• Journal of Nutrition and Health
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• v.46 no.6
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• pp.511-520
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• 2013

Monocyte chemoattractant protein-1 (MCP-1) plays an important role in cardiovascular disease (CVD). Genetic polymorphism in the regulatory regions of MCP-1 could affect MCP-1 expression. The purpose of the study was to explore the possible association of MCP-1 -2518 A/G genetic polymorphism and CVD risk factors in the elderly Korean population. Dietary, anthropometric, and biochemical factors were assessed in 168 subjects. The frequency of A/A, G/A, and G/G genotypes was 14.2%, 45.8%, and 40.0%, respectively. The blood level of MCP-1 was significantly higher in subjects with A/A genotype. The MCP-1 level was significantly higher in A/A genotype with hypercholesterolemia than in other genotypes. Meat intake and percent energy from lipids were significantly positively correlated with the MCP-1 level, especially, stronger in A/A genotype. In the stepwise discriminant analysis, TNF-${\alpha}$ level, meat intake, HDL-C were associated with MCP-1 in all subjects (model $R^2=24%$). TNF-${\alpha}$ level, sugar intake, cholesterol intake, and meat intake affected MCP-1 in A/A genotype (model $R^2=82%$), but not in G/A or G/G. In conclusion, subjects possessing A/A genotype exhibited higher levels of MCP-1 than other genotypes in Korean elders. Further, meat, sugar, and cholesterol intakes affected the MCP-1 level. Therefore, the decrement of meat, sugar, and cholesterol intakes helps to normalize the MCP-1 level and can decrease CVD risk in A/A genotype.

• The Journal of Korean Obstetrics and Gynecology
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• v.25 no.4
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• pp.46-55
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• 2012

Objectives: It is well known that genetic factors and environmental factors play major role in aging skin. In general, son and daughter take after their parents in appearance. But comparability of skin properties in Korean family has not been well estimated. So we evaluated the correlation of skin properties in Korean mother-daughter pairs. Methods: 10 couples of mother and daughter pair(n=20) participate in this study. Mothers and daughters were aged $50.6{\pm}2.459$ and $23.8{\pm}2.15$ years, respectively. Skin moisture, sebum, skin color and elasticity is measured using non-invasive method : Corneometer CM825, Sebumeter(MPA580), Mexameter MX18, Cutometer MPA580. Statistical analysis program we used is Minitab 14 Korea. Results: The Skin moisture of mother group was significantly higher than daughter group. And skin elasticity(R2) of the daughter group was significantly higher than mother group. In the results of correlation analysis between mother and daughter pairs, skin elasticity(R2) had high positive correlation(r=0.729, p=0.026). But skin moisture, sebum, melanin index, erythema index and skin elasticity(R5) did not be confirmed a significant correlation. Conclusions: Skin elasticity(R2) is the only factor that showed high positive correlation significantly in mother and daughter pairs. Mother and daughter share the genetic factors and environmental factors that influence skin aging. So, mother's aging pattern will be a good guide for anti-aging of daughters.

• BMB Reports
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• v.49 no.2
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• pp.111-115
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• 2016

Caffeine has been proposed to have several beneficial effects on obesity and its related metabolic diseases; however, how caffeine affects adipocyte differentiation has not been elucidated. In this study, we demonstrated that caffeine suppressed 3T3-L1 adipocyte differentiation and inhibited the expression of CCAAT/enhancer binding protein (C/EBP)α and peroxisome proliferator-activated receptor (PPAR)γ, two main adipogenic transcription factors. Anti-adipogenic markers, such as preadipocyte secreted factor (Pref)-1 and Krüppel-like factor 2, remained to be expressed in the presence of caffeine. Furthermore, 3T3-L1 cells failed to undergo typical mitotic clonal expansion in the presence of caffeine. Investigation of hormonal signaling revealed that caffeine inhibited the activation of AKT and glycogen synthase kinase (GSK) 3 in a dose-dependent manner, but not extracellular signal-regulated kinase (ERK). Our data show that caffeine is an anti-adipogenic bioactive compound involved in the modulation of mitotic clonal expansion during adipocyte differentiation through the AKT/GSK3 pathway.

• Journal of Korean Society of Forest Science
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• v.86 no.2
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• pp.167-176
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• 1997

Characteristics of leaf morphology and vegetation were examined in 6 populations of rare endemic tree species, Koelreuteria paniculata Laxm. Additionally we studied genetic variation employing isozyme marker. Nested anova showed that there were statistically significant differences among populations as well as among individuals within populations in all 8 leaf morphological traits. In 7 of 8 traits, variance components among populations were larger than those among individuals within populations. Only a few tree species were found within each population and all the populations seemed to have been disturbed by man. Level of genetic diversity for this rare endemic species was very low, especially compared with those of geographically widespread tree species(A/L=1.1, P=9.5%, $H_o=0.021$, $H_e=0.035$) and degree of genetic differentiation was high($F_{ST}=0.114$). Factors contributing to the low level of genetic diversity and high level of genetic differentiation might include genetic drift, inbreeding and limited gene flow. Finally, implications for the conservation of genetic diversity of Koelreuteria paniculata were discussed.

