• Title/Summary/Keyword: risk expression

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Acute Oral Toxicity of dsRNA to Honey Bee, Apis mellifera (꿀벌에 대한 dsRNA의 급성섭식독성 평가)

  • Lim, Hye Song;Jung, Young Jun;Kim, Il Ryong;Kim, Jin;Ryu, Sungmin;Kim, Banni;Lee, Jung Ro;Choi, Wonkyun
    • Korean Journal of Environmental Agriculture
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    • v.36 no.4
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    • pp.241-248
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    • 2017
  • BACKGROUND: RNA interference (RNAi) eliminates or decreases gene expression by disrupting the target mRNA or by interfering with translation. Recently, RNAi technique was applied to generate new crop traits which provide protection against pests. To establish the environmental risk assessment protocol of RNAi LMO in lab scale, we developed dsRNA expression system using E. coli and tested acute oral toxicity assay to honey. METHOD AND RESULTS: The dsRNA expression vector, L4440, was chosen and cloned 240 bp of Snf7 and GFP gene fragment. To develop the maximum dsRNA induction condition in E. coli, we tested induction time, temperature and IPTG concentration in media. To estimate the risk assessment of dsRNA to honey bee, it has been selected and cultured with dsRNA supplement for 48 hours according to OECD guideline. As a result, the optimum condition of dsRNA induction was $37^{\circ}C$, 4 hours and 0.4 mM IPTG concentration and the difference between Snf7 and GFP dsRNA molecules from E. coli was not significant in survival and behavior to honey bee. Furthermore, blast search results indicated that effective match of predicted dsRNA fragments were not existed in honey bee genome. CONCLUSION: In this study, we developed and tested the acute oral toxicity of dsRNA using E. coli expression system to honey bee.

Effects of different cardiorespiratory fitness response to exercise training on cardiovascular disease and adipocytokine in abdominal obesity women (운동 트레이닝을 통한 심폐체력 반응의 차이가 복부비만 여성의 심혈관계 위험요인과 아디포싸이토카인에 미치는 영향)

  • Park, S.H.
    • Exercise Science
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    • v.21 no.1
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    • pp.111-120
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    • 2012
  • The purpose of the study was to assess the effects of different cardiorespiratory fitness response to exercise training on cardiovascular disease and adipocytokine release and gene expression in abdominal obesity women. forty eight middle-age women were divided to a exercise-responder (n=34) group (ERG) and a exercise-nonresponder (n=14) group (ENRG) based on cardiorespiratory fitness after exercise training (12weeks, 1200 kcal/week, moderate-vigorous intensity, walking and jogging). Cardiorespiratory fitness was measured using maximal oxygen uptake with metabolic gas analysis and body composition was determined by bioelectrical impedance. We measured lipid and glucose profiles, blood adipocytokines and adipocytokine genes expression in adipose tissue. Waist girth (p=0.040), and %body fat (p=0.031) were significantly decreased in ERG than ENRG. Triglyceride (p=0.023) and systolic blood pressure (0.046) were significantly decreased in ERG than ENRG. Blood leptin (p=0.022) was significantly decrease in ERG than ENRG but leptin gene expression was decreased both groups (p<0.001). These results show that exercise-responder group improved cardiovascular disease risk factors and adipocytokine more than exercise-nonresponder group after exercise training. Moreover, exercise-nonresponders group show that obese indices and blood leptin and leptin gene expression in adipose tissue were decreased despite the failure to improve fitness. Therefore, regular exercise training seems to give health benefits although the failure to improve fitness.

Association of DNA Base-excision Repair XRCC1, OGG1 and APE1 Gene Polymorphisms with Nasopharyngeal Carcinoma Susceptibility in a Chinese Population

