• Proceedings of the PSK Conference
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• 2002.10a
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• pp.300.2-301
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• 2002

HCV is transmitted via various plasma-derived medicinal products. The transmission of HCV could. however, be prevented by screening plasma pools with NAT and validating HCV viral clearance during the manufacturing of plasma derivatives, Although various screening methods including commercial kits are available. it is yet to develop an analytical method to detect HCV in both plasma and plasma derivatives. The objective of this study was to develop a reliable in house method for reliable for the HCV RNA detection from plasma and plasma derivatives. (omitted)

• Journal of Species Research
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• v.6 no.2
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• pp.91-100
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• 2017

Five bacterial strains, ES10-3-3-1, KKM10-2-2-1, Ant11, JM10-4-1-3, and KMS4-11 assigned to the genus Deinococcus were isolated from soil samples collected from Namyangju-si in Gyeonggi-do, Gangnam-gu and Dongdaemun-gu in Seoul, Korea. In addition, four bacterial strains, KKM10-2-7-2, JM10-2-5, JM10-2-6-2, and KKM10-2-3 assigned to the genus Hymenobacter were isolated from soil samples collected from Gangnam-gu and Dongdaemun-gu in Seoul, in South Korea. The five Deinococcus species were Gram-stain positive, pink-pigmented, and short-rod or coccus shaped. The four Hymenobacter species were Gram-stain negative, red-pigmented, and short-rod shaped. Phylogenetic analysis based on 16S rRNA gene sequences revealed that strains ES10-3-3-1, KKM10-2-2-1, Ant11, JM10-4-1-3, and KMS4-11 were most closely related to Deinococcus citri $NCCP-154^T$ (with 99.8% similarity), Deinococcus grandis DSM $12784^T$ (99.0%), Deinococcus marmoris DSM $12784^T$ (98.8%), Deinococcus claudionis $PO-04-19-125^T$ (98.7%), and Deinococcus radioresistens $8A^T$ (99.8%), respectively. KKM10-2-7-2, JM10-2-5, JM10-2-6-2, and KKM10-2-3 were most closely related to Hymenobacter algoricola $VUG-A23a^T$ (99.1% similarity), Hymenobacter elongatus $VUG-A112^T$ (99.1% similarity), Hymenobacter gelipurpurascens $Txg1^T$ (99.1% similarity), and Hymenobacter psychrotolerans $Tibet-IIU11^T$ (99.3% similarity), respectively. These nine species have never been reported in Korea; thus, five Deinococcus species are reported in the family Deinococcaceae, order Deinococcales, class Deinococci, phylum Deinococcus-Thermus and four Hymenobacter species are reported in the family Cytophagaceae, order Cytophagales, class Cytophagia, phylum Bacteroidetes.

• BMB Reports
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• v.45 no.4
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• pp.247-252
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• 2012

Although previous studies have demonstrated that BMP9 is highly capable of inducing osteogenic differentiation of mesenchymal stem cells, the molecular mechanism involved remains to be fully elucidated. In this study, we showed that BMP9 simultaneously promotes the activation of Smad1/5/8, p38 and ERK1/2 in C3H10T1/2 cells. Knockdown of Smad4 with RNA interference reduced nuclear translocation of Smad1/5/8, and disrupted BMP9-induced osteogenic differentiation. BMP9-induced osteogenic differentiation was blocked by p38 inhibitor SB203580, whereas enhanced by ERK1/2 inhibitor PD98059. SB203580 decreased BMP9-activated Smads singling, and yet PD98059 stimulated Smads singling in C3H10T1/2 cells. The effects of inhibitor were reproduced with adenovirus expressing siRNA targeted p38 and ERK1/2, respectively. Taken together, our findings revealed that Smads, p38 and ERK1/2 are involved in BMP9-induced osteogenic differentiation. Also, it is noteworthy that p38 and ERK1/2 may play opposing regulatory roles in mediating BMP9-induced osteogenic differentiation of C3H10T1/2 cells.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.18
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• pp.7553-7558
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• 2014

The Piwi subfamily comprises two argonaute (Ago) family proteins, which are defined by the presence of PAZ and Piwi domains, with well known roles in RNA silencing. Hiwi, a human Piwi subfamily member, has been shown to play essential roles in stem cell self-renewal and gametogenesis. Recently, accumulating reports have indicated that abnormal hiwi expression is associated with poorer prognosis of multiple types of human cancers, including examples in the breast. However, little is known about details of the oncogenic role of hiwi in breast cancers. In present study, we confirmed overexpression of hiwi in breast cancer specimens and breast cancer cell lines at both mRNA and protein levels. Thus both RT-qPCR and Western blot data revealed significantly higher hiwi in intratumor than peritumor specimens, overexpression being associated with tumor size, lymph node metastasis and histological grade. Hiwi overexpression was also identified in breast cancer cell lines, MDA-MB-231 and MCF-7, and gain-of-function and loss-of-function strategies were adopted to identify the role of hiwi in the MCF-7 cell growth. Results demonstrated that hiwi expression in MCF-7 cells was significantly up- or down-regulated by the two strategies. We next evaluated the influence of hiwi overexpression or knockdown on the growth of breast cancer cells. Both cell count and colony formation assays confirmed promoting roles of hiwi in MCF-7 cells, which could be inhibited by hiwi specific blockage by siRNAs. In summary, the present study confirmed overexpression of hiwi in breast cancer specimens and breast cancer cell lines, and provided e vidence of promotion by hiwi of cell growth. The results imply an oncogenic role of hiwi in breast cancers.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.11
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• pp.6305-6309
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• 2013

