Relevant bibliographies by topics / Gwashu

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Academic literature on the topic 'Gwashu'

Author: Grafiati
Published: 4 June 2021
Last updated: 16 February 2022

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Journal articles on the topic "Gwashu"

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Guo, Michael H., Joel N. Hirschhorn, and Andrew Dauber. "Insights and Implications of Genome-Wide Association Studies of Height." Journal of Clinical Endocrinology & Metabolism 103, no. 9 (July 2, 2018): 3155–68. http://dx.doi.org/10.1210/jc.2018-01126.

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Abstract Context In the last decade, genome-wide association studies (GWASs) have catalyzed our understanding of the genetics of height and have identified hundreds of regions of the genome associated with adult height and other height-related body measurements. Evidence Acquisition GWASs related to height were identified via PubMed search and a review of the GWAS catalog. Evidence Synthesis The GWAS results demonstrate that height is highly polygenic: that is, many thousands of genetic variants distributed across the genome each contribute to an individual’s height. These height-associated regions of the genome are enriched for genes in known biological pathways involved in growth, such as fibroblast growth factor signaling, as well as for genes expressed in relevant tissues, such as the growth plate. GWASs can also uncover previously unappreciated biological pathways, such as theSTC2/PAPPA/IGFBP4 pathway. The genes implicated by GWASs are often the same genes that are the genetic causes of Mendelian growth disorders or skeletal dysplasias, and GWAS results can provide complementary information about these disorders. Conclusions Here, we review the rationale behind GWASs and what we have learned from GWASs for height, including how it has enhanced our understanding of the underlying biology of human growth. We also highlight the implications of GWASs in terms of prediction of adult height and our understanding of Mendelian growth disorders.
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Deja-Muylle, Agnieszka, Boris Parizot, Hans Motte, and Tom Beeckman. "Exploiting natural variation in root system architecture via genome-wide association studies." Journal of Experimental Botany 71, no. 8 (January 20, 2020): 2379–89. http://dx.doi.org/10.1093/jxb/eraa029.

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Abstract Root growth and development has become an important research topic for breeders and researchers based on a growing need to adapt plants to changing and more demanding environmental conditions worldwide. Over the last few years, genome-wide association studies (GWASs) became an important tool to identify the link between traits in the field and their genetic background. Here we give an overview of the current literature concerning GWASs performed on root system architecture (RSA) in plants. We summarize which root traits and approaches have been used for GWAS, mentioning their respective success rate towards a successful gene discovery. Furthermore, we zoom in on the current technical hurdles in root phenotyping and GWAS, and discuss future possibilities in this field of research.
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Schmid, Markus, and Jörn Bennewitz. "Invited review: Genome-wide association analysis for quantitative traits in livestock – a selective review of statistical models and experimental designs." Archives Animal Breeding 60, no. 3 (September 29, 2017): 335–46. http://dx.doi.org/10.5194/aab-60-335-2017.

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Abstract. Quantitative or complex traits are controlled by many genes and environmental factors. Most traits in livestock breeding are quantitative traits. Mapping genes and causative mutations generating the genetic variance of these traits is still a very active area of research in livestock genetics. Since genome-wide and dense SNP panels are available for most livestock species, genome-wide association studies (GWASs) have become the method of choice in mapping experiments. Different statistical models are used for GWASs. We will review the frequently used single-marker models and additionally describe Bayesian multi-marker models. The importance of nonadditive genetic and genotype-by-environment effects along with GWAS methods to detect them will be briefly discussed. Different mapping populations are used and will also be reviewed. Whenever possible, our own real-data examples are included to illustrate the reviewed methods and designs. Future research directions including post-GWAS strategies are outlined.
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Azam, Afifah Binti, and Elena Aisha Binti Azizan. "Brief Overview of a Decade of Genome-Wide Association Studies on Primary Hypertension." International Journal of Endocrinology 2018 (January 30, 2018): 1–14. http://dx.doi.org/10.1155/2018/7259704.

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Primary hypertension is widely believed to be a complex polygenic disorder with the manifestation influenced by the interactions of genomic and environmental factors making identification of susceptibility genes a major challenge. With major advancement in high-throughput genotyping technology, genome-wide association study (GWAS) has become a powerful tool for researchers studying genetically complex diseases. GWASs work through revealing links between DNA sequence variation and a disease or trait with biomedical importance. The human genome is a very long DNA sequence which consists of billions of nucleotides arranged in a unique way. A single base-pair change in the DNA sequence is known as a single nucleotide polymorphism (SNP). With the help of modern genotyping techniques such as chip-based genotyping arrays, thousands of SNPs can be genotyped easily. Large-scale GWASs, in which more than half a million of common SNPs are genotyped and analyzed for disease association in hundreds of thousands of cases and controls, have been broadly successful in identifying SNPs associated with heart diseases, diabetes, autoimmune diseases, and psychiatric disorders. It is however still debatable whether GWAS is the best approach for hypertension. The following is a brief overview on the outcomes of a decade of GWASs on primary hypertension.
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Hill, W. David. "Comment on ‘Large-Scale Cognitive GWAS Meta-Analysis Reveals Tissue-Specific Neural Expression and Potential Nootropic Drug Targets’ by Lam et al." Twin Research and Human Genetics 21, no. 2 (March 19, 2018): 84–88. http://dx.doi.org/10.1017/thg.2018.12.

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Intelligence and educational attainment are strongly genetically correlated. This relationship can be exploited by Multi-Trait Analysis of GWAS (MTAG) to add power to Genome-wide Association Studies (GWAS) of intelligence. MTAG allows the user to meta-analyze GWASs of different phenotypes, based on their genetic correlations, to identify association's specific to the trait of choice. An MTAG analysis using GWAS data sets on intelligence and education was conducted by Lam et al. (2017). Lam et al. (2017) reported 70 loci that they described as ‘trait specific’ to intelligence. This article examines whether the analysis conducted by Lam et al. (2017) has resulted in genetic information about a phenotype that is more similar to education than intelligence.
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Walker, Venexia, Sean Harrison, Alice Carter, Dipender Gill, Ioanna Tzoulaki, and Neil Davies. "The consequences of adjustment, correction and selection in genome-wide association studies used for two-sample Mendelian randomization." Wellcome Open Research 6 (May 10, 2021): 103. http://dx.doi.org/10.12688/wellcomeopenres.16752.1.

