• Asian-Australasian Journal of Animal Sciences
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• v.16 no.9
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• pp.1247-1253
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• 2003

Selection for increased milk production in dairy cows has often resulted in a higher incidence of disease and thus incurred a greater health costs. Considerable interests have been shown in breeding dairy cattle for disease resistance in recent years. This paper discusses the limitations of breeding dairy cattle for genetic resistance in six parts: 1) complexity of disease resistance, 2) difficulty in estimating genetic parameters for planning breeding programs against disease, 3) undesirable relationship between production traits and disease, 4) disease as affected by recessive genes, 5) new mutation of the pathogens, and 6) variable environmental factors. The hidden problems of estimating genetic and phenotypic parameters involving disease incidence were examined in terms of categorical nature, non-independence, heterogeneity of error variance, non-randomness, and automatic relationship between disease and production traits. In light of these limitations, the prospect for increasing genetic resistance by conventional breeding methods would not be so bright as we like. Since the phenomenon of disease is the result of a joint interaction among host genotype, pathogen genotype and environment, it becomes essential to adopt an integrated approach of increasing genetic resistance of the host animals, manipulating the pathogen genotypes, developing effective vaccines and drugs, and improving the environmental conditions. The advances in DNA-based technology show considerable promise in directly manipulating host and pathogen genomes for genetic resistance and producing vaccines and drugs for prevention and medication to promote the wellbeing of the animals.

• Plant Resources
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• v.1 no.1
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• pp.26-32
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• 1998

This paper describes the variations in eight agronomic traits in three unadapted local landraces and an inbred cultivar of corn. To compare the agronomic traits in field evaluation with molecular marker evaluation the genotypes of the plant introduction were also checked by 4 microsatellite-SSR loci. The variations of the eight agronomic traits were higher in the local landrades than in the inbred line. which was substantiated by the high genetic variation in the landrades with microsatellite-SSR loci. The level of genetic variation was also different between landraces. Since the genetic evaluation can be easily quantified by the analysis of microsatellite-SSR loci. the threshold level of genetic homogeneity in the population for parental lines in breeding program can be determined and the effort of maintaining the landrace population would be alleviated. As an example in our analysis. the entry from Whachon should not need the same number of selfing generations as the other two landraces to get the level of inbred state. Since this line showed lowest intra-genetic variation within the population.

• Tuberculosis and Respiratory Diseases
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• v.80 no.2
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• pp.113-135
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• 2017

Asthma is traditionally regarded as a chronic airway disease, and recent literature proves its heterogeneity, based on distinctive clusters or phenotypes of asthma. In defining such asthma clusters, the nature of comorbidity among patients with asthma is poorly understood, by assuming no causal relationship between asthma and other comorbid conditions, including both communicable and noncommunicable diseases. However, emerging evidence suggests that the status of asthma significantly affects the increased susceptibility of the patient to both communicable and noncommunicable diseases. Specifically, the impact of asthma on susceptibility to noncommunicable diseases such as chronic systemic inflammatory diseases (e.g., rheumatoid arthritis), may provide an important insight into asthma as a disease with systemic inflammatory features, a conceptual understanding between asthma and asthma-related comorbidity, and the potential implications on the therapeutic and preventive interventions for patients with asthma. This review discusses the currently under-recognized clinical and immunological phenotypes of asthma; specifically, a higher risk of developing a systemic inflammatory disease such as rheumatoid arthritis and their implications, on the conceptual understanding and management of asthma. Our discussion is divided into three parts: literature summary on the relationship between asthma and the risk of rheumatoid arthritis; potential mechanisms underlying the association; and implications on asthma management and research.

• Asian-Australasian Journal of Animal Sciences
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• v.12 no.6
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• pp.850-853
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• 1999

Angus postweaning daily gain (PWDG) was analyzed to investigate effects of the heterogeneous variance and the genotypes by sex interaction on prediction of EBVs with data sets of various environmental levels. A whole data (16,239 records) was divided into six data sets according to averages of the best linear unbiased estimator (BLUE) of herd environment. The results comparing prediction models showed that single-trait model is adequate for most of the data sets except for the data set of poor environment for both of the bulls and the heifers where the heterogeneity of variance and the genotypes by sex interaction exists. In the prediction with the data set of the low environment level, the bull's EBVs by single-trait models had high product moment correlations with male EBVs of the bulls by the multitrait model. Whereas the heifer's EBVs had moderate correlations with female EBVs by the multitrait model. This moderate correlation seems to be resulted by the heterogeneity of variance and low heritability of the heifer's PWDG. The prediction models with heterogeneity of variance had little effect on the prediction of EBVs for the data sets with moderate to high genetic correlations.