  • Li, Qing;Wang, Jian-Min;Peng, Yu;Zhang, Shi-Heng;Ren, Tao;Luo, Hao;Cheng, Yi;Wang, Dong
    • Asian Pacific Journal of Cancer Prevention
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    • v.14 no.9
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    • pp.5145-5151
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    • 2013
  • Background: Numerous carcinogens and reactive oxygen species (ROS) may cause DNA damage including oxidative base lesions that lead to risk of nasopharyngeal carcinoma. Genetic susceptibility has been reported to play a key role in the development of this disease. The base excision repair (BER) pathway can effectively remove oxidative lesions, maintaining genomic stability and normal expression, with X-ray repair crosscomplementing1 (XRCC1), 8-oxoguanine glycosylase-1 (OGG1) and apurinic/apyimidinic endonuclease 1 (APE1) playing important roles. Aims: To analyze polymorphisms of DNA BER genes (OOG1, XRCC1 and APE1) and explore their associations, and the combined effects of these variants, with risk of nasopharyngeal carcinoma. Materials and Methods: We detected SNPs of XRCC1 (Arg399Gln), OGG1 (Ser326Cys), APE1 (Asp148Glu and -141T/G) using the polymerase chain reaction (PCR) with peripheral blood samples from 231 patients with NPC and 300 healthy people, furtherly analyzing their relations with the risk of NPC in multivariate logistic regression models. Results: After adjustment for sex and age, individuals with the XRCC1 399Gln/Gln (OR=1.96; 95%CI:1.02-3.78; p=0.04) and Arg/Gln (OR=1.87; 95%CI:1.29-2.71; p=0.001) genotype variants demonstrated a significantly increased risk of nasopharyngeal carcinoma compared with those having the wild-type Arg/Arg genotype. APE1-141G/G was associated with a significantly reduced risk of NPC (OR=0.40;95%CI:0.18-0.89) in the smoking group. The OR calculated for the combination of XRCC1 399Gln and APE1 148Gln, two homozygous variants, was significantly additive for all cases (OR=2.09; 95% CI: 1.27-3.47; p=0.004). Conclusion: This is the first study to focus on the association between DNA base-excision repair genes (XRCC1, OGG1 and APE1) polymorphism and NPC risk. The XRCC1 Arg399Gln variant genotype is associated with an increased risk of NPC. APE1-141G/G may decrease risk of NPC in current smokers. The combined effects of polymorphisms within BER genes of XRCC1 399Gln and APE1 148Gln may contribute to a high risk of nasopharyngeal carcinoma.

Person-Situation Benefit Segments of the Female Apparel Market in Seoul by a Prior Segmentation Method Benefit Soughts of Clothing, Perceived Risk, Importanc of Store Attribute, Store-Type Choice - (상황과 인규통계적 특성을 사전적 모형으로 연계시킨 혜택세분화 연구 -추구혜택, 지각된 위험, 상점 속성의 중요도 및 상점 선택 행동에 대한 상호작용효과를 중심으로-)

  • 홍희숙
    • Journal of the Korean Society of Clothing and Textiles
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    • v.20 no.6
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    • pp.1151-1165
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    • 1996
  • The purpose of this study was to identify the pratical applicability of person-situation benefit segmentations of the female apparel market in Seoul by a prior segmentation method. The specific objectives of this study were 1) to identify the useful demographic variables for person-situation benefit segmentations of the female apparel market, 2) to assess that person- situation benefit segmentations of 1.he female apparel market are accessit)le by developing a profile of each segment based on the interactions of situation and personal characteristics on perceived risk, importance of store attributes and store-type choice, and on brand type prefered by each segment. 3) to assess the validity of person-situation benefit segmentations of the female apparel market in terms of easy accessibility. The data were collected via a questionnaire from 601 housewives of ages 20's to 50's living in Seoul, Korea. The data were analyzed by factor analysis, repeated measure two- way ANOVA and X2-test. The results of this study were as follows. First, the age-by-situation segmention basis and the education-by-situation segmention basis were useful for person-situation benefit segmentations of the female apparel market. Second, there were found three benefit segments (Youth/Fashion oriented users, Brand oriented users and Apathetic users of clothing) using age-by-situation segmention basis. Using education-by-situation segmention basis, five segments (Economic-value, Youth/Fashion, Brand/Self-expression Self-expression, and Apathetic users of clothing) were identified. And beifit segments classified by the age-by-situation segmention and education-by-situation segmention approach were accessible. Third, the pratical applicability of person-situation befeift segmentations of the female apparel market by a prior segmentation method were suggested.

