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Dissertations / Theses on the topic 'Genetic risk of disease'

Author: Grafiati
Published: 11 March 2023
Last updated: 31 July 2025

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1

Tilley, Louise. "Genetic risk factors in sporadic Alzheimer's disease." Thesis, University of Nottingham, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.311748.

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2

Salfati, Elias Levy Itshak. "Genetic determinants of cardiovascular disease : heritability and genetic risk score." Thesis, Paris 5, 2014. http://www.theses.fr/2014PA05S014/document.

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Les maladies complexes telles que les maladies cardio-Vasculaires (MCV) sont influencées par des facteurs génétiques et environnementaux. L’estimation du risque cardio-Vasculaire chez un individu est généralement évaluée par la sommation des facteurs de risque reconnu des MCV (p. ex. l’âge, le sexe, le tabac, la pression artérielle et le cholestérol). Dernièrement, plusieurs bio-Marqueurs ont été examiné pour leur aptitude à améliorer la prédiction des maladies cardio-Vasculaires au-Delà des facteurs de risques traditionnels. L’intérêt de découvrir de nouveaux loci est incité notamment par les
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3

Hughes, Katherine Carlson. "Dietary and Genetic Risk Factors for Parkinson's Disease." Thesis, Harvard University, 2016. http://nrs.harvard.edu/urn-3:HUL.InstRepos:27201728.

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Parkinson’s disease (PD) is the second most common neurodegenerative disease. Motor symptoms typically do not manifest until significant neuronal loss has already occurred, highlighting the need for early detection and prevention. In this dissertation, we sought to improve our understanding of PD epidemiology by studying associations between potential modifiable risk factors, including antioxidant vitamins, dairy products, and urate, and PD risk. We conducted prospective analyses within three large cohort studies: the Nurses’ Health Study, the Health Professionals Follow-up Study, and the Canc
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4

Duan, Qingling. "Pharmacogenomics and genetic risk factors of coronary artery disease." Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=115665.

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Coronary artery disease (CAD) is the most prevalent disorder and the leading cause of death worldwide. There are a number of CAD medications, which are effective and safe in most patients, but have been associated with adverse reactions such as angioedema induced by angiotensin I-converting enzyme inhibitors (AE-ACEi). In this study, we identified aminopeptidase P (APP) activity as an endophenotype for AE-ACEi, which is a heritable quantitative trait (heritability =0.336 +/- 0.251 SD) and is significantly reduced in a majority of our cases. Although initial mutation screening did not reveal an
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5

Ossei-Gerning, Nicholas. "Genetic polymorphisms and the risk of coronary artery disease." Thesis, University College London (University of London), 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.391615.

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6

Hayashi, Satomi. "HYPERHOMOCYSTEINEMIA: GENETIC POLYMORPHISMS AND RISK OF CORONARY ARTERY DISEASE." Thesis, The University of Arizona, 2003. http://hdl.handle.net/10150/610473.

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This comprehensive literature review focuses on homocysteine, gene polymorphisms related to homocysteine metabolism and their relationship to coronary artery disease (CAD). Currently, CAD is known as a multifactorial genetic disease, resulting from complex interactions between genetic factors and various environmental influences. In recent years, tremendous knowledge about the hereditary aspect of CAD has been gained, including an understanding of CAD as a multifactorial condition resulting from complex interactions between genetic factors and various environmental influences that trigg
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7

Romagnoli, Martina <1987&gt. "Genetic, immune and environmental risk factors in Alzheimer's disease." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2017. http://amsdottorato.unibo.it/7930/1/Romagnoli_Martina_tesi.pdf.

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Alzheimer's disease (AD) is a complex multi-factorial disease in which several pathogenetic, clinical, environmental and stochastic factors are involved. It is on record that persistent virus infections, the progressive decline of immune competence with ageing and chronic psychological stress exposures might play a pivotal role in AD. This study shows that in patients with clinical and neurological AD diagnosis, antiviral immune response is defective in the majority of AD brain samples. Moreover, gene variants of APOE and IRF7 strongly affect antiviral gene expression profiles in hippocampus.
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8

Ylönen, S. (Susanna). "Genetic risk factors for movement disorders in Finland." Doctoral thesis, Oulun yliopisto, 2019. http://urn.fi/urn:isbn:9789526223988.

