• Journal of Food Hygiene and Safety
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• v.35 no.2
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• pp.103-108
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• 2020

Recently, consumer demand for safe but minimally processed food has rapidly increased. For this reason, many food processing industries are applying hurdle technology to enhance food safety, extend shelf life, and make foods appear minimally processed. Meanwhile, studies have shown that a treatment (stress) meant to inactivate foodborne pathogens may trigger adaptation mechanisms and could even offer cross protection against subsequent treatments. Also, certain routine farm practices such as antibiotic and herbicide use could result in the development of antibiotic-resistant pathogens. Such bacteria may be tolerant to food processing-associated stress and be more likely to remain viable in processed foods. In this review, we discuss the correlation between food processing-associated stress and antibiotic resistance. We also discuss molecular mechanisms such as the use of sigma factors, SOS response pathways and efflux pumps as means of cross protection against antimicrobial compounds and other food processing-associated stresses.

• Journal of Ginseng Research
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• v.46 no.5
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• pp.636-645
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• 2022

Background: Ginsenoside Rg3 and gemcitabine have mutual enhancing antitumor effects. However, the underlying mechanisms are not clear. This study explored the influence of ginsenoside Rg3 on Zinc finger protein 91 homolog (ZFP91) expression in pancreatic adenocarcinoma (PAAD) and their regulatory mechanisms on gemcitabine sensitivity. Methods: RNA-seq and survival data from The Cancer Genome Atlas (TCGA)-PAAD and Genotype-Tissue Expression (GTEx) were used for in-silicon analysis. PANC-1, BxPC-3, and PANC-1 gemcitabine-resistant (PANC-1/GR) cells were used for in vitro analysis. PANC-1 derived tumor xenograft nude mice model was used to assess the influence of ginsenoside Rg3 and ZFP91 on tumor growth in vivo. Results: Ginsenoside Rg3 reduced ZFP91 expression in PAAD cells in a dose-dependent manner. ZFP91 upregulation was associated with significantly shorter survival of patients with PAAD. ZFP91 overexpression induced gemcitabine resistance, which was partly conquered by ginsenoside Rg3 treatment. ZFP91 depletion sensitized PANC-1/GR cells to gemcitabine treatment. ZFP91 interacted with Testis-Specific Y-Encoded-Like Protein 2 (TSPYL2), induced its poly-ubiquitination, and promoted proteasomal degradation. Ginsenoside Rg3 treatment weakened ZFP91-induced TSPYL2 poly-ubiquitination and degradation. Enforced TSPYL2 expression increased gemcitabine sensitivity of PAAD cells and partly reversed induced gemcitabine resistance in PANC-1/GR cells. Conclusion: Ginsenoside Rg3 can increase gemcitabine sensitivity of pancreatic adenocarcinoma at least via reducing ZFP91 mediated TSPYL2 destabilization.

• Proceedings of the Korean Society For Composite Materials Conference
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• 2002.05a
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• pp.109-113
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• 2002

Interfacial and electrical properties for the carbon fiber reinforced epoxy-amine terminated (AT) PEI composites were performed using microdroplet test and electrical resistance measurements. As AT PEI content increased, the fracture toughness of epoxy-AT PEI matrix increased, and IFSS was improved due to the improved toughness and energy absorption mechanisms of AT PEI. The microdroplet in the carbon fiber/neat epoxy composite showed brittle microfailure mode. At 15 wt% AT PEI content, ductile microfailure mode appeared because of improved fracture toughness. After curing, the changes of electrical resistance (ΔR) with increasing AT PEI content increased gradually because of thermal shrinkage. The matrix fracture toughness was correlated to IFSS, TEC and electrical resistance. In cyclic strain test, the maximum stress and their slope of the neat epoxy case were higher than those of 15 wt% AT PEI. The results obtained from electrical resistance measurements under curing process and reversible stress and strain were consistent well with matrix toughness properties.

• KSCE Journal of Civil and Environmental Engineering Research
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• v.32 no.1D
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• pp.33-39
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• 2012

More and more pavements are suffering from damage these days due to the below-zero winter temperatures and frequent snowfalls. From this research, the freeze-thawing mechanisms of pavements will be observed, and the freeze-thawing resistance of porous asphalt concrete mixture is to be evaluated according to various assessment methods. The investigation was conducted through applying rigid and flexible pavements to freeze-thawing resistance experiments, which include various experiments such as deformation rate measurements, Lottman tests, repeated cyclic freeze-thawing experiments, stripping resistance tests and so on. Test results revealed that the porous asphalt concrete had less deformations according to temperatures compared to dense-graded asphalt concrete due to the 20% void gap. In addition, according to the freeze-thawing repetition experiments which are effected by moisture, the porous asphalt concrete mixture showed superior resistance to repeated cyclic freeze-thawing compared to other asphalt concrete mixtures due to the drainage and the voids within the specimen.

