• Journal of Korean Society on Water Environment
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• v.23 no.1
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• pp.87-96
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• 2007

In this paper a methodology of identifying individual pipes according to the internal and external characteristics of pipe is developed, and the methodology is applied to a case study water distribution pipe break database. Using the newly defined individual pipes the hazard rates of the cast iron 6 inch pipes are modeled by implementing the proportional hazards modeling approach for consecutive pipe failures. The covariates to be considered in the modeling procedures are selected by considering the general availability of the data and the practical applicability of the modeling results. The individual cast iron 6 inch pipes are categorized into seven ordered survival time groups according to the total number of breaks recorded in a pipe to construct distinct proportional hazard model (PHM) for each survival time group (STG). The modeling results show that all of the PHMs have the hazard rate forms of the Weibull distribution. In addition, the estimated baseline survivor functions show that the survival probabilities of the STGs generally decrease as the number of break increases. It is found that STG I has an increasing hazard rate whereas the other STGs have decreasing hazard rates. Regarding the first failure the hazard ratio of spun-rigid and spun-flex cast iron pipes to pit cast iron pipes is estimated as 1.8 and 6.3, respectively. For the second or more failures the relative effects of pipe material/joint type on failure were not conclusive. The degree of land development affected pipe failure for STGs I, II, and V, and the average hazard ratio was estimated as 1.8. The effects of length on failure decreased as more breaks occur and the population in a GRID affected the hazard rate of the first pipe failure.

• Journal of Digital Convergence
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• v.14 no.12
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• pp.237-243
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• 2016

Since realtime search keywords of portal sites are arranged in descending order by instant increasing rates of search numbers, they easily show issues increasing in interests for a short time. But they have the limits extracted different results by portal sites and not shown issues by a period. Thus, to find key issues from the whole realtime search keywords for certain period, and to show results of summarizing them and analyzing differences, is significant in providing the basis of understanding issues more practically and in maintaining consistency of them. This paper analyzes differences of week key issues extracted from week analysis of realtime search keywords provided by two typical portal sites. The results of experiments show that the portal group means of realtime search keywords by the independent t-test and the survival functions of realtime search keywords by the survival analysis are statistically significant differences.

• Proceedings of the KAIS Fall Conference
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• 2011.12a
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• pp.170-173
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• 2011

Therapeutic hypothermia(TH) improves neurological outcomes and reduces mortality among survivors of out-of-hospital cardiac arrest. Animal and human studies have shown that TH results in improved salvage of the myocardium, reduced infarct size, reduced left ventricular remodeling and better long-term left ventricular function in settings of regional myocardial ischemia. This study is to investigate the effect of TH on post-resuscitation myocardial dysfunction and survival time after cardiac arrest and resuscitation in a rat model of myocardial infarction (MI). Thoracotomies were performed in 10 Male Sprague-Dawley rats weighing 450-550 g. MI was induced by ligation of the left anterior descending coronary artery (LAD). Ninety min after LAD ligation, ventricular fibrillation induction and subsequent cardiopulmonary resuscitation was performed before defibrillation attempts. Animals were randomized to two groups: a) Acute MI-Normothermia b) Acute MI-Hypothermia ($32^{\circ}C$ for 4 h). Myocardial functions, including cardiac output, left ventricular ejection fraction, and myocardial performance index were measured echocardiographically together with duration of survival. Ejection fraction, cardiac output and myocardial performance index were $54.74{\pm}9.16$, $89.00{\pm}8.89$, $1.30{\pm}0.09$ respectively and significantly better in the TH group than those of the normothermic group at the first 4 h after resuscitation($32.20{\pm}1.85$,$41.60{\pm}8.62$,$1.77{\pm}0.19$)(p=0.00). The survival time of the hypothermic group ($31.8{\pm}14.8$ h) was greater than that of the normothermic group($12.3{\pm}6.5$ h, p<0.05). This study suggested that TH attenuated post resuscitation myocardial dysfunction in acute MI and would be a potential strategy in post resuscitation care.