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Introduction: Genome-wide association studies (GWASs) often adjust for covariates, correct for medication use, or select on medication users. If these summary statistics are used in two-sample Mendelian randomization analyses, estimates may be biased. We used simulations to investigate how GWAS adjustment, correction and selection affects these estimates and performed an analysis in UK Biobank to provide an empirical example. Methods: We simulated six GWASs: no adjustment for a covariate, correction for medication use, or selection on medication users; adjustment only; selection only; correction only; both adjustment and selection; and both adjustment and correction. We then ran two-sample Mendelian randomization analyses using these GWASs to evaluate bias. We also performed equivalent GWASs using empirical data from 306,560 participants in UK Biobank with systolic blood pressure as the exposure and body mass index as the covariate and ran two-sample Mendelian randomization with coronary heart disease as the outcome. Results: The simulation showed that estimates from GWASs with selection can produce biased two-sample Mendelian randomization estimates. Yet, we observed relatively little difference between empirical estimates of the effect of systolic blood pressure on coronary artery disease across the six scenarios. Conclusions: Given the potential for bias from using GWASs with selection on Mendelian randomization estimates demonstrated in our simulation, careful consideration before using this approach is warranted. However, based on our empirical results, using adjusted, corrected or selected GWASs is unlikely to make a large difference to two-sample Mendelian randomization estimates in practice.
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Basile, Kevin J., Matthew E. Johnson, Qianghua Xia, and Struan F. A. Grant. "Genetic Susceptibility to Type 2 Diabetes and Obesity: Follow-Up of Findings from Genome-Wide Association Studies." International Journal of Endocrinology 2014 (2014): 1–13. http://dx.doi.org/10.1155/2014/769671.

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Elucidating the underlying genetic variations influencing various complex diseases is one of the major challenges currently facing clinical genetic research. Although these variations are often difficult to uncover, approaches such as genome-wide association studies (GWASs) have been successful at finding statistically significant associations between specific genomic loci and disease susceptibility. GWAS has been especially successful in elucidating genetic variants that influence type 2 diabetes (T2D) and obesity/body mass index (BMI). Specifically, several GWASs have confirmed that a variant in transcription factor 7-like 2 (TCF7L2) confers risk for T2D, while a variant in fat mass and obesity-associated protein (FTO) confers risk for obesity/BMI; indeed both of these signals are considered the most statistically associated loci discovered for these respective traits to date. The discovery of these two key loci in this context has been invaluable for providing novel insight into mechanisms of heritability and disease pathogenesis. As follow-up studies ofTCF7L2andFTOhave typically lead the way in how to follow up a GWAS discovery, we outline what has been learned from such investigations and how they have implications for the myriad of other loci that have been subsequently reported in this disease context.
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Moll, Matthew, Victoria E. Jackson, Bing Yu, Megan L. Grove, Stephanie J. London, Sina A. Gharib, Traci M. Bartz, et al. "A systematic analysis of protein-altering exonic variants in chronic obstructive pulmonary disease." American Journal of Physiology-Lung Cellular and Molecular Physiology 321, no. 1 (July 1, 2021): L130—L143. http://dx.doi.org/10.1152/ajplung.00009.2021.

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Genome-wide association studies (GWASs) have identified regions associated with chronic obstructive pulmonary disease (COPD). GWASs of other diseases have shown an approximately 10-fold overrepresentation of nonsynonymous variants, despite limited exonic coverage on genotyping arrays. We hypothesized that a large-scale analysis of coding variants could discover novel genetic associations with COPD, including rare variants with large effect sizes. We performed a meta-analysis of exome arrays from 218,399 controls and 33,851 moderate-to-severe COPD cases. All exome-wide significant associations were present in regions previously identified by GWAS. We did not identify any novel rare coding variants with large effect sizes. Within GWAS regions on chromosomes 5q, 6p, and 15q, four coding variants were conditionally significant ( P < 0.00015) when adjusting for lead GWAS single-nucleotide polymorphisms A common gasdermin B ( GSDMB) splice variant (rs11078928) previously associated with a decreased risk for asthma was nominally associated with a decreased risk for COPD [minor allele frequency (MAF) = 0.46, P = 1.8e-4]. Two stop variants in coiled-coil α-helical rod protein 1 ( CCHCR1), a gene involved in regulating cell proliferation, were associated with COPD (both P < 0.0001). The SERPINA1 Z allele was associated with a random-effects odds ratio of 1.43 for COPD (95% confidence interval = 1.17–1.74), though with marked heterogeneity across studies. Overall, COPD-associated exonic variants were identified in genes involved in DNA methylation, cell-matrix interactions, cell proliferation, and cell death. In conclusion, we performed the largest exome array meta-analysis of COPD to date and identified potential functional coding variants. Future studies are needed to identify rarer variants and further define the role of coding variants in COPD pathogenesis.
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Mounier, Ninon, and Zoltán Kutalik. "bGWAS: an R package to perform Bayesian genome wide association studies." Bioinformatics 36, no. 15 (May 29, 2020): 4374–76. http://dx.doi.org/10.1093/bioinformatics/btaa549.

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Abstract Summary Increasing sample size is not the only strategy to improve discovery in Genome Wide Association Studies (GWASs) and we propose here an approach that leverages published studies of related traits to improve inference. Our Bayesian GWAS method derives informative prior effects by leveraging GWASs of related risk factors and their causal effect estimates on the focal trait using multivariable Mendelian randomization. These prior effects are combined with the observed effects to yield Bayes Factors, posterior and direct effects. The approach not only increases power, but also has the potential to dissect direct and indirect biological mechanisms. Availability and implementation bGWAS package is freely available under a GPL-2 License, and can be accessed, alongside with user guides and tutorials, from https://github.com/n-mounier/bGWAS. Supplementary information Supplementary data are available at Bioinformatics online.
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Kong, Yinfei, Pouya Khankhanian, Daniel Himmelstein, Amie E. Hwang, Kristin A. Rand, Dalin Li, David J. Van Den Berg, et al. "Meta-Analysis of Hodgkin Lymphoma and Asthma Genome-Wide Association Scans reveals common variants in GATA3." Blood 124, no. 21 (December 6, 2014): 135. http://dx.doi.org/10.1182/blood.v124.21.135.135.

