer limited uterus or upper vagina and 32 cases with cancer confined to the uterus (including upper vagina) and pelvic lymph node using multivariate analysis. Results: 90% of patients without pelvic lymph node metastasis showed SCC levels of 2.9ng/ml or below. 60.7% of patients with serum SCC level more than 2.9ng/ml exhibited pelvic lymph node metastasis. The marker values exceeding 2.9ng/ml increased risk of nodal metastasis 5 times compared with serum level 2.9ng/ml or below. Multivariate analysis confirmed that the pelvic lymph node metastasis had a large impact on the marker level than did tumor size or depth of stromal infilteration. Conclusion: SCC levels greater than 2.9ng/ml can be considered a high risk zone for nodal metastasis.
김혜영,한진석,이정상,김현리,김진,이중건,이서진,김근호,진호준,전은실,주권욱,나기영,정우경,오지은,엄재호,궁성수 대한신장학회 2000 Kidney Research and Clinical Practice Vol.19 No.5
The purpose of this study was to elucidate whether the molecular defect of acid-base transporters in renal tubules is related to the functional defect of urinary acidification in distal renal tubular acidosis(RTA). We performed NH₄Cl, furosemide, or bicarbonate loading test to evaluate renal acidification function, and immunohistochemistry using antibodies to H^+ -ATPase, Cl^-/HCO₃^- exchanger(band-3 protein), and Na^+/K^+ -ATPase in kidney tissue in 6 patients with RTA and renal cell carcinoma patients as normal controls. Kidney tissue was obtained either by percutaneous needle biopsy(RTA) or nephrectomy(NC). The results were as follows; 1) In all six RTA patients, proton secretory defect of distal acidification was shown by a failure to lower the urine pH after NHC1 loading or furosemide test or abnormally low urine-blood pCO₂ difference during bicarbonate loading. In two patients with RTA, proximal acidification defect was combined, which was demonstrated by increased fractional excretion of bicarbonate. 2) In mal control, intense H^+ -ATPase and band-3 protein staining was observed in collecting ducts. 3) In distal RTA patients, H6+ -ATPase and band-3 protein staining was not demonstrable or markedly decreased in the intercalated cells of distal nephron. 4) In two patients who had both proximal and distal RTA, H^+ -ATPase staining was markedly decreased in the brush border of proximal tubules as well as the distal nephron. In conclusion, the defect of acid-base transporters in renal tubule was related with the functional defect of urinary acidification in distal RTA.
( Eun Ji Yeo ),( Won Sik Eum ),( Hyeon Ji Yeo ),( Yeon Joo Choi ),( Eun Jeong Sohn ),( Hyun Jung Kwon ),( Dae Won Kim ),( Duk-soo Kim ),( Sung-woo Cho ),( Jinseu Park ),( Kyu Hyung Han ),( Keun Wook L 한국응용약물학회 2021 Biomolecules & Therapeutics(구 응용약물학회지) Vol.29 No.3
Oxidative stress plays a crucial role in the development of neuronal disorders including brain ischemic injury. Thioredoxin 1 (Trx1), a 12 kDa oxidoreductase, has anti-oxidant and anti-apoptotic functions in various cells. It has been highly implicated in brain ischemic injury. However, the protective mechanism of Trx1 against hippocampal neuronal cell death is not identified yet. Using a cell permeable Tat-Trx1 protein, protective mechanism of Trx1 against hydrogen peroxide-induced cell death was examined using HT-22 cells and an ischemic animal model. Transduced Tat-Trx1 markedly inhibited intracellular ROS levels, DNA fragmentation, and cell death in H<sub>2</sub>O<sub>2</sub>-treatment HT-22 cells. Tat-Trx1 also significantly inhibited phosphorylation of ASK1 and MAPKs in signaling pathways of HT-22 cells. In addition, Tat-Trx1 regulated expression levels of Akt, NF-κB, and apoptosis related proteins. In an ischemia animal model, Tat-Trx1 markedly protected hippocampal neuronal cell death and reduced astrocytes and microglia activation. These findings indicate that transduced Tat-Trx1 might be a potential therapeutic agent for treating ischemic injury.
( Min Jea Shin ),( Dae Won Kim ),( Yeon Joo Choi ),( Hyun Ju Cha ),( Sung Ho Lee ),( Sunghou Lee ),( Jinseu Park ),( Kyu Hyung Han ),( Won Sik Eum ),( Soo Young Choi ) 생화학분자생물학회(구 한국생화학분자생물학회) 2020 BMB Reports Vol.53 No.2
Glutaredoxin 1 (GLRX1) has been recognized as an important regulator of redox signaling. Although GLRX1 plays an essential role in cell survival as an antioxidant protein, the function of GLRX1 protein in inflammatory response is still under investigation. Therefore, we wanted to know whether transduced PEP-1-GLRX1 protein inhibits lipopolysaccharide (LPS)- and 12-O-tetradecanoyl phorbol-13-acetate (TPA)-induced inflammation. In LPS-exposed Raw 264.7 cells, PEP-1-GLRX1 inhibited cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), activation of mitogen activated protein kinases (MAPKs) and nuclear factor-kappaB (NF-κB) expression levels. In a TPA-induced mouse-ear edema model, topically applied PEP-1-GLRX1 transduced into ear tissues and significantly ameliorated ear edema. Our data reveal that PEP-1-GLRX1 attenuates inflammation in vitro and in vivo, suggesting that PEP-1-GLRX1 may be a potential therapeutic protein for inflammatory diseases. [BMB Reports 2020; 53(2): 106-111]