• The Plant Pathology Journal
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• v.31 no.3
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• pp.226-244
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• 2015

Fusarium head blight is one of the most important and most common diseases of winter wheat. In order to better understanding this disease and to assess the correlations between different factors, 30 cultivars of this cereal were evaluated in a two-year period. Fusarium head blight resistance was evaluated and the concentration of trichothecene mycotoxins was analysed. Grain samples originated from plants inoculated with Fusarium culmorum and naturally infected with Fusarium species. The genetic distance between the tested cultivars was determined and data were analysed using multivariate data analysis methods. Genetic dissimilarity of wheat cultivars ranged between 0.06 and 0.78. They were grouped into three distinct groups after cluster analysis of genetic distance. Wheat cultivars differed in resistance to spike and kernel infection and in resistance to spread of Fusarium within a spike (type II). Only B trichothecenes (deoxynivalenol, 3-acetyldeoxynivalenol and nivalenol) produced by F. culmorum in grain samples from inoculated plots were present. In control samples trichothecenes of groups A (H-2 toxin, T-2 toxin, T-2 tetraol, T-2 triol, scirpentriol, diacetoxyscirpenol) and B were detected. On the basis of Fusarium head blight assessment and analysis of trichothecene concentration in the grain relationships between morphological characters, Fusarium head blight resistance and mycotoxins in grain of wheat cultivars were examined. The results were used to create of matrices of distance between cultivars - for trichothecene concentration in inoculated and naturally infected grain as well as for FHB resistance Correlations between genetic distance versus resistance/mycotoxin profiles were calculated using the Mantel test. A highly significant correlation between genetic distance and mycotoxin distance was found for the samples inoculated with Fusarium culmorum. Significant but weak relationships were found between genetic distance matrix and FHB resistance or trichothecene concentration in naturally infected grain matrices.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.11
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• pp.4689-4695
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• 2014

Background: A great number of studies have shown that cytochrome P450 1A1 (CYP1A1) genetic polymorphisms, CYP1A1 Msp I and CYP1A1 Ile/Val, might be risk factors for digestive tract cancers, including esophageal cancer (EC), gastric cancer (GC), hepatic carcinoma (HC), as well as colorectal cancer (CC), but the results are controversial. In this study, a meta-analysis of this literature aimed to clarify associations of CYP1A1 genetic polymorphisms with digestive tract cancers susceptibility in Chinese populations. Materials and Methods: Eligible case-control studies published until December 2013 were retrieved by systematic literature searches from PubMed, Embase, CBM, CNKI and other Chinese databases by two investigators independently. The associated literature was acquired through deliberate search and selection based on established inclusion criteria. Fixed-effects or random-effects models were used to estimate odds ratios (ORs and 95%CIs). The meta-analysis was conducted using Review Manager 5.2 and Stata 12.0 softwares with stability evaluated by both stratified and sensitivity analyses. Moreover, sensitivity analysis and publication bias diagnostics confirmed the reliability and stability. Results: Eighteen case-control studies with 1,747 cases and 2,923 controls were selected for CYP1A1 MspI polymorphisms, and twenty case-control studies with 3, 790 cases and 4, 907 controls for the CYP1A1 Ile/Val polymorphisms. Correlation associations between CYP1A1 Ile/Val polymorphisms and digestive tract cancers susceptibility were observed in four genetic models in the meta-analysis (GG vs AA:OR= 2.03, 95%CI =1.52- 2.72; AG vs AA: OR=1.26, 95%CI =1.07-1.48; [GG+AG vs AA] :OR =1.42, 95%CI=1.20-1.68, [GG vs AA+AG]:OR=1.80, 95%CI =1.40-2.31). There was no association between CYP1A1 Msp I polymorphisms and digestive tract cancers risk. Subgroup analysis for tumor type showed a significant association of CYP1A1 Ile/Val genetic polymorphisms with EC in China. However, available data collected by the study failed to reveal remarkable associations of GC or HC with CYP1A1 Ile/Val genetic polymorphisms and EC, GC or CC with CYP1A1 MspI genetic polymorphisms. Conclusions: Our results indicated that CYP1A1 Ile/Val genetic polymorphisms, but not CYP1A1 Msp I polymorphisms, are associated with an increased digestive tract cancers risk in Chinese populations. Additional well-designed studies, with larger sample size, focusing on different ethnicities and cancer types are now warranted to validate this finding.

