• Journal of Sport and Applied Science
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• v.6 no.4
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• pp.11-23
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• 2022

New insights into the aetiology of anaemia in athletes have been discovered in recent years. From hemodilution and redistribution, which are thought to commit to so-called "sports anaemia," to iron deficiency triggered by higher requirements, dietary requirements, decreased uptake, enhanced losses, hemolysis, and sequester, to genetic factors of different types of anaemia (some related to sport), anaemia in athletes necessitates a careful and multisystem methodology. Dietary factors that hinder iron absorption and enhance iron bioavailability (e.g., phytate, polyphenols) should be considered. Celiac disease, which is more common in female athletes, may be the consequence of an iron deficiency anaemia that is unidentified. Sweating, hematuria, gastrointestinal bleeding, inflammation, and intravascular and extravascular hemolysis are all ways iron is lost during strength training. In training, evaluating the iron status, particularly in athletes at risk of iron deficiency, may work on improving iron balance and possibly effectiveness. Iron status is influenced by a healthy gut microbiome. To eliminate hemolysis, athletes at risk of iron deficiency should engage in non-weight-bearing, low-intensity sporting activities.

• Journal of the Korean Academy of Child and Adolescent Psychiatry
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• v.35 no.1
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• pp.8-14
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• 2024

Autism spectrum disorder (ASD) is a heterogeneous developmental disorder characterized by impairments in two core areas: 1) social communication and interaction and 2) restricted and repetitive patterns of behaviors and interests. In general, ASD is known to be a lifelong disorder. Follow-up studies from childhood to adulthood have reported that the severity of the key symptoms ASD decreases over time. However, chronic health problems including mental health occur in many patients with ASD. The prevalence of ASD has increased from around 0.04% in the 1970s to 2.8% at present. The average age of diagnosis in developed countries is 38-120 months of age. Recent evidence suggests that biological factors which include genetic, congenital, immunological, neuroanatomical, biochemical, and environmental ones are important in causing autism. Until now, early signs and various risk factors of ASD have been suggested.

• Biomedical Science Letters
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• v.23 no.2
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• pp.133-137
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• 2017

Periodontitis is the major causation of tooth loss in the elderly population. Multiple risk factors include oral microorganisms, smoking, metabolic syndrome, and genetic factors influence periodontitis development. In this study, we conducted a replication study of using previous Korean GWAS results by examining an independent population. The study population was recruited from Mir Dental Clinic, Daegu, Korea. In total, 93 samples were evaluated from July 2016 to January 2017. The sample groups include relatively older patients (>60 years) with no periodontitis (n = 31) and relatively younger patients (range 40~60 years) with severe periodontitis (n = 62). A total of seven markers which were previously reported to be associated with periodontitis were genotyped. Among the seven SNPs, rs16846206 and rs2392510 showed a significant association by logistic regression analysis and Chi square test, respectively. The former SNP showed significant association with severe periodontitis, whereas this study also showed same tendency in which individuals with the minor allele are significantly more frequent in cases than those in controls. The SNP is located on a coding gene (SLC9C2), where the alanine residue 505 is replaced by glycine (Ala505Gly). The later SNP was significant when differed between case and control groups, but there was no significance by logistic regression analysis when controlled for age and sex as covariant. Although the study population size examined in the current study was relatively smaller compared to previous studies, our results implicated that at least the two SNPs (rs16846206 and rs2392510) might be important candidates for the further genetic study.

• The Korean Journal of Malacology
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• v.31 no.4
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• pp.315-322
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• 2015

The sex of bivalves is classified into gonochorism and hermaphroditism, and hermaphroditism is further divided into simultaneous (synchronous or functional), and sequential (asynchronous). The sequential hermaphroditism signifies sex reversal in accordance with seasons. In general, in the case of gonochoristic bivalves, manifestation of sex as female and male, after having identified the morphological sex, is limited to a period of the life cycle in any given individual. In order to accurately identify sex, continuous monitoring of changes in the sex during life cycle is necessary by tagging the sex. In the bivalves, sex reversal and sequential hermaphroditism has been reported in the Ostreidae, Pectinidae, Veneridae and Arcidae etc.. Most of these studies have reached this conclusion based on evidence derived from sex ratio change in accordance with the age within same populations. Sex change in the sequential hermaphroditic bivalves normally occurs when the gonad is undifferentiated between spawning seasons. Two factors are involved in sex determination and sex change in bivalves, namely genetic and environmental. However, more detailed research is needed on the effect of the genetic and environmental factors involved in sex determination and sex change of bivalves.