Background: TIAM2, a Rac guanine nucleotide exchange factor, is closely associated with cell adherence and migration. Here, we aimed to investigate the role of TIAM2 in non-small cell lung cancer (NSCLC) cells. Materials and Methods: A small interference RNA (siRNA) was introduced to silence the expression of TIAM2. Invasion and motility assays were then performed to assess the invasion and motility potential of NSCLC cells. GST-pull down assays were used to detect activation of Rac1. Results: TIAM2 was highly expressed in NSCLC cells. Knockdown of TIAM2 inhibited the invasion and motility, and suppressed activation of Rac1. Further experiments demonstrated that knockdown of TIAM2 could up-regulate the expression of E-cadherin, and down-regulate the expression of MMP-3, Twist and Snail. Conclusions: Our data suggest that TIAM2 can promote invasion and motility of NSCLC cells. Activation of Rac1 and regulation of some EMT/invasion-related genes may be involved in the underlying processes.

• Biomolecules & Therapeutics
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• v.22 no.5
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• pp.390-399
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• 2014

Chalcones (1,3-diaryl-2-propen-1-ones), a flavonoid subfamily, are widely known for their anti-inflammatory properties. Propenone moiety in chalcones is known to play an important role in generating biological responses by chalcones. In the present study, we synthesized chalcone derivatives structurally modified in propenone moiety and examined inhibitory effect on nitric oxide (NO) production and its potential mechanisms. Among the chalcone derivatives used for this study, TI-I-174 (3-(2-Hydroxyphenyl)-1-(thiophen-3-yl)prop-2-en-1-one) most potently inhibited lipopolysaccharide (LPS)-stimulated nitrite production in RAW 264.7 macrophages. TI-I-174 treatment also markedly inhibited inducible nitric oxide synthase (iNOS) expression. However, TI-I-174 did not significantly affect production of IL-6, cyclooxygenase-2 (COX-2) and tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$), implying that TI-I-174 inhibits production of inflammatory mediators in a selective manner. Treatment of macrophages with TI-I-174 significantly inhibited transcriptional activity of activator protein-1 (AP-1) as determined by luciferase reporter gene assay, whereas nuclear factor-${\kappa}B$ (NF-${\kappa}B$) activity was not affected by TI-I-1744. In addition, TI-I-174 significantly inhibited activation of c-Jun-N-Terminal kinase (JNK) without affecting ERK1/2 and p38MAPK, indicating that down-regulation of iNOS gene expression by TI-I-174 is mainly attributed by blockade of JNK/AP-1 activation. We also demonstrated that TI-I-174 treatment led to an increase in heme oxygenase-1 (HO-1) expression both at mRNA and protein level. Transfection of siRNA targeting HO-1 reversed TI-I-174-mediated inhibition of nitrite production. Taken together, these results indicate that TI-I-174 suppresses NO production in LPS-stimulated RAW 264.7 macrophages via induction of HO-1 and blockade of AP-1 activation.

• Asian-Australasian Journal of Animal Sciences
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• v.14 no.2
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• pp.258-262
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• 2001

The study was conducted to evaluate the effects of chromium picolinate (CrP) on growth, carcass characteristics and serum metabolites in growing-finishing pigs. A total of 96 Landrace$\times$Yorkshire$\times$Duroc hybrid pigs, initial live weight about $38.12{\pm}00kg$, were randomly assigned to 2 groups (16 pigs per pen, 3 pens per group), each group had 48 pigs with an equal number of barrows and gilts. The pigs were fed the diet with or without $200{\mu}g/kg$ Cr from CrP. The results indicated that the addition of $200{\mu}g/kg$ CrP increased ADG by 3.58% and decreased feed conversion rate (FCR) by 3.00% compared to the control group. Pigs fed CrP had 7.58% (p<0.05) higher carcass lean percentage, 15.55% (p<0.05) larger longissimus muscle area (LMA) and 10.90% (p<0.05) lower back fat thickness, 15.17% (p<0.05) lower carcass fat percentage. In addition, the IGF-I level in serum was elevated by 79.20% (p<0.05), the Insulin and cortisol level decreased by 27.35% (p<0.05) and 34.58% (p<0.05) respectively with supplementation of CrP. Analysis of subcutaneous fat (10th rib) showed that the activity of hormone sensitive lipase (HSL) increased by 79.58% (p<0.05) and the activities of isocitrate dehydrogenase (ISD) and malate dehydrogenase (MDH) decreased significantly by 15.06% (p<0.05) and 54.53% (p<0.05) respectively in the $200{\mu}g/kg$ CrP group. The concentration of RNA, RNA/DNA in LMA increased by 31.89% (p<0.05) and 5.41% (p<0.05) respectively with the addition of CrP. These results suggest that CrP reduced fat deposits by decreasing lipogenic enzyme activities and increasing HSL activity and may have promoted muscle anabolic metabolism through elevated IGF-I levels.

