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Search Results: 1 - 10 of 20461 matches for " Eunju Kim "
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A simulation-based study of the neutron backgrounds for NaI dark matter experiments
Eunju Jeon,Yeongduk Kim
Physics , 2015, DOI: 10.1016/j.astropartphys.2015.07.004
Abstract: Among the direct search experiments for weakly interacting massive particle (WIMP) dark matter, the DAMA experiment observed an annual modulation signal interpreted as WIMP interactions with a significance of 9.2$\sigma$. Recently, Jonathan Davis claimed that the DAMA modulation may be interpreted on the basis of the neutron scattering events induced by the muons and neutrinos together. We tried to simulate the neutron backgrounds at the Gran Sasso and Yangyang laboratory with and without the polyethylene shielding to quantify the effects of the ambient neutrons on the direct detection experiments based on the crystals.
Function of COP9 Signalosome in Regulation of Mouse Oocytes Meiosis by Regulating MPF Activity and Securing Degradation
Eunju Kim, Se-Jin Yoon, Eun-Young Kim, Yunna Kim, Hyun-Seo Lee, Kyeoung-Hwa Kim, Kyung-Ah Lee
PLOS ONE , 2011, DOI: 10.1371/journal.pone.0025870
Abstract: The COP9 (constitutive photomorphogenic) signalosome (CSN), composed of eight subunits, is a highly conserved protein complex that regulates processes such as cell cycle progression and kinase signalling. Previously, we found the expression of the COP9 constitutive photomorphogenic homolog subunit 3 (CSN3) and subunit 5 (CSN5) changes as oocytes mature for the first time, and there is no report regarding roles of COP9 in the mammalian oocytes. Therefore, in the present study, we examined the effects of RNA interference (RNAi)-mediated transient knockdown of each subunit on the meiotic cell cycle in mice oocytes. Following knockdown of either CSN3 or CSN5, oocytes failed to complete meiosis I. These arrested oocytes exhibited a disrupted meiotic spindle and misarranged chromosomes. Moreover, down-regulation of each subunit disrupted the activity of maturation-promoting factor (MPF) and concurrently reduced degradation of the anaphase-promoting complex/cyclosome (APC/C) substrates Cyclin B1 and Securin. Our data suggest that the CSN3 and CSN5 are involved in oocyte meiosis by regulating degradation of Cyclin B1 and Securin via APC/C.
Gas6 Downregulation Impaired Cytoplasmic Maturation and Pronuclear Formation Independent to the MPF Activity
Kyeoung-Hwa Kim,Eun-Young Kim,Yuna Kim,Eunju Kim,Hyun-Seo Lee,Sook-Young Yoon,Kyung-Ah Lee
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0023304
Abstract: Previously, we found that the growth arrest-specific gene 6 (Gas6) is more highly expressed in germinal vesicle (GV) oocytes than in metaphase II (MII) oocytes using annealing control primer (ACP)-PCR technology. The current study was undertaken to investigate the role of Gas6 in oocyte maturation and fertilization using RNA interference (RNAi). Interestingly, despite the specific and marked decrease in Gas6 mRNA and protein expression in GVs after Gas6 RNAi, nuclear maturation including spindle structures and chromosome segregation was not affected. The only discernible effect induced by Gas6 RNAi was a change in maturation promoting factor (MPF) activity. After parthenogenetic activation, Gas6 RNAi-treated oocytes at the MII stage had not developed further and arrested at MII (90.0%). After stimulation with Sr2+, Gas6-silenced MII oocytes had markedly reduced Ca2+ oscillation and exhibited no exocytosis of cortical granules. In these oocytes, sperm penetration occurred during fertilization but not pronucleus (PN) formation. By roscovitine and colcemid treatment, we found that the Gas6 knockdown affected cytoplasmic maturation directly, independent to the changed MPF activity. These results strongly suggest that 1) the Gas6 signaling itself is important to the cytoplasmic maturation, but not nuclear maturation, and 2) the decreased Gas6 expression and decreased MPF activity separately or mutually influence sperm head decondensation and PN formation.