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Abstract Parkinson’s disease and Huntington’s disease are progressive neurodegenerative movement disorders that typically manifest in adulthood. In this study, genetic risk factors contributing to these two movement disorders were investigated in Finnish patients. Patients with early-onset or late-onset Parkinson’s disease as well as population controls were examined. The p.L444P mutation in GBA was found to contribute to the risk of Parkinson’s disease. POLG1 compound heterozygous mutations were detected in two patients with Parkinson’s disease and rare length variants in POLG1 were associate
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9

Chen, Lu-hua, and 陈璐华. "Genetic risk factors for late-onset Alzheimer's disease in Chinese." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hub.hku.hk/bib/B49617588.

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Alzheimer’s disease (AD) is a progressive neurodegenerative disorder, with genetic factors playing critical roles in its pathogenesis. Mutations in APP, PSEN1 and PSEN2 genes are confirmed to be causative risk factors for early-onset Alzheimer’s disease (EOAD). For late-onset Alzheimer’s disease (LOAD), growing evidence suggests it is caused by multiple genetic risk factors in corporation with the environmental exposures. Although, so far, APOE is the most well recognized common genetic risk factor for LOAD, other susceptible candidate genes, such as CR1, CLU and PICALM, have recently been id
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10

Sarwar, Nadeem. "Emerging molecular and genetic risk factors for coronary heart disease." Thesis, University of Cambridge, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.611549.

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11

Baumgaertel, Johanna, Robert Haußmann, Antonia Gruschwitz, et al. "Education and Genetic Risk Modulate Hippocampal Structure in Alzheimer’s Disease." Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2017. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-214315.

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Genetic and environmental protective factors and risks modulate brain structure and function in neurodegenerative diseases and their preclinical stages. We wanted to investigate whether the years of formal education, a proxy measure for cognitive reserve, would influence hippocampal structure in Alzheimer’s disease patients, and whether apolipoprotein Eε4 (APOE4) carrier status and a first-degree family history of the disease would change a possible association. Fifty-eight Alzheimer’s disease patients underwent 3T magnetic resonance imaging. We applied a cortical unfolding approach to investi
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12

Stojanova, Jana. "Environmental and genetic risk factors for post-transplant lymphoproliferative disease." Limoges, 2013. http://aurore.unilim.fr/theses/nxfile/default/6c517c4c-5de7-490e-a6f5-5fc542155ba9/blobholder:0/2013LIMO310E.pdf.

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Post-transplant lymphoproliferative disorders (PTLDs) represent a serious complication in solid organ transplantation and are the first cause of cancer related mortality in this population. Furtehrmore, lymphomatous PTLD in this setting is frequently extranodal, can behave more aggressively and tends to have a worse prognosis. Previous work addressing risk factors for PTLD have been based on data from large registries, lacking the detail required to address the role of individual maintenance immunosuppressant drugs, taken over time. Studies looking at genetic risk factors for PTLD have focused
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13

Baumgaertel, Johanna, Robert Haußmann, Antonia Gruschwitz, et al. "Education and Genetic Risk Modulate Hippocampal Structure in Alzheimer’s Disease." Aging and Disease, 2016. https://tud.qucosa.de/id/qucosa%3A29982.

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Genetic and environmental protective factors and risks modulate brain structure and function in neurodegenerative diseases and their preclinical stages. We wanted to investigate whether the years of formal education, a proxy measure for cognitive reserve, would influence hippocampal structure in Alzheimer’s disease patients, and whether apolipoprotein Eε4 (APOE4) carrier status and a first-degree family history of the disease would change a possible association. Fifty-eight Alzheimer’s disease patients underwent 3T magnetic resonance imaging. We applied a cortical unfolding approach to investi
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14

Abelson, Anna-Karin. "Genetic Risk Factors for Systemic Lupus Erythematosus : From Candidate Genes to Functional Variants." Doctoral thesis, Uppsala : Universitetsbiblioteket [distributör], 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-9367.

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15

Wanby, Pär W. "On certain genetic and metabolic risk factors for carotid stenosis and stroke." Doctoral thesis, Linköpings universitet, Institutionen för medicin och hälsa, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-7467.