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Abstract Both Hodgkin lymphoma (HL) and asthma are associated with relative isolation from early childhood infectious exposures (hygiene hypothesis) and a T-helper-2 (Th2)-skewed immune response. To test the hypothesis that there is some component of shared genetic etiology between HL and asthma, we examined the genetic overlap in data from genome-wide association study (GWAS) meta-analyses of the two diseases conducted in populations of European ancestry. The HL GWAS meta-analysis consisted of 1,816 HL cases and 7,877 controls, and the asthma GWAS meta-analysis consisted of 2,088 asthma cases and 2,743 controls. The combined HL-asthma GWAS data resulted in 904,634 common single nucleotide polymorphisms (SNPs) genotyped with both arrays. We observed a total of 9 common SNPs associated with both HL and asthma at p<0.0001, compared to 3 SNPs expected in both data sets at that significance level. Out of 66 genetic risk variants associated with HL at a genome-wide significance level of p<10-8, 5 variants replicated in the asthma GWAS dataset at p < 0.05. In a meta-analysis combining the HL and asthma GWAS data, we found genome-wide significant associations with two correlated SNPs (r2 =0.91) in the Th2 transcription factor gene GATA3 (rs422628, ORHL-asthma meta =1.25, p=3.36 x 10-9 and rs444929, ORHL-asthma meta = 1.26, p=2.09 x 10-8) that were not genome-wide significant in either disease alone (Table 1). The association with one SNP remained genome-wide significant in the meta-analysis combined with the nodular sclerosis subset (rs422628, ORHL-asthma meta =1.32, p=3.75 x 10-9), but not with other HL subtypes. An association with a SNP in IKZF3, a gene involved in B lymphocyte differentiation and proliferation, reached genome-wide significance only in the meta-analysis with the HL subset positive for Epstein-Barr virus (EBV) in the tumor (rs9909593, ORHL-asthma meta = 1.19, p=3.80 x 10-8). In a genetic diseasome analysis based on an ontological analysis of published GWAS data, HL, especially nodular sclerosis HL, was more closely related to asthma than to solid cancers. Recognition of overlap in genetic predisposition to HL and other immune diseases sheds light on the complex etiology of HL and may enable novel diagnostic and therapeutic approaches. Abstract 135. Table 1 Genome-wide significant results of a meta-analysis combining Hodgkin lymphoma (HL) and asthma GWAS1data. HL GWAS1 Asthma GWAS1 Combined GWAS1 SNP2 Chr3 BP4 Gene OR5 P-value6 OR5 P-value6 OR5 P-value6 rs422628a 10 8151415 GATA3 1.24 1.13 x 10-5 1.31 6.39 x10-5 1.25 3.26 x 10-9 rs444929b 10 8150030 GATA3 1.26 3.24x 10-6 1.28 8.90 x 10-4 1.26 2.09 x 10-8 rs422628c 10 8151415 GATA3 1.33 7.77 x 10-6 1.31 6.39 x10-5 1.32 3.75 x 10-9 rs9909593d 17 35223675 IKZF3 1.11 2.60 x 10-1 1.25 5.06 x 10-8 1.19 3.80 x 10-8 1Genome-wide association scan 2Single nucleotide polymorphism 3Chromosome 4Base pair position 5Odds ratio 6P-values are derived from a meta-analysis using a fixed effects model with weights proportional to the square root of the number of cases. aAll Hodgkin lymphoma cases bAll Hodgkin lymphoma cases, SNP association reported in Cozen et al., Nat Comm, 2014 cNodular sclerosis cases only dEBV-positive cases only Disclosures No relevant conflicts of interest to declare.
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Dissertations / Theses on the topic "Gwashu"

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Tshaiviti, Thandeka Lovedalia. "Persuasion in the Xhosa drama text Isisila sehobe." Thesis, Stellenbosch : Stellenbosch University, 2008. http://hdl.handle.net/10019.1/2275.

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Thesis (MA (African Languages))--Stellenbosch University, 20008.
The goal of this study is to investigate the speech act of persuasion in the Xhosa drama text Isisila sehobe by Satyo and Gwashu. The investigation into persuasive communication in Isisila sehobe takes as a starting point the persuasive strategies of Larson (1999). The study's main aim is to establish the linguistic realisation through which social aspects of isiXhosa persuasion are expressed in Isisila sehobe. The core persuasive message in this text is concerned with marriage. This study shows that some people take as their reasons for marriage materialistic things such as wealth and as a result such marriages seldom materialise or become stable, because people merely stay together for convenience and not love. In Isisila sehobe the results of such a marriage are disastrous, even leading to death. In addition, this study aims to present an account of how characters in Isisila sehobe realise premises and strategies of persuasion in authentic communication, using the framework of persuasion theory (O’Keefe, 1990).
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Magosi, Lerato Elaine. "Dissecting heterogeneity in GWAS meta-analysis." Thesis, University of Oxford, 2017. https://ora.ox.ac.uk/objects/uuid:c853f7e7-93de-440c-b57c-fcfc03d3bb86.

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Statistical heterogeneity refers to differences among results of studies combined in a meta-analysis beyond that expected by chance. On the one hand, excessive heterogeneity can diminish power to discover genetic signals; on the other, moderate heterogeneity can reveal important biological differences among studies. Given its double-edged nature, this thesis dissects heterogeneity in genetic association meta-analyses from three vantage points. First, a novel multi-variant statistic, M is proposed to detect genome-wide (systematic) heterogeneity patterns in genetic association meta-analyses. This was motivated by the limited availability of appropriate methodology to measure the impact of heterogeneity across genetic signals, since traditional metrics (Q, I2 and T2) measure heterogeneity at individual variants. Second, given that meta-analyses comprising small numbers of studies typically report imprecise summary effect estimates; GWAS-derived empirical heterogeneity priors are used to improve precision in estimation of average genetic effects and heterogeneity in smaller meta-analyses (e.g. ≤ 10 studies). Third, a critical evaluation of the Han-Eskin random-effects model shows how it can identify small effect heterogeneous loci overlooked by traditional fixed and random-effects methods. This work draws attention to the existence of genome-wide heterogeneity patterns, to reveal systematic differences among the ascertainment criteria of participating studies in a meta-analysis of coronary disease (CAD) risk. Furthermore, simulation studies with the Han-Eskin random-effects model revealed inflated genetic signals at small effect loci when heterogeneity levels were high. However, it did reveal an additional CAD risk variant overlooked by traditional meta-analysis methods. We therefore recommend a holistic approach to exploring heterogeneity in meta-analyses which assesses heterogeneity of genetic effects both at individual variants with traditional statistics and across multiple genetic signals with the M statistic. Furthermore, it is critically important to review forest plots for small effect loci identified using the Han-Eskin random-effects model amidst moderate-to-high heterogeneity (I2 ≥ 40%).
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Ooi, Li Yin. "Post-GWAS functional characterisation of colorectal cancer risk loci." Thesis, University of Edinburgh, 2016. http://hdl.handle.net/1842/23514.

