• Journal of Radiation Protection and Research
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• 제42권2호
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• pp.114-129
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• 2017

Background: The purpose of this paper is to confirm the event timings and the magnitude of fission product aerosol release from the Fukushima accident. Over a few hundreds of technical papers have been published on the environmental impact of Fukushima Daiichi accident since the accident occurred on March 11, 2011. However, most of the research used reverse or inverse method based on the monitoring of activities in the remote places and only few papers attempted to estimate the release of fission products from individual reactor core or from individual spent fuel pool. Severe accident analysis code can be used to estimate the radioactive release from which reactor core and from which radionuclide the peaks in monitoring points can be generated. Materials and Methods: The basic material used for this study are the initial core inventory obtained from the report JAEA-Data/Code 2012-018 and the given accident scenarios provided by Japanese Government or Tokyo Electric Power Company (TEPCO) in official reports. In this research a forward method using severe accident progression code is used as it might be useful for justifying the results of reverse or inverse method or vice versa. Results and Discussion: The release timing and amounts to the environment are estimated for volatile radioactive fission products such as noble gases, cesium, iodine, and tellurium up to 184 hours (about 7.7 days) after earthquake occurs. The in-plant fission product behaviors and release characteristics to environment are estimated using the severe accident progression analysis code, MELCOR, for Fukushima Daiichi accident. These results are compared with other research results which are summarized in UNSCEAR 2013 Report and other technical papers. Also it may provide the physically based arguments for justifying or suspecting the rationale for the scenarios provided in open literature. Conclusion: The estimated results by MELCOR code simulation of this study indicate that the release amount of volatile fission products to environment from Units 1, 2, and 3 cores is well within the range estimated by the reverse or inverse method, which are summarized in UNSCEAR 2013 report. But this does not necessarily mean that these two approaches are consistent.

• 암석학회지
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• 제24권2호
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• pp.77-90
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• 2015

피션트랙 검출에 의해 고체 및 액체상태 지질물질 내 우라늄을 정밀정량하는 최적기법을 제안하고 그 적용성을 검증하였다. 우라늄 정량은 중성자 조사에 의해 유도시킨 $^{235}U$의 핵분열 흔적을 트랙 디텍터에 기록하여 고배율 현미경 하에서 계수함으로써 이루어진다. 우라늄-친화력이 좋은 암석(예: 화강암, 석탄)을 분말 펠릿시료로 만들어 건식 검출하면, 그다지 높지 않은 우라늄함량(<5 ppm, 즉 ${\mu}g\;g^{-1}$)에서도 빈번하게 함유된 함-우라늄광물에 기인한 트랙 군집현상으로 인해 시료의 전체평균 함량 결정이 쉽지 않았으며, 트랙 균질부와 군집부를 별도로 검토해야 한다. 시료의 균질성이 유지된다면 백운모-Lexan 디텍터에 의한 중복 측정과 여러 차례 중성자 조사에 의한 반복 측정에서 높은 재현성이 확인되었다. 건고 액체시료 경우에 $10^1ppm$ 수준 및 그 이상의 우라늄함량에서 흔히 나타나는 불균질 현상을 극복하기 위해, 진공 석영튜브를 이용한 습식 검출법을 제안한다. 습식 검출에서 우라늄 균질성은 $10^0ppm$ 수준 이하에서 회복되며, 측정하한은 $10^2ppb$ (i.e. $ng\;g^{-1}$) 수준까지 무난한 것으로 입증되었다.

• BMB Reports
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• 제56권12호
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• pp.663-668
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• 2023

C-reactive protein (CRP) is an inflammatory marker and risk factor for atherosclerosis and cardiovascular diseases. However, the mechanism through which CRP induces myocardial damage remains unclear. This study aimed to determine how CRP damages cardiomyocytes via the change of mitochondrial dynamics and whether survivin, an anti-apoptotic protein, exerts a cardioprotective effect in this process. We treated H9c2 cardiomyocytes with CRP and found increased intracellular ROS production and shortened mitochondrial length. CRP treatment phosphorylated ERK1/2 and promoted increased expression, phosphorylation, and translocation of DRP1, a mitochondrial fission-related protein, from the cytoplasm to the mitochondria. The expression of mitophagy proteins PINK1 and PARK2 was also increased by CRP. YAP, a transcriptional regulator of PINK1 and PARK2, was also increased by CRP. Knockdown of YAP prevented CRP-induced increases in DRP1, PINK1, and PARK2. Furthermore, CRP-induced changes in the expression of DRP1 and increases in YAP, PINK1, and PARK2 were inhibited by ERK1/2 inhibition, suggesting that ERK1/2 signaling is involved in CRP-induced mitochondrial fission. We treated H9c2 cardiomyocytes with a recombinant TAT-survivin protein before CRP treatment, which reduced CRP-induced ROS accumulation and reduced mitochondrial fission. CRP-induced activation of ERK1/2 and increases in the expression and activity of YAP and its downstream mitochondrial proteins were inhibited by TAT-survivin. This study shows that mitochondrial fission occurs during CRP-induced cardiomyocyte damage and that the ERK1/2-YAP axis is involved in this process, and identifies that survivin alters these mechanisms to prevent CRP-induced mitochondrial damage.

• 한국미생물학회:학술대회논문집
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• 한국미생물학회 2005년도 International Meeting of the Microbiological Society of Korea
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• pp.97-100
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• 2005

• 한국원자력학회:학술대회논문집
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• 한국원자력학회 2004년도 추계학술발표회 발표논문집
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• pp.89-89
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• 2004

• 한국원자력학회:학술대회논문집
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• 한국원자력학회 2003년도 춘계학술발표대회 요약집
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• pp.187.2-187.2
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• 2003

• 한국원자력학회:학술대회논문집
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• 한국원자력학회 1998년도 추계학술발표회요약집
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• pp.251-251
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• 1998

• 한국미생물학회:학술대회논문집
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• 한국미생물학회 2009년도 International Meeting of the Microbiological Society of Korea
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• pp.127-128
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• 2009

• 한국동물학회:학술대회논문집
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• 한국동물학회 1994년도 한국생물과학협회 학술발표대회
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• pp.210.2-210
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• 1994

No Abstract, See Full Text

• 한국원자력학회:학술대회논문집
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• 한국원자력학회 1999년도 춘계학술발표회요약집
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• pp.10-10
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• 1999