• Asian Pacific Journal of Cancer Prevention
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• v.17 no.2
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• pp.581-590
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• 2016

Resistance to anoikis, a cell-detachment induced apoptosis, is one of the malignant phenotypes which support tumor metastasis. Molecular mechanisms underlying the establishment of this phenotype require further investigation. This study aimed at exploring protein expression profiles associated with anoikis resistance of a metastatic breast cancer cell. Cell survival of suspension cultures of non-metastatic MCF-7 and metastatic MDA-MB-231 cells were compared with their adherent cultures. Trypan blue exclusion assays demonstrated a significantly higher percentage of viable cells in MDA-MB-231 than MCF-7 cell cultures, consistent with analysis of annexin V-7-AAD stained cells indicating that MDA-MB-231 possess anti-apoptotic ability 1.7 fold higher than MCF-7 cells. GeLC-MS/MS analysis of protein lysates of MDA-MB-231 and MCF-7 cells grown under both culture conditions identified 925 proteins which are differentially expressed, 54 of which were expressed only in suspended and adherent MDA-MB-231 but not in MCF-7 cells. These proteins have been implicated in various cellular processes, including DNA replication and repair, transcription, translation, protein modification, cytoskeleton, transport and cell signaling. Analysis based on the STITCH database predicted the interaction of phospholipases, PLC and PLD, and 14-3-3 beta/alpha, YWHAB, with the intrinsic and extrinsic apoptotic signaling network, suggesting putative roles in controlling anti-anoikis ability. MDA-MB-231 cells grown in the presence of inhibitors of phospholipase C, U73122, and phospholipase D, FIPI, demonstrated reduced ability to survive in suspension culture, indicating functional roles of PLC and PLD in the process of anti-anoikis. Our study identified intracellular mediators potentially associated with establishment of anoikis resistance of metastatic cells. These proteins require further clarification as prognostic and therapeutic targets for advanced breast cancer.

• The Korean Journal of Physiology and Pharmacology
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• v.22 no.1
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• pp.43-51
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• 2018

Although cisplatin is one of the most effective antitumor drugs for ovarian cancer, the emergence of chemoresistance to cisplatin in over 80% of initially responsive patients is a major barrier to successful therapy. The precise mechanisms underlying the development of cisplatin resistance are not fully understood, but alteration of DNA methylation associated with aberrant gene silencing may play a role. To identify epigenetically regulated genes directly associated with ovarian cancer cisplatin resistance, we compared the expression and methylation profiles of cisplatin-sensitive and -resistant human ovarian cancer cell lines. We identified ${\alpha}$-N-acetylgalactosaminidase (NAGA) as one of the key candidate genes for cisplatin drug response. Interestingly, in cisplatin-resistant cell lines, NAGA was significantly down-regulated and hypermethylated at a promoter CpG site at position +251 relative to the transcriptional start site. Low NAGA expression in cisplatin-resistant cell lines was restored by treatment with a DNA demethylation agent, indicating transcriptional silencing by hyper-DNA methylation. Furthermore, overexpression of NAGA in cisplatin-resistant lines induced cytotoxicity in response to cisplatin, whereas depletion of NAGA expression increased cisplatin chemoresistance, suggesting an essential role of NAGA in sensitizing ovarian cells to cisplatin. These findings indicate that NAGA acts as a cisplatin sensitizer and its gene silencing by hypermethylation confers resistance to cisplatin in ovarian cancer. Therefore, we suggest NAGA may be a promising potential therapeutic target for improvement of sensitivity to cisplatin in ovarian cancer.