• The Plant Pathology Journal
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• v.26 no.2
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• pp.159-169
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• 2010

Lesion mimic mutant (LMM) plants display spontaneous necrotic lesions on their leaves without any pathogenic infection. Specific rice LMMs designated as spotted leaf (spl) including spl1, spl3, spl4, spl5 and spl6 are genetically known as lesion resembling disease (lrd) mutant. The inheritance patterns in the $F_1$ and $F_2$ progenies of these mutants are controlled by recessive genetic factors. Lesion development in the rice LMMs were controlled by both development stages and environmental factors. The rice LMMs exhibited higher numbers of spots under $45^{\circ}C$ temperature than those under $30^{\circ}C$. Contents of chlorophyll were drastically reduced at 60 days old LMM leaves when the spot formation was severe. The levels of endogenous hydrogen peroxide were highest at 45 days old mutants but reduced at 60 days old. Transcription levels of stress related genes including thioredoxin peroxidase and protein disulfide isomerase were reduced in spotted leaves than those of non spotted leaves. It could be suggested that scavenging system against reactive oxygen species induced by either stresses or innate metabolisms may not work properly in the rice LMMs. As these rice LMMs autonomously expressed clear lesions of lrd phenotype without pathogen infection, it could be useful to understand stresses responses in plants.

• 대한예방의학회:학술대회논문집
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• 1999.10a
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• pp.1-15
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• 1999

In a case-control study to evaluate the factors involved in the development of hepatocellular carcinoma, polymorphisms of the p53 gene were compared in 68 cases mostly infected with hepatitis C virus (HCV) and 68 controls matched for sex and age: DNA from peripheral blood leukocytes was analyzed by the polymerase chain reaction-single strand conformation polymorphism method and direct sequencing. Polymorphisms analyzed were those in exon 4 (CCC vs. CGC, Pro vs. Arg at codon 72, Al allele vs. A2 allele), intron 2 (C vs. G at nucleotide 38, Al vs. A2), intron 3 (C vs. A at nucleotide 65, Al vs. A2; absence and presence of 16 base pair repeat at nucleotides 24 to 39, Al vs. A2), intron 6 (A vs. G at nucleotide 62, Al vs. A2) and intron 7 (C and T vs. T and G at nucleotides 72 and 92, Al vs. A2). A significantly higher frequency of the allele for CCC (Pro, Al) at codon 72 of exon 4 was found in cases (39%) than in controls (26%) (p<0.05). Highly significant linkage of the polymorphisms in exon 4, intron 2, intron 3 and intron 7, and between the intron 3-16 bp duplication and polymorphism in intron 6 also was found. Matched Fair analysis showed significantly higher frequencies of certain haplotypes (1-1-1-1-2-2 or 1-1-2-1-2-1 for exon 4, intron 2, intron 3, the intron 3-16 bp duplication, intron 6 and intron 7) in cases than in controls (p=0.014, OR=2.27, 95% CI= 1.08-5.12). No preference of specific p53 polymorphisms for specific HCV genotype was detected. These findings suggest that in hepatocarcinogenesis mainly due to HCV infection, genetic factors may be involved and that genetic markers can serve as predictors of a high-risk group for hepatocarcinogenesis.

• Korean Journal of Biological Psychiatry
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• v.7 no.2
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• pp.115-122
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• 2000

The development of molecular biology has brought many changes in psychiatry. Molecular biology makes us possible to know the cause of mental disorders that provide the way to prevent the disorders, and to develop various accurate diagnostic and treatment methods for mental disorders. The author discusses the concept, cause, and treatment of mental disorders in the aspect of molecular biology. Importing the methods of molecular biology into psychiatry, we can anticipate to get a number of the goals of psychiatric genetics, including identification of specific susceptibility genes, clarification of the pathophysiological processes whereby these genes lead to symptoms, establishment of epigenetic factors that interact with these genes to produce disease, validation of nosological boundaries that more closely reflect the actions of these genes, and development of effective preventive and therapeutic interventions based on genetic counseling, gene therapy, and modification of permissive or protective environmental influences. In addition to their capacity to accelerate the discovery of new molecules participating in the nervous system's response to disease or to self-administered drugs, molecular biological strategies can also be used to determine how critical a particular gene product may be in mediating a cellular event with behavioral importance. Molecular biology probably enables us discover the environmental factors of mental disorders and allow rational drug design and gene therapies for mental disorders, by isolation of gene products that facilitate a basic understanding of the pathogenesis of these disorders. A specific genetic linkage may suggest a novel class of drugs that has not yet been tried. With respect to gene therapy, the hypothetical method would use a gene delivery system, most likely a modified virus, to insert a functional copy of a mutant gene into those brain cells that require the gene for normal function.

