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In-Gyu Kim,Byung Seup Kim,Jang Yong Jeon,Jae Woo Kwon,Joo Seop Kim,Doo Jin Kim,Jae Pil Jung,Seong Eun Chon,Han Joon Kim,Eui Yong Jeon,Min-Jeong Kim,Kwanseop Lee 한국간담췌외과학회 2011 한국간담췌외과학회지 Vol.15 No.3
Liver transplantation with preservation of the recipient vena cava (piggyback technique) has been performed as an alternative to the conventional method. Outflow disturbance or obstruction of the vena cava in the early period after liver transplantation is associated with high morbidity and mortality. We used side-to-side cavo-caval anastomosis (modified piggyback technique) in a deceased-donor liver transplantation (DDLT) for venous outflow reconstruction. On postoperative day 9, the patient developed abdominal discomfort, and abnormal liver function showing serum total bilirubin of 6.2 mg/dl and serum AST/ALT of 297/597 IU/L. Doppler ultrasound showed mono-phasic wave forms of the hepatic vein. Computed tomography showed focal narrowing of 9.5 mm±2 mm in diameter at the cavo-caval anastomosis site. Liver biopsy was showed that there was no evidence of acute allograft rejection. Direct venogram showed stenosis of the cavo-caval anastomosis with a pressure gradient of 12 mmHg. An interventional stent was inserted in the stenotic site of the inferior vena cava, and the pressure gradient decreased to 2 mmHg. He was discharged from hospital on postoperative day 23 without any other complications. Herein we report a case of deceased-donor liver transplantation using the modified piggyback technique, who received an inferior vena cava stent due to stricture of the reconstructed orifice of the vena cava. (Korean J Hepatobiliary Pancreat Surg 2011;15:184-188)
Kim, Hoon-Seop,Lee, Dong-Hyun,Seok, Moo-Young,Zhao, Yakai,Kim, Woo-Jin,Kwon, Dongil,Jin, Hyung-Ha,Kwon, Junhyun,Jang, Jae-il Elsevier 2017 Journal of nuclear materials Vol.487 No.-
<P><B>Abstract</B></P> <P>While nanoindentation is a very useful tool to examine the mechanical properties of ion irradiated materials, there are some issues that should be considered in evaluating the properties of irradiated layer. In this study, in order to properly extract the hardness of only-irradiated layer from nanoindentation data, a new procedure is suggested in consideration of the geometry of indentation-induced plastic zone. By applying the procedure to an ion irradiated Fe-12Cr alloy, the reasonable results were obtained, validating its usefulness in the investigation of practical effect of irradiation on the mechanical behavior of future nuclear materials.</P>
Kwon, Mi Jung,Jeon, Jang Yong,Park, Hye-Rim,Nam, Eun Sook,Cho, Seong Jin,Shin, Hyung Sik,Kwon, Ji Hyun,Kim, Joo Seop,Han, Boram,Kim, Dong Hoon,Choi, Yoon-La RAVEN PRESS PUBLISHERS 2015 PANCREAS Vol.44 No.3
OBJECTIVES: Low prevalence and prognostic relevance of KRAS mutations in Korean pancreatic ductal adenocarcinomas (PDACs) need to be validated with sensitive detection method. METHODS: Peptide nucleic acid (PNA)–mediated polymerase chain reaction (PCR) clamping was used to precisely detect KRAS mutation in 72 paraffinized tumor samples and was validated by pancreatic cell lines to compare the efficiency of direct sequencing. RESULTS: The PNA-mediated PCR clamping detected mutant allele proportions of as low as 0.5% against a background of wild-type DNA and was 20-fold more sensitive than direct sequencing through the validation of pancreatic cell lines. Peptide nucleic acid–mediated PCR clamping detected KRAS mutations in 47.2% of 72 PDACs. Low tumor cellularity and low PCR amplification efficiency led to be undetected or failed by direct sequencing in pancreatic paraffinized samples.KRAS mutations were an independent worse prognostic factor predicting a reduced progression-free survival rate in the postoperative chemotherapy group. CONCLUSIONS: Peptide nucleic acid clamp real-time PCR was a sensitive method for detecting KRAS status in paraffinized PDAC samples. We identified a low KRAS mutation rate among the Korean PDAC patients using PNA clamp real-time PCR, potentially implicating epidemiological characteristics. The low KRAS mutation rate and its prognostic role may suggest the further survival benefit in Korean PDAC patients.