Income-related health inequalities across regions in Korea
Eunju Hong, Byung Ahn
International Journal for Equity in Health , 2011, DOI: 10.1186/1475-9276-10-41
Abstract: We considered a total of 45,233 subjects (≥ 19 years) drawn from the four waves of the Korean National Health and Nutrition Examination Survey (KNHANES). We considered true health as a latent variable following a lognormal distribution. We obtained ill-health scores by matching self-rated health (SRH) to its distribution and used the Gini Coefficient (GC) and an income-related ill-health Concentration Index (CI) to examine inequalities in income and health, respectively.The GC estimates were 0.3763 and 0.0657 for overall and spatial inequalities, respectively. The overall CI was -0.1309, and the spatial CI was -0.0473. The spatial GC and CI estimates were smaller than their counterparts, indicating substantial inequalities in income (from 0.3199 in Daejeon to 0.4233 Chungnam) and income-related health inequalities (from -0.1596 in Jeju and -0.0844 in Ulsan) within regions.The results indicate a positive relationship between the GC and the average ill-health and a negative relationship between the CI and the average ill-health. Those regions with a low level of health tended to show an unequal distribution of income and health. In addition, there was a negative relationship between the GC and the CI, that is, the larger the income inequalities, the larger the health inequalities were. The GC was negatively related to the average regional income, indicating that an increase in a region's average income reduced income inequalities in the region. On the other hand, the CI showed a positive relationship, indicating that an increase in a region's average income reduced health inequalities in the region.The results suggest that reducing health inequalities across regions require a more equitable distribution of income and a higher level of average income and that the higher the region's average income, the smaller its health inequalities are.Socioeconomic inequalities have represented one of the most controversial issues in Korea, mainly because Korea has achieved consider
Storage Allocation Under Processor Sharing I: Exact Solutions and Asymptotics
Eunju Sohn,Charles Knessl
Mathematics , 2009,
Abstract: We consider a processor sharing storage allocation model, which has m primary holding spaces and infinitely many secondary ones, and a single processor servicing the stored items (customers). All of the spaces are numbered and ordered. An arriving customer takes the lowest available space. We define the traffic intensity rho to be lambda/mu where lambda is the customers' arrival rate and mu is the service rate of the processor. We study the joint probability distribution of the numbers of occupied primary and secondary spaces. For 0 < rho < 1, we obtain the exact solutions for m = 1 and m = 2. For arbitrary m we study the problem in the asymptotic limit rho -> 1 with m fixed. We also develop a semi-numerical semi-analytic method for computing the joint distribution.
Storage Allocation Under Processor Sharing II: Further Asymptotic Results
Eunju Sohn,Charles Knessl
Mathematics , 2009,
Abstract: We consider a processor sharing storage allocation model, which has m primary holding spaces and infinitely many secondary ones, and a single processor servicing the stored items (customers). All of the spaces are numbered and ordered. An arriving customer takes the lowest available space. We define the traffic intensity rho to be lambda/mu where lambda is the customers' arrival rate and mu is the service rate of the processor. We study the joint probability distribution of the numbers of occupied primary and secondary spaces. We study the problem in two asymptotic limits: (1) m -> infinity with a fixed rho <1, and (2) rho -> 1, m -> infinity with m(1-rho)= O(1).
Weight Change as a Predictor of Incidence and Remission of Insulin Resistance
Yoosoo Chang, Eunju Sung, Kyung Eun Yun, Hyun-Suk Jung, Chan-Won Kim, Min-Jung Kwon, Sung-Il Cho, Seungho Ryu
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0063690
Abstract: Objective The objective of this study was to assess the longitudinal relationship of weight change on incidence and remission of insulin resistance (IR). Methods We performed a cohort study in apparently healthy Korean men, 30 to 59 years of age, who underwent a health checkup and were followed annually or biennially between 2002 and 2009. The computer model of homeostasis model assessment, HOMA2-IR, was obtained at each visit, and IR was defined as HOMA2-IR ≥75th percentile. Results For IR development, 1,755 of the 6,612 IR-free participants at baseline developed IR (rate 5.1 per 100 person-years) during 34,294.8 person-years of follow-up. The hazard ratios (95% confidence intervals) for incident IR with weight changes of <?0.9 kg, 0.6–2.1 kg and ≥2.2 kg from visit 1 to visit 2 (average 1.8 years) compared to weight change of ?0.9–0.5 kg (reference) were 0.78 (0.68–0.90), 1.19 (1.04–1.35) and 1.26 (1.11–1.44), respectively. This association persisted in normal-weight individuals or those without any metabolic syndrome traits and remained significant after introducing weight categories and confounders as time-dependent exposures (P-trend <0.001). For IR remission, 903 of 1,696 IR participants had no IR (remission rate 10.3 per 100 person-years) during 8,777.4 person-years of follow-up. IR remission decreased with increasing quartiles of weight change (P-trend <0.001) and this association persisted in normal-weight individuals. Conclusions Weight gain was associated with increased IR development and decreased IR remission regardless of baseline BMI status. Preventing weight gain, even in healthy and normal-weight individuals, is an important strategy for reducing IR and its associated consequences.
Radiological Diagnosis of Congenital Diaphragmatic Hernia in 17th Century Korean Mummy
Yi-Suk Kim, In Sun Lee, Go-Un Jung, Myeung Ju Kim, Chang Seok Oh, Dong Su Yoo, Won-Joon Lee, Eunju Lee, Soon Chul Cha, Dong Hoon Shin
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0099779
Abstract: Congenital diaphragmatic hernia (CDH) is a birth defect of the diaphragm resulting in pulmonary sequelae that threaten the lives of infants. In computed tomography (CT) images of a 17th century middle-aged male mummy (the Andong mummy), we observed that the abdominal contents had protruded into the right thoracic cavity through the diaphragmatic defect, accompanied by a mediastinal shift to the left. On autopsy, the defect in the right posterolateral aspect of the diaphragm was reconfirmed, as was the herniation of the abdominal organs. The herniated contents included the right lobe of the liver, the pyloric part of the stomach, a part of the greater omentum, and the right colic flexure connecting the superior part of the ascending colon and the right part of the transverse colon. Taking our CT and autopsy results together, this case was diagnosed as the Bochdalek-type CDH. Herein we make the first ever report of a CT-assisted diagnosis of a pre-modern historical case of CDH. Our results show the promising utility of this modality in investigations of mummified human remains archaeologically obtained.