• Asian Pacific Journal of Cancer Prevention
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• v.17 no.2
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• pp.591-595
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• 2016

The liver is one of the most common sites of cancer in the world, hepatocellular carcinoma (HCC) predominating. Chronic hepatitis B virus infection (CHB) is considered as an important potential risk factors for HCC. Different people have diverse responses to HBV infection regarding the likelihood of HCC development, and host factors such as single nucleotide polymorphisms (SNPs) might account for this. The present study was conducted to evaluate any association between SNP frequencies in two genes, XRCC4 (rs1805377) and ATF6 (rs2070150), and the risk of CHB and HCC development in Thai patients. The study covered 369 subjects including 121 HCC patients, 141 with chronic hepatitis B virus infection (CHB) and 107 healthy controls. With TaqMan real-time PCR, the results showed that no significant association between XRCC4 (rs1805377) and ATF6 (rs2070150) and risk of HCC in the Thai population. From this first study of the 2 polymorphisms and HCC in Thailand it can concluded that rs1805377 and rs2070150 polymorphisms may not be applicable as genetic markers in the Thai population for HCC assessment.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.1
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• pp.21-25
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• 2013

Background: Genetic factors and environmental factors play a role in pathogenesis of esophageal squamous cell carcinoma (ESCC). Previous studies regarding the association of folate intake and Methylenetetrahydrofolate reductase C677T polymorphism with ESCC was conflicting. We conducted a meta-analysis to investigate the association of MTHFR C677T and folate intake with esophageal cancer risk. Methods: MEDLINE, EMBASE and the Chinese Biomedical Database were searched in our study. The quality of studies were evaluated by predefined scale, and The association of polymorphisms of MTHFR C677T and folate intake and ESCC risk was estimated by Odds ratio (ORs) with 95% confidence intervals (CIs). Results: 19 studies (4239 cases and 5575 controls) were included for meta-analysis. A significant association was seen between individuals with MTHFR 677 CT [OR(95%)=1.47(1.32-1.63)] and TT [OR(95%)=1.69(1.49-1.91)] genotypes and ESCC risk (p<0.05). Low intake of folate had significantly higher risk of esophageal cancer among individuals with CT/TT genotype [OR(95%)=1.65(1.1-2.49)], while high intake of folate did not find significant high risk of esophageal cancer among individuals with CT/TT genotype [OR(95%)=1.64 (0.82-3.26)]. Conclusions: Our meta-analysis indicated the folate intake and MTHFR 677CT/TT are associated with the risk of ESCC, and folate showed a significant interaction with polymorphism of MTHFR C677T.

• BMB Reports
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• v.40 no.3
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• pp.448-452
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• 2007

We examined the contribution of CYP2C9 and CYP2C19 genotypes and drug interactions to the phenytoin metabolism among 97 Korean epileptic patients to determine if pharmacogenetic testing could be utilized in routine clinical practice. The CYP2C9 polymorphism is a wellknown major genetic factor responsible for phenytoin metabolism. The CYP219 polymorphism, with a high incidence of variant alleles, has a minor influence on phenytoin treated Koran patients. Using a multiple regression model for evaluation of the CYP2C9 and CYP2C19 genotypes, together with other non-genetic variables, we explained 39.6% of the variance in serum phenytoin levels. Incorporation of genotyping for CYP2C9 and CYP2C19 into a clinical practice may be of some help in the determination of phenytoin dosage. However, because concurrent drug treatment is common in patients taking phenytoin and many environmental factors are likely to play a role in drug metabolism, these factors may overwhelm the relevance of CYP polymorphisms in the clinical setting. Further investigations with an approach to dose assessment that includes comprehensive interpretation of both pharmacogenetic and pharmacokinetic data along with understanding of the mechanism of drug interactions in dosage adjustment is warranted.