• Asian Pacific Journal of Cancer Prevention
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• v.16 no.18
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• pp.8041-8045
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• 2016

Cervical cancer is one of the most common cancers in women worldwide. During their life time the vast majority of women become infected with human papillomavirus (HPV), but interestingly only a small portion develop cervical cancer and in the remainder infection regresses to a normal healthy state. Beyond HPV status, associated molecular characterization of disease has to be established. However, initial work suggests the existence of several different molecular classes, based on the biological features of differentially expressed genes in each subtype. This suggests that additional risk factors play an important role in the outcome of infection. Host genomic factors play an important role in the outcome of such complex or multifactor diseases such as cervical cancer and are also known to regulate the rate of disease progression. The aim of this review was to compile advances in the field of host genomics of HPV positive and negative cervical cancer and their association with clinical response.

• Proceedings of the Korean Society of Plant Biotechnology Conference
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• 2005.11a
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• pp.367-370
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• 2005

The risk from genetically modified (GM) plants results from the possibility of gene contamination producing adverse effects on biological diversity by introducing herbicide or insect resistance into related plants or weeds (NAS 2002). The concern about the leakage of genes from GM plants into the environment has primarily focused on pollen that could be wind-borne for long distances. During the period of fisk assessment in Japan, physical containment is applied as a measure of reducing gene flow via the dispersal of pollen from GM plants into the surrounding environment In this study, we tried to estimate the effect of physically contained greenhouse covered by 1-mm fine mesh to reduce pollen dispersal by researching cross pollination rate between non-GM yellow maize in a greenhouse and silver maize outside the greenhouse.

• Toxicological Research
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• v.31 no.1
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• pp.1-9
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• 2015

Environmental toxicants such as toxic metals can alter epigenetic regulatory features such as DNA methylation, histone modification, and non-coding RNA expression. Heavy metals influence gene expression by epigenetic mechanisms and by directly binding to various metal response elements in the target gene promoters. Given the role of epigenetic alterations in regulating genes, there is potential for the integration of toxic metal-induced epigenetic alterations as informative factors in the risk assessment process. Here, we focus on recent advances in understanding epigenetic changes, gene expression, and biological effects induced by toxic metals.

• YAKHAK HOEJI
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• v.52 no.3
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• pp.212-218
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• 2008

Manganese is a naturally occurring element which is widespread in the environment. Also, manganese is an essential trace element and plays a key role in important biological reactions catalyzed by enzymes. However, exposure to high levels of manganese can cause toxicity in neurone and inhalation system, also damage in various tissues. We investigated the toxicity induced by manganese compound ($MnCl_2$) in cultured rat cardiomyocytes. Treatment of manganese to cultured cardiomyocyte led to cell death, reactive oxygen species (ROS) increase, and cytosolic caspase-3 activation. The ROS increase was related with the decreased level of glutathione. Expressions of ROS related genes such as heme oxygenase-1, thioredoxin reductase, and NADH quinone oxidase were significantly induced in manganese treated cells. These results suggest that manganese induce oxidative stress and apoptosis in cardiomyocytes, and may be the one of risk factors to cause heart dysfunction in vivo.

• Genomics & Informatics
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• v.8 no.1
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• pp.41-49
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• 2010

Statins are competitive inhibitors of hydroxy-3-methyl glutaryl coenzyme A (HMG-CoA) reductase and used most frequently to reduce plasma cholesterol levels and to decrease cardiovascular events. However, statins also have been reported to have undesirable side effects such as myotoxicity and hepatotoxicity associated with their intrinsic efficacy mechanisms. Clinical studies recurrently reported that statin therapy elevated the level of liver enzymes such as ALT and AST in patients suggesting possible liver toxicity due to statins. This observation has been drawn great attention since statins are the most prescribed drugs and statin-therapy was extended to a larger number of high-risk patients. Here we employed rat primary hepatocytes and microarray technique to understand underlying mechanism responsible for statin-induced liver toxicity on cell level. We isolated genes whose expressions were commonly modulated by statin treatments and examined their biological functions. It is of interest that those genes have function related to response to stress in particular immunity and defense in cells. Our study provided the basic information on cellular mechanism of statin-induced cytotoxicity and may serve for finding indicator genes of statin -induced toxicity in rat primary hepatocytes.