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Associations between Single Nucleotide Polymorphisms of COX-2 and MMP-2 Genes and Colorectal Cancer Susceptibility in the Saudi Population

  • Shalaby, Manal Ali;Nounou, Howaida Attia;Alanazi, Mohammad Saud;Alharby, Othman;Azzam, Nahla;Saeed, Hesham Mahmoud
    • Asian Pacific Journal of Cancer Prevention
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    • v.15 no.12
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    • pp.4989-4994
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    • 2014
  • Background: It has been reported that COX-2 expression is associated with MMP-2 expression in thyroid and breast cancers, suggesting that MMPs are linked to COX-2-mediated carcinogenesis. Several polymorphisms within the MMP2 promoter region have been reported in cases with oncogenesis and tumor progression, especially in colorectal carcinogenesis. Materials and Methods: This research evaluated risk of association of the SNPs, including genes for COX-2 (AIG transition at +202) and MMP-2 (Crr transition at-1306), with colorectal cancer in 125 patients and 125 healthy controls. Results and Conclusions: Our data confirmed that MMP2 C-1306 T mutations were significantly more common in colon cancer patients than in our control Saudi population; p=O.0121. On the other hand in our study, there was no significant association between genotype distribution ofthe COX2 polymorphism and colorectal cancer; p=0.847. An elevated frequency ofthe mutated genotype in the control group as compared to the patients subjects indeed suggested that this polymorphism could decrease risk in the Saudi population. Our study confirmed that the polymorphisms that could affect the expressions of MMP-2 and COX-2 the colon cancer patients were significantly higher than that in the COX-2 negative group. The frequency of individuals with MMP2 polymorphisms in colon cancer patients was higher than individuals with combination of COX2 and MMP2 polymorphisms. Our study confirmed that individuals who carried the polymorphisms that could affect the expressions ofCOX2 are more susceptible to colon cancer. MMP2 regulatory polymorphisms could be considered as protective; further studies need to confirm the results with more samples and healthy subjects.

Roles of Combined Glypican-3 and Glutamine Synthetase in Differential Diagnosis of Hepatocellular Lesions

  • Wasfy, Rania Elsayed;Eldeen, Aliaa Atef Shams
    • Asian Pacific Journal of Cancer Prevention
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    • v.16 no.11
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    • pp.4769-4775
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    • 2015
  • Background: Hepatocellular carcinoma (HCC) is the fifth most prevalent cancer and thirdly leading cause of cancer-related death worldwide. The estimated risk of hepatocellular carcinoma is 15 to 20 times as high among persons infected with HCV as it is among those who are not infected, with most of the excess risk limited to those with advanced hepatic fibrosis or cirrhosis. Glypican3 (GPC3) plays a key role in relation to signaling with growth factors, regulating the proliferative activity of cancer cells. Glutamine synthetase (GS) catalyzes the synthesis of glutamine from glutamate and ammonia in the mammalian liver. GS was suggested as a specific marker for tracing cell lineage relationships during hepatocarcinogenesis. In normal liver, GS expression is seen in pericentral hepatocytes, but not by midzonal or periportal hepatocytes. In HCC, strong and diffuse GS expression in seen in tumor cells. Results: Glypican3 immunopositvity was highly specific and sensitive indicator for hepatocellular carcinoma as well as glutamine synthetase which was found to be a sensitive and specific indicator for development of hepatocellular carcinoma when compared to cirrhosis, liver cell dyspalsia and metastatic carcinomas. Statistical analysis revealed a significant association between GPC3 and GS with tumor size (P=0.003, p=0.006, respectively). Diffuse staining significantly associated with large tumor size while, focal and mixed staining was detected more with small tumor size. Studying the relation with tumor grade also revealed significant association between diffuse GPC3 and GS staining with high tumor grade. Diffuse staining was detected in 91.7% and 100% respectively of poorly differentiated specimens and only in 33.3% and 22.2% of well differentiated specimens. Conclusions: While using GPC3 and GS to screen for premalignant hepatic lesions remains controversial, our data suggest that GPC3 and GS may be a reliable diagnostic immunomarkers to distinguish HCC from benign hepatocellular lesions. However, negative immunostaining should not exclude the diagnosis of HCC.