• Journal of Life Science
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• v.24 no.6
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• pp.612-617
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• 2014

The phenetic relationships among six natural populations of Equisetum pratense in Korea were investigated at the population level by constructing a tree based on Random Amplified Polymorphic DNA (RAPD) markers. RAPD analysis was also conducted to estimate genetic diversity and the population structure of E. pratense. A mean of 26.7% at the six population levels indicated polymorphism. E. pratense was found to have fewer alleles per locus (1.267) and fewer effective alleles per locus (1.176). Genetic diversity (0.102) in E. pratense is lower than the average for species with similar life history traits. Total genetic diversity values (HT) varied between 0.112 (OPD-07) and 0.445 (OPD-16), for an average overall polymorphic locus of 0.141. Inter-locus variation in the within-population genetic diversity ($H_S$) was low (0.102). Asexual reproduction, small population size, and the colonization process are proposed as possible factors contributing to the observed low genetic diversity in E. pratense. On a per-locus basis, the proportion of total genetic variation due to differences among populations ($G_{ST}$) ranged from 0.129 for OPD-07 to 0.455 for OPD-09, with a mean of 0.277. This indicated that about 27.7% of the total variation was among populations. Thus, genetic variation (72.3%) resided within populations. This study contributes new information for research on the taxonomy and population genetics of E. pratense.

• Journal of Ginseng Research
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• v.39 no.1
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• pp.61-68
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• 2015

Background: Korean Red Ginseng (KRG) is a representative traditional herbal medicine with many different pharmacological properties including anticancer, anti-atherosclerosis, anti-diabetes, and anti-inflammatory activities. Only a few studies have explored the molecular mechanism of KRG-mediated anti-inflammatory activity. Methods: We investigated the anti-inflammatory mechanisms of the protopanaxadiol saponin fraction (PPD-SF) of KRG using in vitro and in vivo inflammatory models. Results: PPD-SF dose-dependently diminished the release of inflammatory mediators [nitric oxide (NO), tumor necrosis factor-${\alpha}$, and prostaglandin $E_2$], and downregulated the mRNA expression of their corresponding genes (inducible NO synthase, tumor necrosis factor-${\alpha}$, and cyclooxygenase-2), without altering cell viability. The PPD-SF-mediated suppression of these events appeared to be regulated by a blockade of p38, c-Jun N-terminal kinase (JNK), and TANK (TRAF family member-associated NF-kappa-B activator)-binding kinase 1 (TBK1), which are linked to the activation of activating transcription factor 2 (ATF2) and interferon regulatory transcription factor 3 (IRF3). Moreover, this fraction also ameliorated HCl/ethanol/-induced gastritis via suppression of phospho-JNK2 levels. Conclusion: These results strongly suggest that the anti-inflammatory action of PPD-SF could be mediated by a reduction in the activation of p38-, JNK2-, and TANK-binding-kinase-1-linked pathways and their corresponding transcription factors (ATF2 and IRF3).

• Clinical and Experimental Pediatrics
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• v.57 no.5
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• pp.205-210
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• 2014

Atopic sensitization is a complex phenomenon that changes dynamically with age throughout childhood; its prevalence increases with age in young children. Additionally, with increasing age, the prevalence of sensitization to inhalant allergens and the prevalence of polysensitization to allergens increase. It is also well established that the development of atopic sensitization is the result of a complex interplay of genetic and environmental factors. However, there is considerable heterogeneity in the literature in terms of the effect of different environmental exposures in young children on the subsequent risk of atopic sensitization and allergic diseases. Previous studies on the relationship, in early life, between pet ownership, sex, exposure to secondhand smoke, exposure to traffic-related air pollution components, and atopic sensitization have yielded different results. Recent studies have highlighted the importance of gene-environment interactions, especially during early childhood, on the risk of subsequent atopic sensitization and allergic diseases. Therefore, pediatricians should consider the genetic and environmental determinants of atopic sensitization in infants and young children when diagnosing and treating patients with allergic diseases. Determining ways in which early exposure to these risk factors in young children may be reduced could be beneficial in preventing the likelihood of developing atopic sensitization.

• Journal of Environmental Health Sciences
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• v.36 no.1
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• pp.1-13
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• 2010

Evidences supporting gene-environment interaction are accumulating in terms of environmental exposure including lifestyle factors and related genetic variants. One form of defense mechanism against cancer development involves a series of genes whose role is to metabolize (activation/detoxification) and excrete potentially toxic compounds and to repair subtle mistakes in DNA. The purpose of this article is to provide a brief review of the notion of gene-environment interaction, environmental/occupational carcinogens and related cancers, and previous studies of gene-environment interaction on cancers caused by exposure to carcinogenesis. With a number of studies on the interaction between lifestyle factors (e.g., smoking and diet) and genetic polymorphisms in genes involved in xenobiotic metabolism and DNA repair excluded, only several studies have been conducted on the interactive effects between polymorphisms of CYPs, GSTs, ERCCs, XRCCs and environmental/occupational carcinogens such as vinyl chloride, benzo[a]pyrene, and chloroform on carcinogenesis or genotoxicity. Future studies may need to be conducted with sufficient number of subjects and based on occupational cohorts to provide useful information in terms of advanced risk assessment and regulation of exposure level.