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Large bowel cancer, or colorectal cancer (CRC) is the third most common cause of cancer worldwide and the fourth biggest cause of cancer mortality. Twin studies have shown that the heritable contribution is ~35%, with ~5% of cases due to rare, high-penetrance mutations. In the last decade, the use of genome-wide association studies on large, well-characterised case-control cohorts of CRC has facilitated the identification of over 25 common genetic variants that carry with them an increased predisposition to colorectal cancer, invoking the common-disease common variant paradigm. As almost all of these variants lie within non-coding regions, the underlying causal mechanism is to-date poorly understood for the majority of these loci, and it is thought that they mediate risk by influencing gene expression levels. To test this hypothesis, an agnostic approach that utilises expression quantitative trait loci (eQTL) analysis was first carried on 115 normal colorectal mucosa samples and 59 peripheral blood mononuclear cells (PBMC). As these heritable variation on gene expression are likely to be subtle, there is a strong emphasis on the technical methodology to minimise experimentally-induced non-biological variations, including the extraction of high-quality RNA from primary tissue, the selection and validation of reference genes for normalisation of gene expression quantification, as well as internal validation of the samples and data processing. Thereafter, the association between the 25 CRC risk variants and the expression of their cis-genes were examined systematically, demonstrating that ten of these variants are also tissue-specific eQTLs. This intermediate phenotype strongly suggests that they confer risk, at least in part, by modifying regulatory mechanisms. One of the best eQTL associations (Xp22.2) is investigated in further detail to reveal a novel indel polymorphism (Indel24) at the distal promoter region of target gene SHROOM2 that influenced both transcript abundance and CRC risk more than the original tagging SNP. Functional verification with gene reporter assays indicated that Indel24 displays differential allelic control over transcriptional activity. Further in silico analysis and mutations to the reporter gene constructs provided evidence that Indel24 modulates transcription by modifying the spacing between CCAAT motifs and the consequent binding affinity of NF-Y transcription factor. siRNA depletion of NF-Y was associated with a reduction in transcriptional activity of the Indel24 gene construct as well as endogenous SHROOM2, which is strongly supportive of the interaction between Indel24 and NF-Y in the transcriptional activation of SHROOM2. Preliminary evidence is suggestive of SHROOM2 being expressed at the top of the intestinal epithelial crypt and playing a role in cell cycle regulation. Hypothesis-driven approaches can also be of utility in demonstrating functionality of CRC risk variants, complementing the hypothesis-free approach of eQTL analysis. Guided by a recently discovered gene-environment interaction between the 16q22.1 risk variant and circulating vitamin D levels, the influence of the rs9929218 SNP on CDH1 gene expression was examined, in relation to the expression of putative regulatory genes derived from in silico analysis and studies of other target genes. Although there was no direct association between rs9929218 and CDH1 expression, there were multiple two-way interactions that were together suggestive of rs9929218 influencing the VDR/FOXO4 regulation of CDH1. This provides functional support for the mechanism underlying the epidemiological observation of the gene-environment interaction between 16q22.1 and vitamin D, and demonstrates a candidate-based approach in deciphering the link between genetic locus and CRC susceptibility. In summary, the research presented in this thesis has validated the experimental rationale of utilising expression studies of normal colorectal mucosa to hone in on the molecular mechanisms and susceptibility genes underlying the association between common genetic variation and CRC risk.
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Hu, Xianghong. "Statistical methods for Mendelian randomization using GWAS summary data." HKBU Institutional Repository, 2019. https://repository.hkbu.edu.hk/etd_oa/639.

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Mendelian Randomization (MR) is a powerful tool for accessing causality of exposure on an outcome using genetic variants as the instrumental variables. Much of the recent developments is propelled by the increasing availability of GWAS summary data. However, the accuracy of the MR causal effect estimates could be challenged in case of the MR assumptions are violated. The source of biases could attribute to the weak effects arising because of polygenicity, the presentence of horizontal pleiotropy and other biases, e.g., selection bias. In this thesis, we proposed two works, expecting to deal with these issues.In the first part, we proposed a method named 'Bayesian Weighted Mendelian Randomization (BMWR)' for causal inference using summary statistics from GWAS. In BWMR, we not only take into account the uncertainty of weak effects owning to polygenicity of human genomics but also models the weak horizontal pleiotropic effects. Moreover, BWMR adopts a Bayesian reweighting strategy for detection of large pleiotropic outliers. An efficient algorithm based on variational inference was developed to make BWMR computationally efficient and stable. Considering the underestimated variance provided by variational inference, we further derived a closed form variance estimator inspired by a linear response method. We conducted several simulations to evaluate the performance of BWMR, demonstrating the advantage of BWMR over other methods. Then, we applied BWMR to access causality between 126 metabolites and 90 complex traits, revealing novel causal relationships. In the second part, we further developed BWMR-C: Statistical correction of selection bias for Mendelian Randomization based on a Bayesian weighted method. Based on the framework of BWMR, the probability model in BWMR-C is built conditional on the IV selection criteria. In such way, BWMR-C delicated to reduce the influence of the selection process on the causal effect estimates and also preserve the good properties of BWMR. To make the causal inference computationally stable and efficient, we developed a variational EM algorithm. We conducted several comprehensive simulations to evaluate the performance of BWMR-C for correction of selection bias. Then, we applied BWMR-C on seven body fat distribution related traits and 140 UK Biobank traits. Our results show that BWMR-C achieves satisfactory performance for correcting selection bias. Keywords: Mendelian Randomization, polygenicity, horizontal pleiotropy, selection bias, variation inference.
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Martin, Paul. "Post-GWAS bioinformatics and functional analysis of disease susceptibility loci." Thesis, University of Manchester, 2017. https://www.research.manchester.ac.uk/portal/en/theses/postgwas-bioinformatics-and-functional-analysis-of-disease-susceptibility-loci(cc0e6cee-5c32-4b75-b3d3-f7c18b6f126d).html.