Molecular and genomic features of <i>Mycobacterium bovis</i> strain 1595 isolated from Korean cattle
Kim, Narae,Jang, Yunho,Kim, Jin Kyoung,Ryoo, Soyoon,Kwon, Ka Hee,Kim, Miso,Kang, Shin Seok,Byeon, Hyeon Seop,Lee, Hee Soo,Lim, Young-Hee,Kim, Jae-Myung The Korean Society of Veterinary Science 2017 Journal of Veterinary Science Vol.18 No.-
<P>The aim of this study was to investigate the molecular characteristics and to conduct a comparative genomic analysis of <I>Mycobacterium</I> (<I>M.</I>) <I>bovis</I> strain 1595 isolated from a native Korean cow. Molecular typing showed that <I>M. bovis</I> 1595 has spoligotype SB0140 with mycobacterial interspersed repetitive units-variable number of tandem repeats typing of 4-2-5-3-2-7-5-5-4-3-4-3-4-3, representing the most common type of <I>M. bovis</I> in Korea. The complete genome sequence of strain 1595 was determined by single-molecule real-time technology, which showed a genome of 4351712 bp in size with a 65.64% G + C content and 4358 protein-coding genes. Comparative genomic analysis with the genomes of <I>Mycobacterium tuberculosis</I> complex strains revealed that all genomes are similar in size and G + C content. Phylogenetic analysis revealed all strains were within a 0.1% average nucleotide identity value, and MUMmer analysis illustrated that all genomes showed positive collinearity with strain 1595. A sequence comparison based on BLASTP analysis showed that <I>M. bovis</I> AF2122/97 was the strain with the greatest number of completely matched proteins to <I>M. bovis</I> 1595. This genome sequence analysis will serve as a valuable reference for improving understanding of the virulence and epidemiologic traits among <I>M. bovis</I> isolates in Korea.</P>
Kim, Kyu-pyo,Park, Seong Joon,Kim, Jeong-Eun,Hong, Yong Sang,Lee, Jae-Lyun,Bae, Kyun-Seop,Cha, Hyunju,Kwon, Sool-Ki,Ro, Seonggu,Cho, JoongMyung,Kim, Tae Won Springer-Verlag 2015 Investigational new drugs Vol.33 No.5
<P>Purpose The aim of the present study was to assess the safety, maximum tolerated dose (MTD), pharmacokinetics, pharmacodynamics, and efficacy of single and multiple doses of intravenous CG200745, a novel histone deacetylase (HDAC) inhibitor, in patients with advanced solid malignancies. Experimental Design Two to six patients received intravenous CG200745 according to the 2?+?4 dose-escalating method. This first-in-human trial was comprised of two parts: Part 1 was a single ascending dose, and Part 2 was multiple ascending doses weekly for 3?weeks, and then 1?week off. For the first cycle, pharmacokinetic sampling for CG200745 and pharmacodynamic sampling for acetylated histone H4 in peripheral blood mononuclear cells (PBMCs) were performed on day 1 for Part 1 and on days 1 and 15 for Part 2. Examination of acetylated histone H4 in pre- and post-biopsy samples was performed in accessible patients. Results In all, 28 patients were treated at 13 dose levels (1.8-250?mg/m(2)) and received a total of 71 cycles of CG200745. Hematologic toxicities included grade 3/4 neutropenia (22.2?%) that did not last a week and non-hematologic toxicities included fatigue (22.2?%) and anorexia (16.7?%) that did not exceed grade 2. No dose-limiting toxic effects were noted. Dose proportionality was observed for both the maximum concentration and area under the curve. The elimination half-life was 5.67??2.69?h (mean??standard deviation). An increase in PBMC acetylated histone H4 was observed at dose levels up to 51?mg/m(2), which plateaued at higher dose levels. At 24?h, 75?% of patients (6/8) showed higher relative acetylation in tumor tissue compared to PBMCs. Although there was no partial or complete response, 57.1?% of patients (16/28) had stable disease that lasted at least 6?weeks. Conclusions CG200745 can be safely administered at effective dose levels that inhibit HDAC in PBMCs and tumor tissue. Although MTD was not reached, further escalation was not performed because acetylated histone H4 plateaued at dose levels higher than 51?mg/m(2). Additional phase II trials are recommended at 250?mg/m(2).</P>