• The Korean Journal of Applied Statistics
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• v.34 no.3
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• pp.411-425
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• 2021

Accelerated failure time (AFT) model represents a linear relationship between the log-survival time and covariates. We are interested in the inference of covariate's effect affecting the variation of survival times in the AFT model. Thus, we need to model the variance as well as the mean of survival times. We call the resulting model mean and variance AFT (MV-AFT) model. In this paper, we propose a variable selection procedure of regression parameters of mean and variance in MV-AFT model using penalized likelihood function. For the variable selection, we study four penalty functions, i.e. least absolute shrinkage and selection operator (LASSO), adaptive lasso (ALASSO), smoothly clipped absolute deviation (SCAD) and hierarchical likelihood (HL). With this procedure we can select important covariates and estimate the regression parameters at the same time. The performance of the proposed method is evaluated using simulation studies. The proposed method is illustrated with a clinical example dataset.

• Journal of Microbiology and Biotechnology
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• v.32 no.3
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• pp.365-377
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• 2022

Mammalian target of rapamycin (mTOR) is a serine-threonine kinase member of the cellular phosphatidylinositol 3-kinase (PI3K) pathway, which is involved in multiple biological functions by transcriptional and translational control. mTOR is a downstream mediator in the PI3K/Akt signaling pathway and plays a critical role in cell survival. In cancer, this pathway can be activated by membrane receptors, including the HER (or ErbB) family of growth factor receptors, the insulin-like growth factor receptor, and the estrogen receptor. In the present work, we congregated an electronic network of mTORC1 built on an assembly of data using natural language processing, consisting of 470 edges (activations/interactions and/or inhibitions) and 206 nodes representing genes/proteins, using the Cytoscape 3.6.0 editor and its plugins for analysis. The experimental design included the extraction of gene expression data related to five distinct types of cancers, namely, pancreatic ductal adenocarcinoma, hepatic cirrhosis, cervical cancer, glioblastoma, and anaplastic thyroid cancer from Gene Expression Omnibus (NCBI GEO) followed by pre-processing and normalization of the data using R & Bioconductor. ExprEssence plugin was used for network condensation to identify differentially expressed genes across the gene expression samples. Gene Ontology (GO) analysis was performed to find out the over-represented GO terms in the network. In addition, pathway enrichment and functional module analysis of the protein-protein interaction (PPI) network were also conducted. Our results indicated NOTCH1, NOTCH3, FLCN, SOD1, SOD2, NF1, and TLR4 as upregulated proteins in different cancer types highlighting their role in cancer progression. The MCODE analysis identified gene clusters for each cancer type with MYC, PCNA, PARP1, IDH1, FGF10, PTEN, and CCND1 as hub genes with high connectivity. MYC for cervical cancer, IDH1 for hepatic cirrhosis, MGMT for glioblastoma and CCND1 for anaplastic thyroid cancer were identified as genes with prognostic importance using survival analysis.

• Korean Journal of Clinical Laboratory Science
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• v.51 no.4
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• pp.475-483
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• 2019

The use of stem cells in cell-based therapy has attracted extensive interest in the field of regenerative medicine, and it has been applied to numerous incurable diseases due to the inherent abilities of self-renewal and differentiation. However, there still exist some severe obstacles, such as requirement of cell expansion before the treatment, and low survival at the treated site. To overcome these disadvantages of stem cells, we used the carcinoembryonic antigen-related cell adhesion molecule 6 (CEACAM 6) gene, which functions to increase cell-cell interaction as well as anti-apoptosis. We first confirmed whether CEACAM 6 is expressed in various cell lines at the protein level (including in stem cells), followed by evaluating and selecting the optimal transfection conditions into stem cells. The CEACAM 6 gene was transfected into stem cells to prolong cell survival and preserve from damage by oxidative stress. After confirming the CEACAM 6 expression in transfected stem cells, the cell survival was assessed under oxidative condition by exposing to hydrogen peroxide (H₂O₂) to mimic the chronic environment-induced cellular damage. CEACAM 6 expressing stem cells show increased cell viability compared to the non-CEACAM 6 expressing cells. We propose that the application of the CEACAM 6 gene is a potential option, capable of expanding and enhancing the therapeutic effects of stem cells.