• Asian-Australasian Journal of Animal Sciences
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• v.12 no.6
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• pp.846-849
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• 1999

Angus postweaning daily gain (PWDG) were analyzed to investigate heterogeneous variance by sex. A set of data (16,239 records) was divided into six sub-data sets according to level of environment. REML estimation was conducted by a multitrait model, where PWDG in each sex was treated as a separate trait. Estimates showed diversity among environmental levels, where the heritability for heifers was high in good environment but low in poor environment. The bull's estimates varied among environmental levels. The largest heterogeneity of phenotypic variance between sexes was estimated in a data set of the poor environment level. The genetic correlations between the heifer's PWDG and the bull's PWDG were high in the good environment and low in the poor environment (-0.17). The results suggest existence of genotype by sex interaction in the poor environment.

• Genomics & Informatics
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• v.16 no.4
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• pp.17.1-17.6
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• 2018

Tumor heterogeneity, the cellular mosaic of multiple lineages arising from the process of clonal evolution, has continued to thwart multi-omics analyses using traditional bulk sequencing methods. The application of single-cell sequencing, in concert with existing genomics methods, has enabled high-resolution interrogation of the genome, transcriptome, epigenome, and proteome. Applied to cancers, these single-cell multi-omics methods bypass previous limitations on data resolution and have enabled a more nuanced understanding of the evolutionary dynamics of tumor progression, immune evasion, metastasis, and treatment resistance. This review details the growing number of novel single-cell multi-omics methods applied to tumors and further discusses recent discoveries emerging from these approaches, especially in regard to immunotherapy.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.10
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• pp.4457-4463
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• 2015

Common genetic variation Q192R in the paraoxonase 1 (PON1) gene has been considered to be implicated in the development of many cancers. Nevertheless, results from the related studies were inconsistent. To elucidate the association, we performed a meta-analysis for 8,112 cases and 10,037 controls from 32 published case-control studies. Odds ratios (ORs) with 95% confidence intervals (CIs) were used to assess the strength of the association by STATA 12.0 software. Overall, we revealed that the PON1-192R allele was associated with a reduced risk of the overall cancers. Moreover, in the stratified analysis by cancer types (breast cancer, prostate cancer, brain cancer etc.), the results showed that PON1-192R allele was associated with a decreased risk in breast cancer (R vs Q: OR=0.605, 95% CI=0.378-0.967, $P_{heterogeneity}=0.000$; RR vs QQ: OR=0.494, 95% CI=0.275-0.888, $P_{heterogeneity}=0.002$; RQ vs QQ: OR=0.465, 95% CI=0.259-0.835, $P_{heterogeneity}=0.000$; and RR+RQ vs QQ: OR=0.485, 95% CI=0.274-0.857, $P_{heterogeneity}=0.000$), and associated with prostate cancer in homozygote (RR vs QQ: OR=0.475, 95% CI=0.251-0.897, $P_{heterogeneity}=0.001$) and recessive models (RR vs RQ+QQ: OR=0.379, 95% CI=0.169-0.853, $P_{heterogeneity}=0.000$), while an increased risk was identified in lymphoma (R vs Q: OR=1.537, 95% CI=1.246-1.896, $P_{heterogeneity}=0.944$; RR vs QQ: OR=2.987, 95% CI=1.861-4.795, $P_{heterogeneity}=0.350$; RR+RQ vs QQ: OR=1.354, 95% CI=1.021-1.796, $P_{heterogeneity}=0.824$; and RR vs RQ+QQ: OR=2.934, 95% CI=1.869-4.605, $P_{heterogeneity}=0.433$), and an increased risk in prostate cancer under heterozygote comparison (RQ vs QQ: OR=1.782, 95% CI=1.077-2.950, $P_{heterogeneity}=0.000$) and dominant models (RR+RQ vs QQ: OR=1.281, 95% CI=1.044-1.573, $P_{heterogeneity}=0.056$). When subgroup analysis that performed by the control source (hospital based or population based), a decreased risk of the overall cancers was revealed by homozygote (RR vs QQ: OR=0.601, 95% CI=0.366-0.987, $P_{heterogeneity}=0.000$) and dominant models (RR vs RQ+QQ: OR= 0.611, 95% CI=0.384-0.973, $P_{heterogeneity}=0.000$) in hospital based group. Stratifying by ethnicity, a significantly reduced risk of the overall cancers under allele contrast model (R vs Q: OR=0.788, 95% CI=0.626-0.993, $P_{heterogeneity}=0.000$) was uncovered in Caucasian. In summary, these findings suggested that PON1 Q192R polymorphism was associated with a reduced risk of the overall cancers, nevertheless, it might increase cancer susceptibility of prostate and lymphoma risk. Large well-designed epidemiological studies will be continued on this issue of interest.