Single-Switch Single Power-Conversion PFC Converter Using Regenerative Snubber
Kim, Kwang-Seop,Kwon, Jung-Min,Kwon, Bong-Hwan IEEE 2018 IEEE transactions on industrial electronics Vol.65 No.7
<P>This paper presents a single-switch single power-conversion (S<TEX>$^\text{3}$</TEX>PC) power factor correction (PFC) converter. Using the series-resonant circuit, the S <TEX>$^\text{3}$</TEX>PC converter provides bidirectional core excitation for the transformer and obtains higher power capability compared with the conventional single-switch PFC converters. Also, the series-resonant circuit provides zero-current switching turn-off for the output diodes, so that the reverse-recovery loss is alleviated. The regenerative snubber not only avoids the voltage spike of the switch but also recycles the absorbed energy. Because these features are obtained with only a single switch and through single power-conversion, the S<TEX>$^\text{3}$</TEX>PC converter has high efficiency and simple structure. The control algorithm derived from feedback linearization enables the S<TEX>$^\text{3}$</TEX>PC converter to obtain good controllability. Also, by using this control algorithm, the proposed converter performs both PFC control and output power control through single power-conversion. With these advantages, the S<TEX>$^\text{3}$</TEX>PC converter provides maximum efficiency of 96.4% and high power factor in excess of 0.994. The proposed converter is theoretically analyzed in detail, and experimental results are applied to a 1-kW prototype to show its validity.</P>
C/EBP homologous protein deficiency inhibits statin-induced myotoxicity
Kim, Won Ho,Lee, Chi-Ho,Han, Jung-Hwa,Kim, Sujin,Kim, Seong Yong,Lim, Jae Hyang,Park, Kwon Moo,Shin, Duk Seop,Woo, Chang-Hoon Elsevier 2019 Biochemical and biophysical research communication Vol.508 No.3
<P><B>Abstract</B></P> <P>It has been well established that HMG-CoA reductase inhibitors (statins) cause adverse side effects in skeletal muscle ranging from mild to fatal myotoxicity upon dose, drug interaction, and exercise. However, the underlying mechanisms by which statins induce myotoxicity have not been fully addressed. Recent reports showed that statins induce endoplasmic reticulum (ER) stress and cell death in immune cells and myoblasts <I>in vitro</I>. Therefore, the goal of study is to investigate the molecular mechanism by which statins induce skeletal muscle cell death and myopathy via the regulation of ER stress. Biochemical data showed that TUDCA, an ER stress inhibitor, inhibited atorvastatin- and simvastatin-induced protein cleavages of PARP-1 and caspase-3, respectively. Actually, statin treatment activated marker proteins of unfolded protein responses (UPR) including ATF6, CHOP, and spliced XBP1 and these responses were inhibited by TUDCA. In addition, statin treatment induced mRNA levels of UPR marker genes, suggesting that statins activate ER stress in a transcriptional regulation. The physiological relevance of ER stress in statin-induced myopathy was demonstrated in a mouse model of myopathy, in which instillation of simvastatin and atorvastatin led to myopathy. Notably, the reduction of muscular endurance in response to statin instillation was significantly improved in TUDCA treating group compared to vehicle control group. Moreover, CHOP deficiency mice showed restoration of statin-induced reduction of muscular endurance, suggesting that statin induces myopathy via ER stress and in a CHOP-dependent manner. Taken together, these findings indicate that statins specifically induce myopathy in an ER stress-dependent manner, suggesting the therapeutic potential of ER stress regulation in preventing adverse effects of statin.</P> <P><B>Highlights</B></P> <P> <UL> <LI> We examine the role of ER stress in statin-induced myotubule injury and myopathy. </LI> <LI> TUDCA and CHOP depletion inhibits statin-induced myotubule apoptosis. </LI> <LI> TUDCA and CHOP deficiency ameliorates statin-induced myopathy <I>in vivo</I>. </LI> </UL> </P>