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Monte Carlo Simulation for Designing a CZT-based Fork Detection System
Wooseong Hong,Geehyun Kim 한국방사성폐기물학회 2022 한국방사성폐기물학회 학술논문요약집 Vol.20 No.2
The detector response was simulated to design a fork detection system for verifying the characteristics of spent fuel. The fork detection system currently used consists of two fission chamber and an ion chamber, and it is nuclear safeguard equipment that measures the gross neutrons and gross gamma rays emitted from the spent fuel assembly to identify the characteristics of the spent fuel and verify the authenticity of the operation history. In order to improve the current fork detection system, we are developing a system that applies CZT, a room temperature semiconductor detector, and a stilbene detector, which is an organic scintillator. Depletion calculations were performed using the ORIGEN code to determine the radiological characteristics emitted from spent nuclear fuel assembly. The flux of radiation emitted from the spent nuclear fuel assembly was calculated by changing the conditions such as initial enrichment, burnup, and cooling time, which are major variables of spent fuel assembly. The calculated result is used as the source term of the particle transport code. Considering the general operating conditions of the pressurized light water reactor, the conditions were changed in the range of 3-5% for initial enrichment and 30-72 GWD/MTU for burnup, and the cooling time was given within 10 years. MCNP 6.2, a Monte Carlo simulation code, was used to simulate the detector response to radiation emitted from spent nuclear fuel assembly. According to the shape, size, and position of the CZT detector, the gamma counts incident on the detector were calculated and derived the initial design of our fork detection system.
Differentially expressed genes in human peripheral blood as potential markers for statin response.
Won, Hong-Hee,Kim, Suk Ran,Bang, Oh Young,Lee, Sang-Chol,Huh, Wooseong,Ko, Jae-Wook,Kim, Hyung-Gun,McLeod, Howard L,O'Connell, Thomas M,Kim, Jong-Won,Lee, Soo-Youn Springer 2012 Journal of molecular medicine Vol.90 No.2
<P>There is a considerable inter-individual variation in response to statin therapy and one third of patients do not meet their treatment goals. We aimed to identify differentially expressed genes that might be involved in the effects of statin treatment and to suggest potential markers to guide statin therapy. Forty-six healthy Korean subjects received atorvastatin; their whole-genome expression profiles in peripheral blood were analyzed before and after atorvastatin administration in relation with changes in lipid profiles. The expression patterns of the differentially expressed genes were also compared with the data of familial hypercholesterolemia (FH) patients and controls. Pairwise comparison analyses revealed differentially expressed genes involved in diverse biological processes and molecular functions related with immune responses. Atorvastain mainly affected antigen binding, immune or inflammatory response including interleukin pathways. Similar expression patterns of the genes were observed in patients with FH and controls. The Charcol-Leyden crystal (CLC), CCR2, CX3CR1, LRRN3, FOS, LDLR, HLA-DRB1, ERMN, and TCN1 genes were significantly associated with cholesterol levels or statin response. Interestingly, the CLC gene, which was significantly altered by atorvastatin administration and differentially expressed between FH patients and controls, showed much bigger change in high-responsive group than in low-responsive group. We identified differentially expressed genes that might be involved in mechanisms underlying the known pleiotropic effects of atorvastatin, baseline cholesterol levels, and drug response. Our findings suggest CLC as a new candidate marker for statin response, and further validation is needed.</P>
Kim, Hyunjeong,Kim, Wooseong,Yum, Soohwan,Hong, Sungchae,Oh, Jeong-Eun,Lee, Ji-Woo,Kwak, Mi-Kyoung,Park, Eun Ji,Na, Dong Hee,Jung, Yunjin Elsevier 2013 FREE RADICAL BIOLOGY AND MEDICINE Vol.65 No.-
<P><B>Abstract</B></P> <P>Caffeic acid phenethyl ester (CAPE) is a polyphenolic natural product that possesses numerous biological activities including anti-inflammatory effects. CAPE-mediated nuclear factor-erythroid 2 p45 (NF-E2)-related factor 2 (Nrf2) activation is likely responsible for some of its biological effects. CAPE was chemically modified to yield CAPE analogues that were subjected to experiments examining cellular Nrf2 activity. CAPE and the CAPE analogue with a catechol moiety, but not the other analogues, activated the Nrf2 pathway. In addition, only biotin-labeled CAPE analogues with the catechol moiety precipitated Kelch-like ECH associated protein 1 (Keap1) when incubated with cell lysates and streptavidin agarose beads. Sodium hypochlorite (NaOCl) oxidation of the catechol moiety in CAPE produced an oxidized, electrophilic form of CAPE (Oxi-CAPE) and greatly enhanced the ability of CAPE to activate Nrf2 and to bind to Keap1. Rectal administration of CAPE ameliorated 2,4,6-trinitrobenzene sulfonic acid-induced rat colitis and activated the Nrf2 pathway in the inflamed colon, and incubation of CAPE in the lumen of the inflamed distal colon generated Oxi-CAPE. However, these biological effects and chemical change of CAPE were not observed in the normal colon. Our data suggest that CAPE requires the catechol moiety for the oxidation-enhanced activation of the Nrf2 pathway and has potential as a pathologically targeted Nrf2-activating agent that is exclusively activated in pathological states with oxidative stress such as colonic inflammation.</P> <P><B>Highlights</B></P> <P> <UL> <LI> The catechol moiety in caffeic acid phenethyl ester (CAPE) is required for CAPE activation of Nrf2. </LI> <LI> Oxidized CAPE (most likely an electrophilic <I>o</I>-quinone form) is responsible for the biological activity of CAPE. </LI> <LI> CAPE ameliorates experimental rat colitis and generates the oxidized form of CAPE in the inflamed colonic tissues. </LI> <LI> CAPE activates the Nrf2 pathway in the inflamed colonic tissues but not in the normal colonic tissues. </LI> </UL> </P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>
( Hye Soo Lee ),( Hun-suk Song ),( Hong-ju Lee ),( Sang Hyun Kim ),( Min Ju Suh ),( Jang Yeon Cho ),( Sion Ham ),( Yun-gon Kim ),( Hwang-soo Joo ),( Wooseong Kim ),( Sang Ho Lee ),( Dongwon Yoo ),( Sh 한국미생물 · 생명공학회 2021 Journal of microbiology and biotechnology Vol.31 No.8
Community-associated Methicillin-Resistant Staphylococcus aureus (CA-MRSA) is notorious as a leading cause of soft tissue infections. Despite several studies on the Agr regulator, the mechanisms of action of Agr on the virulence factors in different strains are still unknown. To reveal the role of Agr in different CA-MRSA, we investigated the LACΔagr mutant and the MW2Δagr mutant by comparing LAC (USA300), MW2 (USA400), and Δagr mutants. The changes of Δagr mutants in sensitivity to oxacillin and several virulence factors such as biofilm formation, pigmentation, motility, and membrane properties were monitored. LACΔagr and MW2Δagr mutants showed different oxacillin sensitivity and biofilm formation compared to the LAC and MW2 strains. Regardless of the strain, the motility was reduced in Δagr mutants. And there was an increase in the long chain fatty acid in phospholipid fatty acid composition of Δagr mutants. Other properties such as biofilm formation, pigmentation, motility, and membrane properties were different in both Δagr mutants. The Agr regulator may have a common role like the control of motility and strain-dependent roles such as antibiotic resistance, biofilm formation, change of membrane, and pigment production. It does not seem easy to control all MRSA by targeting the Agr regulator only as it showed strain-dependent behaviors.