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Genome-wide association studies (GWAS) have been tremendously successful in identifying genetic variants associated with complex diseases, such as rheumatoid arthritis (RA). However, the majority of these associations lie outside traditional protein coding regions and do not necessarily represent the causal effect. Therefore, the challenges post-GWAS are to identify causal variants, link them to target genes and explore the functional mechanisms involved in disease. The aim of the work presented here is to use high level bioinformatics to help address these challenges. There is now an increasing amount of experimental data generated by several large consortia with the aim of characterising the non-coding regions of the human genome, which has the ability to refine and prioritise genetic associations. However, whilst being publicly available, manually mining and utilising it to full effect can be prohibitive. I developed an automated tool, ASSIMILATOR, which quickly and effectively facilitated the mining and rapid interpretation of this data, inferring the likely functional consequence of variants and informing further investigation. This was used in a large extended GWAS in RA which assessed the functional impact of associated variants at the 22q12 locus, showing evidence that they could affect gene regulation. Environmental factors, such as vitamin D, can also affect gene regulation, increasing the risk of disease but are generally not incorporated into most GWAS. Vitamin D deficiency is common in RA and can regulate genes through vitamin D response elements (VDREs). I interrogated a large, publicly available VDRE ChIP-Seq dataset using a permutation testing approach to test for VDRE enrichment in RA loci. This study was the first comprehensive analysis of VDREs and RA associated variants and showed that they are enriched for VDREs, suggesting an involvement of vitamin D in RA.Indeed, evidence suggests that disease associated variants effect gene regulation through enhancer elements. These can act over large distances through physical interactions. A newly developed technique, Capture Hi-C, was used to identify regions of the genome which physically interact with associated variants for four autoimmune diseases. This study showed the complex physical interactions between genetic elements, which could be mediated by regions associated with disease. This work is pivotal in fully characterising genetic associations and determining their effect on disease. Further work has re-defined the 6q23 locus, a region associated with multiple diseases, resulting in a major re-evaluation of the likely causal gene in RA from TNFAIP3 to IL20RA, a druggable target, illustrating the huge potential of this research. Furthermore, it has been used to study the genetic associations unique to multiple sclerosis in the same region, showing chromatin interactions which support previously implicated genes and identify novel candidates. This could help improve our understanding and treatment of the disease. Bioinformatics is fundamental to fully exploit new and existing datasets and has made many positive impacts on our understanding of complex disease. This empowers researchers to fully explore disease aetiology and to further the discovery of new therapies.
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Loken, Erik. "Identifying functional variation in schizophrenia GWAS loci by pooled sequencing." VCU Scholars Compass, 2014. http://scholarscompass.vcu.edu/etd/3515.

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Schizophrenia demonstrates high heritability in part accounted for by common simple nucleotide variants (SNV), rare copy number variants (CNV) and, most recently, rare SNVs Although heritability explained by rare SNVs and CNVs is small compared to that explained by common SNVs, rare SNVs in functional sequences may identify specific disease mechanisms. However, current exome methods do not capture a large proportion of potentially functional bases where rare variation may impact disease risk: as much as two-thirds of conserved sequences lie outside the exome in non-coding regions of cross-species evolutionary constraint. We reasoned that the candidate loci from the Psychiatric Genomics Consortium Phase 1 (PGC-1) schizophrenia study represent good target loci to test for the impact of rare SNVs in non-coding constrained regions. We developed custom reagents to capture mammalian constrained non-coding regions, exons, and 5’- and 3’-untranslated regions (UTRs) in the 12 PGC-1 loci for pooled sequencing in 912 cases and 936 controls. Compared to our coding targets, our noncoding targets contain substantially more highly conserved bases (46,412 vs. 31,609) and variants (390 vs. 193). Using C-alpha to detect excess variance due to aggregate risk increasing or decreasing rare SNV effects, we identified signals attributable to alleles with MAF < 0.1% in both coding sequences and in functional non-coding sequences, including variants within ENCODE transcription factor binding sites, DNase hypersensitive regions, and histone modification sites in neuronal cell lines. We also observed significant excess risk-altering variation in the CUB domain of CSMD1, a gene expressed in the developing central nervous system. These results support the hypothesis that common and rare variants in the same loci contribute to schizophrenia risk, but highlight the need to expand capture strategies in order to detect trait-relevant sequence variation in a broader set of functional sequences.
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Evans-Jones, Gareth Hugh. "'Mae'r Beibl o'n tu' : y dadleuon Beiblaidd ynghylch caethwasiaeth ar dudalennau gwasg gyfnodol Gymraeg America, 1838-1868." Thesis, Bangor University, 2017. https://research.bangor.ac.uk/portal/en/theses/maer-beibl-on-tu-y-dadleuon-beiblaidd-ynghylch-caethwasiaeth-ar-dudalennau-gwasg-gyfnodol-gymraeg-america-18381868(fc2aa9ed-df9c-44d0-9959-350aea287da9).html.