• Asian-Australasian Journal of Animal Sciences
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• v.22 no.9
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• pp.1341-1350
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• 2009

Dietary lipids are rapidly hydrolysed and biohydrogenated in the rumen resulting in meat and milk characterised by a high content of saturated fatty acids and low polyunsaturated fatty acids (PUFA), which contributes to increases in the risk of diseases including cardiovascular disease and cancer. There has been considerable interest in altering the fatty acid composition of ruminant products with the overall aim of improving the long-term health of consumers. Metabolism of dietary lipids in the rumen (lipolysis and biohydrogenation) is a major critical control point in determining the fatty acid composition of ruminant lipids. Our understanding of the pathways involved and metabolically important intermediates has advanced considerably in recent years. Advances in molecular microbial technology based on 16S rRNA genes have helped to further advance our knowledge of the key organisms responsible for ruminal lipid transformation. Attention has focused on ruminal biohydrogenation of lipids in forages, plant oils and oilseeds, fish oil, marine algae and fat supplements as important dietary strategies which impact on fatty acid composition of ruminant lipids. Forages, such as grass and legumes, are rich in omega-3 PUFA and are a useful natural strategy in improving nutritional value of ruminant products. Specifically this review targets two key areas in relation to forages: i) what is the fate of the lipid-rich plant chloroplast in the rumen and ii) the role of the enzyme polyphenol oxidase in red clover as a natural plant-based protection mechanism of dietary lipids in the rumen. The review also addresses major pathways and micro-organisms involved in lipolysis and biohydrogenation.

• Environmental Analysis Health and Toxicology
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• v.21 no.1 s.52
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• pp.71-79
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• 2006

Epidemiologic studies have showed a close correlation between arsenic exposure and heart disease such as, cardiovascular problem, ischemic heart disease, infarction, atherosclerosis and hypertension in human. It may increase the mortality of high risk group with heart disease. Regarding the mechanism studies of heart failure, blood vessel, vascular smooth muscle cells and endothelial cells have long been focused as the primary targets in arsenic exposure but there are only a few studies on the cardiomyocytes. In this study, the generation of oxidative stress by low dose of arsenic trioxide was investigated in rat cardiomyocytes. By direct measurement of reactive oxygen species and fluorescent microscopic observation using fluorescent dye 2',7'-dichlorofluorescin diacetate, reactive oxygen species were found to be generated without cell death, where cells are treated with 0.1 ppm arsenic for 24 hours. With the induction of reactive oxygen species, GSH level was decreased by the same treatment. However, DNA damage did not seem to be serious by DAPI staining, while high dose of arsenic (2 ppm for 24 hrs) caused fragmentation of DNA. To identify the molecular biomarkers of low-dose arsenic exposure, gene expression was also investigated with whole genome microarray. As results, 9,022 genes were up-regulated including heme oxygenase-l and glutathione S-transrerase, which are well-known biomarkers of oxidative stress. 9,404 genes were down-regulated including endothelial type gp 91-phox gene by the treatment of 0.1 ppm arsenic for 24 hours. This means that biological responses of cardiomyocytes may be altered by ROS induced by low level arsenic without cell death, and this alteration may be detected clearly by molecular biomarkers such as heme oxygenase-1.

• Asian Pacific Journal of Cancer Prevention
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• v.17 no.5
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• pp.2491-2497
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• 2016