• Journal of Korean Neurosurgical Society
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• v.60 no.2
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• pp.130-137
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• 2017

Objective : Autophagy is one of the key responses of cells to programmed cell death. Memantine, an approved anti-dementia drug, has an antiproliferative effect on cancer cells but the mechanism is poorly understood. The aim of the present study was to test the possibility of induction of autophagic cell death by memantine in glioma cell lines. Methods : Glioma cell lines (T-98 G and U-251 MG) were used for this study. Results : The antiproliferative effect of memantine was shown on T-98 G cells, which expressed N-methyl-D-aspartate 1 receptor (NMDAR1). Memantine increased the autophagic-related proteins as the conversion ratio of light chain protein 3-II (LC3-II)-/LC3-I and the expression of beclin-1. Memantine also increased formation of autophagic vacuoles observed under a transmission electron microscope. Transfection of small interfering RNA (siRNA) to knock down NMDAR1 in the glioma cells induced resistance to memantine and decreased the LC3-II/LC3-I ratio in T-98 G cells. Conclusion : Our study demonstrates that in glioma cells, memantine inhibits proliferation and induces autophagy mediated by NMDAR1.

• Journal of Microbiology and Biotechnology
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• v.23 no.12
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• pp.1785-1790
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• 2013

The synthetic machinery of ATF4 (activating transcription factor 4) is activated in response to various stress conditions involved in nutrient restriction, endoplasmic reticulum homeostasis, and oxidation. Stress-induced inhibition of proteasome activity triggers the unfolded protein response and endoplasmic reticulum stress, where ATF4 is crucial for consequent biological events. In the current study, we showed that the $NAD^+$-dependent deacetylase, SIRT1, suppresses ATF4 synthesis during proteasome inhibition. SIRT1 depletion via transfection of specific siRNA into HeLa cells resulted in a significant increase in ATF4 protein, which was observed specifically in the presence of the proteasome inhibitor MG132. Consistent with SIRT1 depletion data, transient transfection of cells with SIRT1-overexpressing plasmid induced a decrease in the ATF4 protein level in the presence of MG132. Interestingly, however, ATF4 mRNA was not affected by SIRT1, even in the presence of MG132, indicating that SIRT1-induced suppression of ATF4 synthesis occurs under post-transcriptional control. Accordingly, we propose that SIRT1 serves as a negative regulator of ATF4 protein synthesis at the post-transcriptional level, which is observed during stress conditions, such as proteasome inhibition.

• The Korean Journal of Physiology and Pharmacology
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• v.15 no.2
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• pp.83-88
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• 2011

A large body of evidence has indicated that induction of endogenous antioxidative proteins seems to be a reasonable strategy for delaying the progression of cell injury. In our previous study, cilostazol was found to increase the expression of the antioxidant enzyme heme oxygenase-1 (HO-1) in synovial cells. Thus, the present study was undertaken to examine whether cilostazol is able to counteract tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$)-induced cell death in endothelial cells via the induction of HO-1 expression. We exposed human umbilical vein endothelial cells (HUVECs) to TNF-${\alpha}$ (50 ng/ml), with or without cilostazol ($10{\mu}M$). Pretreatment with cilostazol markedly reduced TNF-${\alpha}$-induced viability loss in the HUVECs, which was reversed by zinc protoporphyrine IX (ZnPP), an inhibitor of HO-1. Moreover, cilostazol increased HO-1 protein and mRNA expression. Cilostazol-induced HO-1 induction was markedly attenuated not only by ZnPP but also by copper-protoporphyrin IX (CuPP). In an assay measuring peroxisome proliferator-activated receptor-${\gamma}$ (PPAR-${\gamma}$) transcription activity, cilostazol directly increased PPAR-${\gamma}$ transcriptional activity which was completely abolished by HO-1 inhibitor. Furthermore, increased PPAR-${\gamma}$ activity by cilostazol and rosiglitazone was completely abolished in cells transfected with HO-1 siRNA. Taken together, these results indicate that cilostazol up-regulates HO-1 and protects cells against TNF-${\alpha}$-induced endothelial cytotoxicity via a PPAR-${\gamma}$-dependent pathway.