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Amcan yr astudiaeth hon yw archwilio rôl y Beibl ymysg Cymry America’r bedwaredd ganrif ar bymtheg wrth iddynt ymateb i gaethwasiaeth, un o brif heriau eu gwlad fabwysiedig. Ymdriniwyd â’r mater yn helaeth ar dudalennau gwasg gyfnodol Gymraeg America, a defnyddid testunau Beiblaidd a chysyniadau Cristnogol yn fynych er mwyn trafod yr hyn a ystyrid gan amryw yn un o ‘bechodau mwyaf ysgeler’ yr Unol Daleithiau. Gan fod y diwylliant print yn hynod ddylanwadol yn y bedwaredd ganrif ar bymtheg, canolbwyntia’r traethawd hwn ar yr ymateb llenyddol a gafwyd i gaethwasiaeth gan Gymry America yn eu cyfnodolion a gyhoeddid yn ystod y cyfnod 1838-1868: oes aur y wasg gyfnodol Gymraeg yn yr Unol Daleithiau. Er mwyn ystyried eu defnydd o’r Beibl yng nghyd-destun y broblem gyfoes, archwilir defnydd Cymry America o bedwar testun neu thema Feiblaidd unigol ym mhedair pennod gyntaf y thesis. Cynnwys y rhain: Cham a Gomer, deddfau’r Pumllyfr a’r Jiwbili, y Gaethglud ym Mabilon, ac Iesu a’r Testament Newydd. Wrth asesu’r modd y defnyddiwyd y testunau a’r themâu hyn, ystyrir pa mor debyg yr oedd ymdriniaeth gwahanol awduron ohonynt. Yn ogystal, ymholir i ba raddau yr oedd holl Gymry America’n gwrthwynebu caethwasiaeth, ac a oedd rhai, mewn gwirionedd, wedi parhau i gefnogi’r gyfundrefn ar bwys y Beibl. Mae’r bumed bennod o natur wahanol i’r rhelyw gan y cymerir cyfraith a basiwyd gan lywodraeth yr Unol Daleithiau, a oedd yn arwyddocaol i’r ymgyrch diddymol, Cyfraith Caeth Ffoëdig 1850 fel astudiaeth achos, ac ystyrir y modd yr ymatebwyd iddi ar seiliau Beiblaidd. Awgrymir yn y bennod hon i radicaliaeth y Cymry ei hamlygu ei hun ymhellach yn sgil pasio cyfraith ddadleuol 1850. Daw’r thesis i glo drwy bwyso a mesur arwyddocâd y dadleuon Beiblaidd mewn trafodaethau ynglŷn â chaethwasiaeth, a chasglu i’r Ysgrythur fod yn ddylanwadol yng ngweithgarwch llenyddol, gwleidyddol a chymdeithasol hil Gomer yr Unol Daleithiau.
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Mitropanopoulos, Sotiris. "GWAS for Bipolar Disorder in a European Cohort with CNV Discovery." Thesis, The University of Arizona, 2012. http://hdl.handle.net/10150/221248.

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A Thesis submitted to The University of Arizona College of Medicine - Phoenix in partial fulfillment of the requirements for the Degree of Doctor of Medicine.
Background: Bipolar disorder (BD) is a disabling disorder whereby individuals suffer from episodes of mania and depression. The mode of inheritance of BD is complex and likely multifactorial. The specific number of susceptibility loci, the recurrence risk ratio attributable to each locus, and the degree of interaction between loci are unknown. By determining whether single nucleotide polymorphisms (SNPs) or copy number variants (CNVs) predispose individuals to bipolar disorder, therapeutics and diagnostic tests may be developed. Method: A Genome Wide Association Study (GWAS) was performed using cases of bipolar disorder and normal controls hybridized on Affymetrix 6.0 Genome-Wide Human SNP Arrays. Data preprocessing removed 595 individuals from 2205 arrays. The probe intensities of the remaining 880 cases and 730 controls were normalized. A modified t-test algorithm was used to determine p-values for each SNP. A sliding window analysis was performed on SNPs ordered by chromosome and locus. The mean probe intensities of the cases and controls from regions of significance were then reanalyzed for differences. Results: Analysis yielded several SNPs and CNVs that may have involvement in the pathophysiology of bipolar disorder. One region was 15kbp within the Neuron Navigator 2 (NAV2) gene. A second region was found in the Down Syndrome Cell Adhesion Molecule Like 1 (DSCAML1) gene. A third region was within the Voltage-dependent Calcium Channel Alpha 1G (CACNA1G). Conclusion: Multiple SNPs and CNVs may play a role in the phenotype of Bipolar Disorder. A convergent functional genomics approach with a gene network analysis maybe warranted elucidating possible pathophysiologies involving the gene products found to be significant in this study.
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Aldasoro, Alex-Ander. "Post-GWAS Investigations for discovering pleiotropic gene effects in cardiovascular diseases." Thesis, Université de Lorraine, 2017. http://www.theses.fr/2017LORR0247/document.

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Les maladies cardiovasculaires (MCV) sont d’une étiologie complexe et elles sont soumises à de nombreux facteurs environnementaux ainsi que génétiques. Malgré les succès obtenus, pendant la dernière décennie, et pour réduire la mortalité CV il est nécessaire l’identification de nouveaux biomarqueurs en utilisant des approches différentes. Cette thèse propose une approche intégrative pour découvrir de nouvelles associations génétiques associés avec les MCV. Nous avons d’abord réuni les résultats existants grâce à des GWAS précédents, puis nous avons recherché la pléiotropie de ces gènes et nous avons dirigé nos efforts vers une possible traduction des résultats obtenus dans l’application clinique. Nous avons détecté les effets pléiotropiques de différent gènes (IL-6R et ABO) avec différents phénotypes lipidiques et inflammatoires. Par ailleurs, nous avons trouvé quelques associations gène-genre intéressantes pour certains gènes étudiés (ABO et GNB3). Concernant l’implémentation clinique des connaissances obtenues par cette thèse, une SNP dans le gène TREM-1, pourrait être utilisé comme un marqueur de risque pour différentes maladies, et nous avons déposé un brevet Européen et nous envisageons de mener des essais cliniques de chez les patients. D’autre part, nous avons détecté une haplotype du gène IL6R qui pourrait être utilisés dans la médecine personnalisée. Nos résultats aident à mieux comprendre comment les gènes étudiés exercent leurs effets au niveau moléculaire, en influant finalement sur l’état des patients souffrant de MCV. Nous espérons que nos résultats vont être pris en compte pour faire progresser la médecine personnalisée
Cardiovascular diseases (CVD) are complex diseases where many environmental and genetic factors are involved. Although the genetic aetiology of the CVD has been extensively investigated the last two decades, alternative approaches are needed in order to keep advancing in the pathophysiology of CVD. In this thesis, we propose an integrative approach to discover new genetic associations potentially involved in CVD. We chose previous GWAS hits and we centred our efforts in studying the pleiotropic and gene-gender interaction effects. Finally, we focused on the implementation of personalized genome-based therapy of the results obtained. New pleiotropic effects were discovered in the IL-6R and ABO genes relating them with different inflammatory and lipid phenotypes. In addition, we studied the gene-gender interaction effects, finding some sex-specific associations in two of the genes studied (ABO and GNB3). Further, we centered our efforts in implementing the results obtained during the thesis at the clinical level. One SNP within the TREM-1 gene was associated with increased levels of its protein and could be used as a predictor or risk biomarker for different diseases. Due to the high potential of this SNP, we applied a European patent and we are planning to start clinical trials in patients. Also, one haplotype in the IL-6R gene could be used in the treatment of personalized medicine. During this thesis, we discovered new gene-phenotype associations involved in CVD and other diseases. Our results help to better understand how the studied genes are exerting their effects at the molecular level. Our results will hopefully be taken into account in future personalized treatments
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Resende, Rafael Tassinari. "Regional Heritability Mapping and GWAS for molecular breeding in eucalyptus hybrids." Universidade Federal de Viçosa, 2017. http://www.locus.ufv.br/handle/123456789/11670.