• Journal of Microbiology and Biotechnology
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• v.11 no.5
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• pp.788-797
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• 2001

The usefulness of three PCR methods were evaluated for the epidemiological typing of Staphylococcus aureus: an enterobacterial repetitive intergenic consensus sequence PCR (ERIC-PCR), repetitive extragenic palindromic element PCR (REP-PCR), and 16S-23S intergenic spacer PCR (ITS-PCR). The analysis was performed using a collection of S. aureus strains comprised of 6 reference and 79 isolates from patients with various diseases. Among the 85 S. aureus strains tested, 6 references and 6 isolates were found to be susceptible to methicillin, whereas the remaining 73 isolates were resistant to it. PCR methods are of special concern, as conventional phenotypic methods are unable to clearly distinguish among methicillin-resistant S. aureus (MRSA) strains. The ability of the techniques to detect different unrelated types was found to be as follows: ERIC-PCR, 19 types; REP-PCR, 36 types; and ITS-PCR, 14 types. On the basis of combining the ERIC, REP, and ITS fingerprints, the 85 S. aureus strains were grouped into 56 genetic types (designated G1 to G56). The diversities for the 85 S. aureus strains, calculated according to Simpson\`s index, were 0.88 for an ERIC-PCR, 0.93 for a REP-PCR, and 0.48 for an ITS-PCR, and the diversity increased up to 0.97 when an ERIC-PCR and REP-PCR were combined. The above discrimination indices imply that the genetic heterogeneity of S. aureus strains is high. Accordingly, this study demonstrates that DNA sequences from highly conserved repeats of a genome, particularly a combination of ERIC sequences and REP elements, are a convenient and accurate tool for the subspecies-specific discrimination and epidemiologic tracking of S. aureus.

• Journal of The Korean Society of Inherited Metabolic disease
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• v.23 no.2
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• pp.1-7
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• 2023

Inherited metabolic disorders (IMD) are a group of disorders involving various metabolic pathways. Genetic diagnosis of IMD has been challenging because of extremely heterogeneous nature and extensive laboratory and/or phenotype overlap. Conventional genetic diagnosis was a gene-by-gene approach that needs a priori information on the causative genes that might underlie the IMD. Recent implementation of next-generation sequencing (NGS) technologies has changed the process of genetic diagnosis from a gene-by-gene approach to simultaneous analysis of targeted genes possibly associated with the IMD using gene panels or using whole exome/genome sequencing (WES/WGS) covering entire human genes. Clinical NGS tests can be a cost-effective approach for the rapid diagnosis of IMD with genetic heterogeneity and are becoming standard diagnostic procedures.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.15
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• pp.6131-6136
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• 2014

Objective: Epidemiology studies have reported conflicting results between glutathione S-transferase Mu-1 (GSTM1), glutathione S-transferase theta-1 (GSTT1) and glutathione S-transferase pi-1 (GSTP1) and ovarian cancer (OC) susceptibility. In this study, an updated meta-analysis was applied to determine whether the deletion of GSTM1, GSTT1 and GSTP1 has an influence on OC susceptibility. Methods: A published literature search was performed through PubMed, Embase, Cochrane Library, and Science Citation Index Expanded database for articles published in English. Pooled odds ratios (ORs) and 95% confidence intervals (95%CIs) were calculated using random or fixed effects models. Heterogeneity between studies was assessed using the Cochrane Q test and $I^2$ statistics. Sub-group analysis was conducted to explore the sources of heterogeneity. Sensitivity analysis was employed to evaluate the respective influence of each study on the overall estimate. Results: In total, 10 published studies were included in the final analysis. The combined analysis revealed that there was no significant association between GSTM1 null genotype and OC risk (OR=1.01, 95%CI: 0.91-1.12). Additionally, there was no significant association between GSTT1 genetic polymorphisms and OC risk (OR=0.98, 95% CI: 0.85-1.13). Similalry, no significant associations were found concerning the GSTP1 rs1695 locus and OC risk. Meanwhile, subgroup analysis did not show a significant increase in eligible studies with low heterogeneity. However, sensitivity analysis, publication bias and cumulative analysis demonstrated the reliability and stability of the current meta-analysis. Conclusions: These findings suggest that GSTs genetic polymorphisms may not contribute to OC susceptibility. Large epidemiological studies with the combination of GSTM1 null, GSTT1 null and GSTP1 Ile105Val polymorphisms and more specific histological subtypes of OC are needed to prove our findings.