rs12904 Polymorphism in the 3'UTR of EFNA1 is Associated with Colorectal Cancer Susceptibility in a Chinese Population

  • Mao, Ying-Ying;Jing, Fang-Yuan;Jin, Ming-Juan;Li, Ying-Jun;Ding, Ye;Guo, Jing;Wang, Fen-Juan;Jiang, Long-Fang;Chen, Kun
    • Asian Pacific Journal of Cancer Prevention
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    • v.14 no.9
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    • pp.5037-5041
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    • 2013
  • Accumulated evidence has indicated that Ephrin A1 (EFNA1) is associated with angiogenesis and tumorigenesis in various types of malignancies, including colorectal cancer (CRC). In the current study, we performed an online search using the public microarray database to investigate whether EFNA1 expression might be altered in CRC tissues. We then conducted a case-control study including 306 subjects (102 cases and 204 well-matched controls) in Xiaoshan County to assess any association between genetic polymorphisms in EFNA1 and CRC susceptibility. Searches in the Oncomine expression profiling database revealed EFNA1 to be overexpressed in CRC tissue compared with adjacent normal tissue. The rs12904 G-A variant located in the 3' untranslated region (UTR) of EFNA1 was observed to be associated with CRC susceptibility. Compared with the AA homozygous genotype, those carrying GA genotype had a decreased risk of developing CRC (odds ratio (OR)=0.469, 95% confidence interval (CI): 0.225-0.977, and P=0.043). The association was stronger among smokers and tea drinkers, however, no statistical evidence of interaction between rs12904 polymorphism and smoking or tea drinking on CRC risk was found. Our results suggest that EFNA1 is involved in colorectal tumorigenesis, and rs12904 A>G polymorphism in the 3' UTR of EFNA1 is associated with CRC susceptibility. Larger studies and further mechanistic investigations are warranted to confirm our findings.

Genome-Wide Association Study of Metabolic Syndrome in Koreans

  • Jeong, Seok Won;Chung, Myungguen;Park, Soo-Jung;Cho, Seong Beom;Hong, Kyung-Won
    • Genomics & Informatics
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    • v.12 no.4
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    • pp.187-194
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    • 2014
  • Metabolic syndrome (METS) is a disorder of energy utilization and storage and increases the risk of developing cardiovascular disease and diabetes. To identify the genetic risk factors of METS, we carried out a genome-wide association study (GWAS) for 2,657 cases and 5,917 controls in Korean populations. As a result, we could identify 2 single nucleotide polymorphisms (SNPs) with genome-wide significance level p-values (< $5{\times}10^{-8}$), 8 SNPs with genome-wide suggestive p-values ($5{\times}10^{-8}{\leq}$ p < $1{\times}10^{-5}$), and 2 SNPs of more functional variants with borderline p-values ($5{\times}10^{-5}{\leq}$ p < $1{\times}10^{-4}$). On the other hand, the multiple correction criteria of conventional GWASs exclude false-positive loci, but simultaneously, they discard many true-positive loci. To reconsider the discarded true-positive loci, we attempted to include the functional variants (nonsynonymous SNPs [nsSNPs] and expression quantitative trait loci [eQTL]) among the top 5,000 SNPs based on the proportion of phenotypic variance explained by genotypic variance. In total, 159 eQTLs and 18 nsSNPs were presented in the top 5,000 SNPs. Although they should be replicated in other independent populations, 6 eQTLs and 2 nsSNP loci were located in the molecular pathways of LPL, APOA5, and CHRM2, which were the significant or suggestive loci in the METS GWAS. Conclusively, our approach using the conventional GWAS, reconsidering functional variants and pathway-based interpretation, suggests a useful method to understand the GWAS results of complex traits and can be expanded in other genomewide association studies.

Hormone Receptor, HER2/NEU and EGFR Expression in Ovarian Carcinoma - is here a Prognostic Phenotype?