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Conselho Nacional de Desenvolvimento Científico e Tecnológico
Embora os estudos de associação genômica (GWAS) forneçam informações valiosas na descodificação das relações entre a variação gênica e os fenótipos complexos, esta técnica explica uma pequena fração da herdabilidade. O mapeamento de herdabilidades regionais (RHM) fornece estimativas de herdabilidade para segmentos genômicos que contêm efeitos alélicos raros e que contribuem individualmente com baixa variação ao ponto de serem detectados pela GWAS. Neste estudo foi realizado a GWAS e o RHM para sete características de crescimento, madeira e resistência à doenças em uma população 768 árvores híbridas de Eucalyptus usando o moderno Chip Illumina EuCHIP60K. As herdabilidades genômicas totais representaram grandes proporções (64-89%) de herdabilidades baseadas em pedigree, fornecendo evidências adicionais de que características complexas em eucaliptos são controlados por muitas variantes ao longo do genoma, cada uma com pequenas contribuições para a variância fenotípica. O RHM detectou 26 QTLs (Quantitative Trait Loci) abrangendo 2.191 SNPs (Single Nucleotide Polymorphism), enquanto que a GWAS detectou 13 associações. Os QTLs detectados via RHM e GWAS explicaram individualmente 5 a 15% e 4 a 6% da herdabilidade genômica, respectivamente. O RHM foi superior à GWAS na captura de maiores proporções de herdabilidade genômica. Semelhantemente a QTLs previamente mapeados, os resultados destacaram as regiões genômicas que podem ser utilizadas em estudos mais aprofundados para descoberta de genes. Os RHM-QTLs contendo uma combinação de variantes comuns e raras representam um avanço para incorporar conhecimento prévio da arquitetura genética subjacente em modelos de predição genômica.
Although genome-wide association studies (GWAS) have provided valuable insights into the decoding of the relationships between sequence variation and complex phenotypes, they have explained little heritability. Regional heritability mapping (RHM) provides heritability estimates for genomic segments containing both common and rare allelic effects that individually contribute too little variance to be detected by GWAS. We carried out GWAS and RHM for seven growths, wood and disease resistance traits in a breeding population of 768 Eucalyptus hybrid trees using EuCHIP60K. Total genomic heritabilities accounted for large proportions (64 89%) of pedigree-based trait heritabilities, providing additional evidence that complex traits in eucalypts are controlled by many sequence variants across the frequency spectrum, each with small contributions to the phenotypic variance. RHM detected 26 quantitative trait loci (QTLs) encompassing 2,191 single nucleotide polymorphisms (SNPs), whereas GWAS detected 13 single SNP trait associations. RHM and GWAS QTLs individually explained 5 15% and 4 6% of the genomic heritability, respectively. RHM was superior to GWAS in capturing larger proportions of genomic heritability. Equated to previously mapped QTLs, our results highlighted genomic regions for further examination towards gene discovery. RHM-QTLs bearing a combination of common and rare variants could be useful enhancements to incorporate prior knowledge of the underlying genetic architecture in genomic prediction models.
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Books on the topic "Gwashu"

1

Dowd, Anthony. The special bindings of Gwasg Gregynog: An illustrated catalogue of the special bindings produced at Gregynog between 1977 and 2002. Newtown, Powys: Gwasg Gregynog, 2004.

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Dowd, Anthony. The special bindings of Gwasg Gregynog: An illustrated catalogue of the special bindings produced at Gregynog between 1977 and 2002. Newtown: Gwasg Gregynog, 2004.

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Creu argraff: Atgofion teulu Gwasg Gomer. Llandysul, Ceredigion: Gomer, 2012.

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Hughes, Mair Wynn. Gwas y stabl. Llandysul: Gomer, 2004.

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Gwas y gwaredwr. Abertawe: T^y John Penry, 1991.

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Nicieja, Stanisław Sławomir. Z Kijowa na Piccadilly: Wokół biografii Tadeusza Zabłockiego-Gwasza. Opole: Wydawn. Helionia, 1993.

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Z kijowa na Picadilly: Wokół biografii Tadeusza Zabłockiego-Gwasza. Opole: Helionia, 1994.

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The archaeology of Rutland Water: Excavations at Empingham in Gwash Valley, Rutland, 1967-73 and 1990. Leicester: University of Leicester Archaeological Services, 2000.

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Harrop, Dorothy A. The Gregynog Press Gwasg Gregynog: Three essays Tair ysgrif. [Newtown, Powys]: [Gwasg Gregynog], 2003.

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Glaz, Kazimir. From the Essence Series: Istota rzeczy : works on paper, gwasze, 1985-2005. Toronto: Toronto Center for Contemporary Art, 2005.

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Book chapters on the topic "Gwashu"

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Stram, Daniel O. "Post-GWAS Analyses." In Design, Analysis, and Interpretation of Genome-Wide Association Scans, 285–327. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-9443-0_8.

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Kim, Ju Han. "GWAS Data Analysis." In Genome Data Analysis, 281–97. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-1942-6_16.

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Krawczak, Michael. "Genomweite Assoziationsstudien (GWAS)." In Handbuch Ethik und Recht der Forschung am Menschen, 39–42. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-35099-3_7.