Background: Human leukocyte antigen (HLA) genes have been implicated in cervical cancer in several populations. Objectives: To study the predispositions of HLA alleles/haplotypes with cervical cancer. Materials and Methods: Clinically diagnosed and PAP smear confirmed cervical cancer patients (n 48) and age matched controls (n 47) were genotyped for HLA-A,-B,-DRB1* and DQB1* alleles by PCR-SSP methods. Results: The frequencies of alleles DRB1*04 (OR=2.57), DRB1*15 (OR=2.04), DQB1*0301 (OR=4.91), DQB1*0601 (OR=2.21), B*15 (OR=13.03) and B*07 (OR=6.23) were higher in cervical cancer patients than in the controls. The frequencies of alleles DRB1*10 (OR=0.22) and B*35 (OR=0.19) were decreased. Strong disease associations were observed for haplotypes DRB1*15-DQB1*0601 (OR=6.56; p< $3.5{\times}10^{-4}$), DRB1*14-DQB1*0501 (OR=6.51; p<0.039) and A*11-B*07 (OR=3.95; p<0.005). The reduced frequencies of haplotypes DRB1*10-DQB1*0501 (OR=0.45), A*03-B*35 (OR=0.25) and A*11-B*35 (OR= 0.06) among patients suggested a protective association. HLA-C* typing of 8 patients who possessed a unique three locus haplotype 'A*11-B*07-DRB1*04' (8/48; 16.66%; OR=6.51; p<0.039) revealed the presence of a four locus haplotype 'A*11-B*07-C*01-DRB1*04' in patients (4/8; 50%). Amino acid variation analysis of susceptible allele DQB1*0601 suggested 'tyrosine' at positions ${\beta}9$ and ${\beta}37$ and tyrosine-non-tyrosine genotype combination increased the risk of cervical cancer. Conclusions: Strong susceptible associations were documented for HLA alleles B*15, B*07, DRB1*04, DRB1*15, DQB1*0301, DQB1*0601 and haplotypes DRB1*15-DQB1*0601 and DRB1*14-DQB1*0501. Further, protective associations were evidenced for alleles B*35 and DRB1*10 and haplotypes A*11-B*35 and DRB1*10-DQB1*0501 with cervical cancer in South India.

• Journal of Microbiology and Biotechnology
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• v.27 no.3
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• pp.417-428
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• 2017

Diseases caused by foodborne or waterborne pathogens are emerging. Many pathogens can enter into the viable but nonculturable (VBNC) state, which is a survival strategy when exposed to harsh environmental stresses. Pathogens in the VBNC state have the ability to evade conventional microbiological detection methods, posing a significant and potential health risk. Therefore, controlling VBNC bacteria in food processing and the environment is of great importance. As the typical one of the gram-negatives, Escherichia coli (E. coli) is a widespread foodborne and waterborne pathogenic bacterium and is able to enter into a VBNC state in extreme conditions (similar to the other gram-negative bacteria), including inducing factors and resuscitation stimulus. VBNC E. coli has the ability to recover both culturability and pathogenicity, which may bring potential health risk. This review describes the concrete factors (nonthermal treatment, chemical agents, and environmental factors) that induce E. coli into the VBNC state, the condition or stimulus required for resuscitation of VBNC E. coli, and the methods for detecting VBNC E. coli. Furthermore, the mechanism of genes and proteins involved in the VBNC E. coli is also discussed in this review.

• Korean Journal of Biological Psychiatry
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• v.8 no.1
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• pp.62-70
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• 2001

Alzheimer's disease(AD) is associated with a characteristic neuropathology. The major hallmarks of AD are senile plaques (SPs) and neurofibrillary tangles(NFTs). ${\beta}$-amyloid protein($A{\beta}$) is derived from the proteolysis of amyloid precursor protein(APP) and then converted to SPs. Mature SPs produce cytotoxicity through direct toxic effects and activation of microglia and complement. NFTs are composed of paired helical filaments(PHFs) including abnormally phosphorylated form of the microtubule-associated protein(MAP) tau and increased tau level in cerebrospinal fluid may be observed in most AD. The aggregation of $A{\beta}$ and tau formation are thought to be a final common pathway of AD. Acetylcholine, dopamine, serotonin, GABA and their receptors are associated with AD. Especially, decreased nicotinic acetylcholine receptors(nAChRs) in AD are reported. Genetic lesions associated with AD are mutations in the structural genes for the APP located on chromosome 21, presenilin(PSN)1 located on chromosome 14 and PSN2 located on chromosome 1. Also, trisomy 21, Apo-E gene located on chromosome 19, PMF locus, low density lipoprotein receptor-related protein and ${\alpha}$-macroglobulin increase risk of AD. In this article, we will review about the neurobiology of AD and some newly developed research areas.