Activation of p53 with Ilimaquinone and Ethylsmenoquinone, Marine Sponge Metabolites, Induces Apoptosis and Autophagy in Colon Cancer Cells
Hyun-Young Lee,Kyu Jin Chung,In Hyun Hwang,Jungsuk Gwak,Seoyoung Park,Bong Gun Ju,Eunju Yun,Dong-Eun Kim,Young-Hwa Chung,MinKyun Na,Gyu-Yong Song,Sangtaek Oh
Marine Drugs , 2015, DOI: 10.3390/md13010543
Abstract: The tumor suppressor, p53, plays an essential role in the cellular response to stress through regulating the expression of genes involved in cell cycle arrest, apoptosis and autophagy. Here, we used a cell-based reporter system for the detection of p53 response transcription to identify the marine sponge metabolites, ilimaquinone and ethylsmenoquinone, as activators of the p53 pathway. We demonstrated that ilimaquinone and ethylsmenoquinone efficiently stabilize the p53 protein through promotion of p53 phosphorylation at Ser15 in both HCT116 and RKO colon cancer cells. Moreover, both compounds upregulate the expression of p21 WAF1 /CIP1, a p53-dependent gene, and suppress proliferation of colon cancer cells. In addition, ilimaquinone and ethylsmenoquinone induced G 2/M cell cycle arrest and increased caspase-3 cleavage and the population of cells that positively stained with Annexin V-FITC, both of which are typical biochemical markers of apoptosis. Furthermore, autophagy was elicited by both compounds, as indicated by microtubule-associated protein 1 light chain 3 (LC3) puncta formations and LC3-II turnover in HCT116 cells. Our findings suggest that ilimaquinone and ethylsmenoquinone exert their anti-cancer activity by activation of the p53 pathway and may have significant potential as chemo-preventive and therapeutic agents for human colon cancer.
Role of Serotonin Neurons in L-DOPA- and Graft-Induced Dyskinesia in a Rat Model of Parkinson's Disease
Eunju Shin,Elisabetta Tronci,Manolo Carta
Parkinson's Disease , 2012, DOI: 10.1155/2012/370190
Abstract: L-DOPA, the most effective drug to treat motor symptoms of Parkinson's disease, causes abnormal involuntary movements, limiting its use in advanced stages of the disease. An increasing body of evidence points to the serotonin system as a key player in the appearance of L-DOPA-induced dyskinesia (LID). In fact, exogenously administered L-DOPA can be taken up by serotonin neurons, converted to dopamine and released as a false transmitter, contributing to pulsatile stimulation of striatal dopamine receptors. Accordingly, destruction of serotonin fibers or silencing serotonin neurons by serotonin agonists could counteract LID in animal models. Recent clinical work has also shown that serotonin neurons are present in the caudate/putamen of patients grafted with embryonic ventral mesencephalic cells, producing intense serotonin hyperinnervation. These patients experience graft-induced dyskinesia (GID), a type of dyskinesia phenotypically similar to the one induced by L-DOPA but independent from its administration. Interestingly, the 5-HT1A receptor agonist buspirone has been shown to suppress GID in these patients, suggesting that serotonin neurons might be involved in the etiology of GID as for LID. In this paper we will discuss the experimental and clinical evidence supporting the involvement of the serotonin system in both LID and GID. 1. Introduction Parkinson’s disease (PD) is the second most common neurodegenerative disease and is characterized by loss of dopamine (DA) neurons in the substantia nigra. The cell loss results in decreased activation of striatal DA receptors, thus causing motor impairments, such as tremor, rigidity, bradykinesia, and postural instability. The DA precursor L-3,4-dihydroxyphenylalanine (L-DOPA) represents the most effective drug to alleviate the motor symptoms. Although this medication is very efficient during the first few years of administration, its efficacy gradually diminishes overtime, and uncontrolled excessive movements, known as dyskinesia, appear as a side effect after a variable number of years in most of patients, limiting the use of L-DOPA in advanced stages of the disease. A better understanding of the mechanisms underlying the appearance of dyskinesia has been achieved during recent years using animal models of L-DOPA-induced dyskinesia (LID). In fact, abnormal involuntary movements (AIMs) develop in response to sub-chronic L-DOPA treatment in 6-hydroxydopamine (6-OHDA)-lesioned rats and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated monkeys, resembling peak-dose dyskinesia seen in patients [1–4].
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