  • Demir, Lutfiye;Yigit, Seyran;Sadullahoglu, Canan;Akyol, Murat;Cokmert, Suna;Kucukzeybek, Yuksel;Alacacioglu, Ahmet;Cakalagaoglu, Fulya;Tarhan, Mustafa Oktay
    • Asian Pacific Journal of Cancer Prevention
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    • v.15 no.22
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    • pp.9739-9745
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    • 2014
  • Purpose: We aimed to evaluate the effects of hormone receptor, HER2, and epidermal growth factor receptor (EGFR) expression on epithelial ovarian cancer (EOC) prognosis and investigate whether or not phenotypic subtypes might exist. Materials and Methods: The medical records of 82 patients who were diagnosed with EOC between 2003 and 2012 and treated by platinum-based chemotherapy were retrospectively evaluated. Expression of EGFR, oestrogen (ER), progesterone (PR), and cerbB2 (HER2) receptors were assessed immunohistochemically on paraffin-embedded tissues of these patients. Three phenotypic subtypes were defined according to ER, PR, and HER2 expression and associations of these with EGFR expression, clinicopathologic features, platinum sensitivity, and survival were investigated. Results: When we classified EOC patients into three subtypes, 63.4% had hormone receptor positive (HR(+)) (considering breast cancer subtypes, luminal A), 18.3% had triple negative, and 18.3% had HER2(+) disease. EGFR positivity was observed in 37 patients (45.1%) and was significantly more frequent with advanced disease (p=0.013). However, no significant association with other clinicopathologic features and platinum sensitivity was observed. HER2(+) patients had significantly poorer outcomes than HER2(-) counterparts (triple negative and HR positive patients) (p=0.019). Multivariate analysis demonstrated that the strongest risk factor for death was residual disease after primary surgery. Conclusions: Triple negative EOC may not be an aggressive phenotype as in breast cancer. The HER2 positive EOC has more aggressive behaviour compared to triple negative and HR(+) phenotypes. EGFR expression is more frequent in advanced tumours, but is not related with poorer outcome. Additional ovarian cancer molecular subtyping using gene expression analysis may provide more reliable data.

High-fat diet alters the thermogenic gene expression to β-agonists or 18-carbon fatty acids in adipocytes derived from the white and brown adipose tissue of mice

  • Seonjeong Park;Seung A Ock;Yun Jeong Park;Yoo-Hyun Lee;Chan Yoon Park;Sunhye Shin
    • Journal of Nutrition and Health
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    • v.57 no.2
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    • pp.171-184
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    • 2024
  • Purpose: Although activating thermogenic adipocytes is a promising strategy to reduce the risk of obesity and related metabolic disorders, emerging evidence suggests that it is difficult to induce adipocyte thermogenesis in obesity. Therefore, this study aimed to investigate the regulation of adipocyte thermogenesis in diet-induced obesity. Methods: Adipose progenitor cells were isolated from the white and brown adipose tissues of control diet (CD) or high-fat diet (HFD) fed mice, and fully differentiated white and brown adipocytes were treated with β-agonists or 18-carbon fatty acids for β-adrenergic activation or peroxisome proliferator-activated receptor (PPAR) activation. Results: Compared to the CD-fed mice, the expression of uncoupling protein 1 (Ucp1) was lower in the white adipose tissue of the HFD-fed mice; however, this was not observed in the brown adipose tissue. The expression of peroxisome proliferator-activated receptor gamma (Pparg) was lower in the brown adipose progenitor cells isolated from HFD-fed mice than in those isolated from the CD-fed mice. Norepinephrine (NE) treatment exerted lesser effect on peroxisome proliferator-activated receptor-γ coactivator (Pgc1a) upregulation in white adipocytes derived from HFD-fed mice than those derived from CD-fed mice. Regardless which 18-carbon fatty acids were treated, the expression levels of thermogenic genes including Ucp1, Pgc1a, and positive regulatory domain zinc finger region protein 16 (Prdm16) were higher in the white adipocytes derived from HFD-fed mice. Oleic acid (OLA) and γ-linolenic acid (GLA) upregulated Pgc1a expression in white adipocytes derived from HFD-fed mice. Brown adipocytes derived from HFD-fed mice had higher expression levels of Pgc1a and Prdm16 compared to their counterparts. Conclusion: These results indicate that diet-induced obesity may downregulate brown adipogenesis and NE-induced thermogenesis in white adipocytes. Also, HFD feeding may induce thermogenic gene expression in white and brown primary adipocytes, and OLA and GLA could augment the expression levels.