• Journal of Veterinary Science
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• v.23 no.1
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• pp.8.1-8.15
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• 2022

Background: Brucella infection induces brucellosis, a zoonotic disease. The intracellular circulation process and virulence of Brucella mainly depend on its type IV secretion system (T4SS) expressing secretory effectors. Secreted protein BspJ is a nucleomodulin of Brucella that invades the host cell nucleus. BspJ mediates host energy synthesis and apoptosis through interaction with proteins. However, the mechanism of BspJ as it affects the intracellular survival of Brucella remains to be clarified. Objectives: To verify the functions of nucleomodulin BspJ in Brucella's intracellular infection cycles. Methods: Constructed Brucella abortus BspJ gene deletion strain (B. abortus ∆BspJ) and complement strain (B. abortus pBspJ) and studied their roles in the proliferation of Brucella both in vivo and in vitro. Results: BspJ gene deletion reduced the survival and intracellular proliferation of Brucella at the replicating Brucella-containing vacuoles (rBCV) stage. Compared with the parent strain, the colonization ability of the bacteria in mice was significantly reduced, causing less inflammatory infiltration and pathological damage. We also found that the knockout of BspJ altered the secretion of cytokines (interleukin [IL]-6, IL-1β, IL-10, tumor necrosis factor-α, interferon-γ) in host cells and in mice to affect the intracellular survival of Brucella. Conclusions: BspJ is extremely important for the circulatory proliferation of Brucella in the host, and it may be involved in a previously unknown mechanism of Brucella's intracellular survival.

• BMB Reports
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• v.49 no.3
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• pp.191-196
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• 2016

Vascular endothelial growth factor (VEGF) is a key mediator of angiogenesis and critical for normal embryonic development and repair of pathophysiological conditions in adults. Although phospholipase D (PLD) activity has been implicated in angiogenic processes, its role in VEGF signaling during angiogenesis in mammals is unclear. Here, we found that silencing of PLD2 by siRNA blocked VEGF-mediated signaling in immortalized human umbilical vein endothelial cells (iHUVECs). Also, VEGF-induced endothelial cell survival, proliferation, migration, and tube formation were inhibited by PLD2 silencing. Furthermore, while Pld2-knockout mice exhibited normal development, loss of PLD2 inhibited VEGF-mediated ex vivo angiogenesis. These findings suggest that PLD2 functions as a key mediator in the VEGF-mediated angiogenic functions of endothelial cells.

• Animal cells and systems
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• v.11 no.2
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• pp.205-213
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• 2007

Nek6 belongs to NIMA1 (never in mitosis, gene A) related kinase, which was originally identified in Aspergillus nidulans as a serine/threonine kinase critical for cell cycle progression. We noticed that the putative SUMOylation site is localized on the $K^{252}$ residue in $^{251}FKsD^{254}$ of Nek6, based on the consensus sequence ${\Phi}KxE$; where ${\Phi}$ represents L, I, V or F and x is any amino acid. We observed that the Nek6 SUMO mutant (K252R) has decreased protein kinase activity, nuclear speckle localization and protein stability, compared with that of the Nek6 wild type. However, the Nek6 SUMO mutant increased the cell survival rate of COS-1 cells as determined by FACS analysis. Therefore, our data suggest that SUMOylation on the $K^{252}$ residue of Nek6 is required for its normal functions, such as proper nuclear localization, kinase activity and protein stability, to control cell cycle.

• Clinical and Experimental Reproductive Medicine
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• v.41 no.3
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• pp.97-107
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• 2014

The placenta is a temporary fetomaternal organ capable of supporting fetal growth and development during pregnancy. In particular, abnormal development and dysfunction of the placenta due to cha nges in the proliferation, differentiation, cell death, and invasion of trophoblasts induce several gynecological diseases as well as abnormal fetal development. Autophagy is a catalytic process that maintains cellular structures by recycling building blocks derived from damaged microorganelles or proteins resulting from digestion in lysosomes. Additionally, autophagy is necessary to maintain homeostasis during cellular growth, development, and differentiation, and to protect cells from nutritional deficiencies or factors related to metabolism inhibition. Induced autophagy by various environmental factors has a dual role: it facilitates cellular survival in normal conditions, but the cascade of cellular death is accelerated by over-activated autophagy. Therefore, cellular death by autophagy has been known as programmed cell death type II. Autophagy causes or inhibits cellular death via the other mechanism, apoptosis, which is programmed cell death type I. Recently, it has been reported that autophagy increases in placenta-related obstetrical diseases such as preeclampsia and intrauterine growth retardation, although the mechanisms are still unclear. In particular, abnormal autophagic mechanisms prevent trophoblast invasion and inhibit trophoblast functions. Therefore, the objectives of this review are to examine the characteristics and functions of autophagy and to investigate the role of autophagy in the placenta and the trophoblast as a regulator of cell death.