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Frommlet, Florian, Małgorzata Bogdan, and David Ramsey. "Statistical Analysis of GWAS." In Computational Biology, 105–61. London: Springer London, 2016. http://dx.doi.org/10.1007/978-1-4471-5310-8_5.

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Lu, Yang, Katherine Perez-Morera, and Rita M. Cantor. "GWAS for Drug Discovery." In Nonclinical Statistics for Pharmaceutical and Biotechnology Industries, 157–76. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-23558-5_7.

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Waugh, Robbie, Bill Thomas, Andrew Flavell, Luke Ramsay, Jordi Comadran, and Joanne Russell. "Genome-Wide Association Scans (GWAS)." In Biotechnological Approaches to Barley Improvement, 345–65. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-662-44406-1_18.

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Fernando, Rohan L., and Dorian Garrick. "Bayesian Methods Applied to GWAS." In Methods in Molecular Biology, 237–74. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-447-0_10.

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Wagner, Peter, Frank C. Mooren, Hidde J. Haisma, Stephen H. Day, Alun G. Williams, Julius Bogomolovas, Henk Granzier, et al. "Genome-Wide Association Study (GWAS)." In Encyclopedia of Exercise Medicine in Health and Disease, 363. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_2436.

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Galik, Elizabeth, Shin Fukudo, Yukari Tanaka, Yori Gidron, Tavis S. Campbell, Jillian A. Johnson, Kristin A. Zernicke, et al. "Genome-Wide Association Study (GWAS)." In Encyclopedia of Behavioral Medicine, 852–54. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-1005-9_697.

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Pare, Guillaume, and Matthew P. A. Henderson. "Genome-Wide Association Studies (GWAS)." In Stroke Genetics, 25–50. London: Springer London, 2012. http://dx.doi.org/10.1007/978-0-85729-209-4_3.

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Conference papers on the topic "Gwashu"

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Slaten, Marianne. "HAPPI GWAS: Holistic Analysis with Pre and Post Integration GWAS." In ASPB PLANT BIOLOGY 2020. USA: ASPB, 2020. http://dx.doi.org/10.46678/pb.20.1374646.

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Fienberg, Stephen E., Aleksandra Slavkovic, and Caroline Uhler. "Privacy Preserving GWAS Data Sharing." In 2011 IEEE International Conference on Data Mining Workshops (ICDMW). IEEE, 2011. http://dx.doi.org/10.1109/icdmw.2011.140.

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Marin, Belen, Carlos Alquezar-Baeta, Monica Hernandez, and Elvira Mayordomo. "Evolution of GWAS results through ADNI cohorts." In 2018 IEEE International Conference on Bioinformatics and Biomedicine (BIBM). IEEE, 2018. http://dx.doi.org/10.1109/bibm.2018.8621358.

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WARDE-FARLEY, DAVID, MICHAEL BRUDNO, QUAID MORRIS, and ANNA GOLDENBERG. "MIXTURE MODEL FOR SUB-PHENOTYPING IN GWAS." In Proceedings of the Pacific Symposium. WORLD SCIENTIFIC, 2011. http://dx.doi.org/10.1142/9789814366496_0035.

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Zhang, Yanjun, Xin Zhao, Xue Li, Mingyang Zhong, Caitlin Curtis, and Chen Chen. "Enabling Privacy-Preserving Sharing of Genomic Data for GWASs in Decentralized Networks." In WSDM '19: The Twelfth ACM International Conference on Web Search and Data Mining. New York, NY, USA: ACM, 2019. http://dx.doi.org/10.1145/3289600.3290983.

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Ahmed, Zeeshan, Saman Zeeshan, and Bruce T. Liang. "PAS-SNP: iOS App with GWAS SNP-Disease Database for Personalized Genomics Research: PAS-SNP for GWAS SNP-Disease." In 2019 IEEE International Conference on Bioinformatics and Biomedicine (BIBM). IEEE, 2019. http://dx.doi.org/10.1109/bibm47256.2019.8983389.

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Mutalib, Sofianita, and Azlinah Mohamed. "A brief survey on GWAS and ML algorithms." In 2011 11th International Conference on Hybrid Intelligent Systems (HIS 2011). IEEE, 2011. http://dx.doi.org/10.1109/his.2011.6122184.

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Wang, Zhengkui, Yue Wang, Kian-Lee Tan, Limsoon Wong, and Divyakant Agrawal. "CEO a cloud epistasis computing model in GWAS." In 2010 IEEE International Conference on Bioinformatics and Biomedicine (BIBM 2010). IEEE, 2010. http://dx.doi.org/10.1109/bibm.2010.5706542.

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Wang, Liya, Doreen Ware, Nirav Merchant, and Carol Lushbough. "Building an open Genome Wide Association Study (GWAS) platform." In 2013 IEEE International Conference on Cluster Computing (CLUSTER). IEEE, 2013. http://dx.doi.org/10.1109/cluster.2013.6702696.

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Alipanah, Neda, Hyeoneuoi Kim, and Lucila Ohno-Machado. "Building an Ontology of Phenotypes for Existing GWAS Studies." In 2012 IEEE Second International Conference on Healthcare Informatics, Imaging and Systems Biology (HISB). IEEE, 2012. http://dx.doi.org/10.1109/hisb.2012.36.

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Reports on the topic "Gwashu"

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Hermosilla, Manuel, and Jorge Lemus. Therapeutic Translation of Genomic Science: Opportunities and limitations of GWAS. Cambridge, MA: National Bureau of Economic Research, November 2017. http://dx.doi.org/10.3386/w23989.

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Thibodeau, Stephen. Use of eQTL Analysis for the Discovery of Target Genes Identified by GWAS. Fort Belvoir, VA: Defense Technical Information Center, April 2014. http://dx.doi.org/10.21236/ada604737.

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Thibodeau, Stephen. Use of eQTL Analysis for the Discovery of Target Genes Identified by GWAS. Fort Belvoir, VA: Defense Technical Information Center, April 2013. http://dx.doi.org/10.21236/ada591115.

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Thibodeau, Stephen. Use of eQTL Analysis for the Discovery of Target Genes Identified by GWAS. Fort Belvoir, VA: Defense Technical Information Center, April 2012. http://dx.doi.org/10.21236/ada561870.

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