• Korean Journal of Microbiology
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• v.31 no.3
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• pp.255-260
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• 1993

The Enterobacter cloacae biofilms developed on slide glasses and galvanized-iron coupons were applied to test the attached bacterial resistance to chlorination. The chlorine resistances of biofilm bacteria grown on the slide glasses and galvanized-iron coupons were 14 and 480 times that of the suspended bacteria, respectively. The chlorine resistance of particleattached bacterial populations was 48 times that of suspended bacterial populations. The biofilm bacterial densities developed on the slide glasses and galvanized-iron coupons which were immersed in the flowing tap water for 75 days were $4.75 {\times} 10^{4}$ and $1.12 {\times} 10^5 cfu/cm^{2}$ It is concluded that main mechanisms of enteric or HPC bacterial resistance to chlorination in tap waters are bacterial attachment or . adsorption to particles or bacterial aggregations and formation of biofilms on the inner wall of distribution systems by escaped bacteria from chlorination in water treatment processes, which results in bacterial regrowth in water distribution systems.

• BMB Reports
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• v.40 no.6
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• pp.853-860
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• 2007

Resistance to anticancer drugs is a major obstacle in the effective treatment of tumors. To understand the mechanisms responsible for multidrug resistance (MDR), a proteomic approach was used to identify proteins that were expressed in different levels by the adriamycinresistant human gastric cancer cell line, SGC7901/ADR, and its parental cell line, SGC7901. Two-dimensional gel electrophoresis (2-DE) and image analysis was used to determine which protein spots were expressed in different levels by the two cell lines. These spots were then partially identified using ESI-Q-TOF mass spectrometry, and the differential expressional levels of the partially identified proteins were then determined by western blot analysis and real-time RT-PCR. Additionally, the association of Nucleophosmin (NPM1), a protein that was highly expressed by SGC7901/ADR, with MDR was analyzed using siRNA. As a result of this study, well-resolved, reproducible 2-DE patterns of SGC7901/ADR and SGC7901 were established, and 16 proteins that may playa role in the development of thermo resistance were identified. Additionally, suppression of NPMl expression was found to enhance adriamycin chemosensitivity in SGC7901/ADR. These results provide a fundamental basis for the elucidation of the molecular mechanism of MDR, which may assist in the treatment of gastric cancer.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.12
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• pp.6435-6439
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• 2012

Chemoresistance to cancer therapy is a major obstacle to the effective treatment of human cancers with cisplatin (DDP), but the mechanisms of cisplatin-resistance are not clear. In this study, we established a cisplatin-resistant human ovarian cancer cell line (COC1/DDP) and identified differentially expressed proteins related to cisplatin resistance. The proteomic expression profiles in COC1 before and after DDP treatment were examined using 2-dimensional electrophoresis technology. Differentially expressed proteins were identified using matrix-assisted laser desorption/ ionization time-of-flight mass spectrometry (MALDI-TOF-MS) and high performance liquid chromatography-electrospray tandem MS (NanoUPLC-ESI-MS/MS). 5 protein spots, for cytokeratin 9, keratin 1, deoxyuridine triphosphatase (dUTPase), aarF domain containing kinase 4 (ADCK 4) and cofilin1, were identified to be significantly changed in COC1/DDP compared with its parental cells. The expression of these five proteins was further validated by quantitative PCR and Western blotting, confirming the results of proteomic analysis. Further research on these proteins may help to identify novel resistant biomarkers or reveal the mechanism of cisplatin-resistance in human ovarian cancers.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.8
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• pp.3517-3522
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• 2015

Background: Glucose regulated protein 78 (GRP78) is a type of molecular chaperone. It is a possible candidate protein that contributes to development of drug resistance. We first examined the involvement of GRP78 in chemotherapy-resistance in human ovarian cancer cell. Materials and Methods: The expression of GRP78 mRNA and protein were examined by RT-PCR and western blotting, respectively, in human ovarian cancer cells line (HO-8910). Sensitivity of HO-8910 to paclitaxel was determined with methyl thiazolyl tetrazolium (MTT). Suppression of GRP78 expression was performed using specific small-interfering RNA (siRNA) in HO-8910 cells, and cell apoptosis was assessed by flow cytometry. Statistical analysis was performed using the SPSS 15.0 statistical package. Results: HO-8910 cells, with high basal levels of GRP78, exhibited low sensitivity to paclitaxel. The mRNA and protein levels of GRP78 were dramatically decreased at 24h, 48h and 72h after transfection and the sensitivity to paclitaxel was increased when the GRP78 gene was disturbed by specific siRNA transfection. Conclusions: The results suggested that high GRP78 expression might be one of the molecular mechanisms causing resistance to paclitaxel, and therefore siRNA of GRP78 may be useful in tumor-specific gene therapy for ovarian cancer.