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The present study evaluated genetic and metabolic factors influencing the risk of acute cerebrovascular disease (CVD) and internal carotid artery stenosis (ICA stenosis) in a Swedish community. The threonine (T) containing protein of the FABP2 A54T gene polymorphism has a greater affinity for long chain fatty acids (FFAs) than the alanine (A) containing protein. This altered affinity for FFAs has been shown to affect the intestinal absorption of fatty acids and consequently the fatty acid composition of serum lipids, in particularly postprandially. Endothelium derived NO is a potent vasodilato
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16

Daavittila, I. (Iita). "Genetic risk factors for lumbar intervertebral disc disease characterized by sciatica." Doctoral thesis, University of Oulu, 2007. http://urn.fi/urn:isbn:9789514283666.

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Abstract Genetic factors have been shown to have an important role in intervertebral disc disease. The associations of known genetic risk factors and whole-body vibration, a proposed environmental risk factor, for intervertebral disc disease (IDD) were evaluated. Eleven variations in eight genes (COL9A2, COL9A3, COL11A2, IL1A, IL1B, IL6, MMP-3 and VDR) were genotyped in 150 male train engineers with an average of 21-year exposure to whole-body vibration and 61 male paper mill workers with no occupational exposure to vibration. The number of individuals belonging to the IDD group was significan
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17

Caglayan, Safak [Verfasser]. "SORLA/SORL1 as genetic risk factor in Alzheimer disease / Safak Caglayan." Berlin : Freie Universität Berlin, 2013. http://d-nb.info/1043480935/34.

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18

Shah, S. H. "Discovery and application of genetic determinants of cardiovascular disease risk factors." Thesis, University College London (University of London), 2014. http://discovery.ucl.ac.uk/1417181/.

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The focus of my PhD has been two-­‐fold: First, to improve the understanding of the biology behind a well-­‐known cardiovascular disease (CVD) risk factor -­‐ left ventricular mass, by identifying novel genetic loci associated with this risk factor. A large-­‐scale association meta-­‐analysis in over 10,000 individuals identified four novel loci associated with electrocardiographically-­‐determined left ventricular mass. Second, to explore the application of known genetic determinants of the main blood lipid fractions, the latter being well-­‐known CVD risk factors and therapeutic targets. I a
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19

McVey, David Graham. "Investigating genetic risk factors of coronary artery disease using genome editing." Thesis, University of Leicester, 2016. http://hdl.handle.net/2381/36614.

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Genome-wide association studies (GWAS) have identified the genetic loci associated with many complex diseases including coronary artery disease (CAD). The challenge now is to elucidate the biological and cellular pathways affected by disease-associated loci. In order to fully understand the functional mechanisms, the causal genetic variants need to be identified. The majority of GWAS loci lack candidate genes, and may instead be located in regulatory regions, making the functional effects of specific variants difficult to appreciate. Recently, genome editing techniques have become available th
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20

Rodrigo, Undugodage Linduni Madushika. "Identifying novel, conditional and joint genetic effects on Parkinson's disease risk." Thesis, Queensland University of Technology, 2021. https://eprints.qut.edu.au/212754/1/Undugodage_Rodrigo_Thesis.pdf.

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This study is an analysis of existing ExomeChip-based genome-wide association data to demonstrate the utility of genotype imputation with whole genome sequence-based haplotype reference panels, and recently developed statistical and machine learning approaches to identify novel common and rare genetic variants and their interactions associated with Parkinson’s disease risk.
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21

Petersen, Desiree C. "Genetic aspects of HIV-1 risk in an African setting." Thesis, Link to the online version, 2006. http://hdl.handle.net/10019.1/1294.

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22

Almontashiri, Naif Ahmad. "The Genetic and Proteomic Detereminants of the Risk of Coronary Artery Disease." Thesis, Université d'Ottawa / University of Ottawa, 2015. http://hdl.handle.net/10393/32382.

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Coronary artery disease (CAD) remains the number one cause of morbidity and mortality in the world. CAD or atherosclerosis of the coronary arteries, results from the interaction of environmental and genetic risks factors and it is postulated that 50% of the susceptibility to CAD is genetic. With knowledge of specific genetic predispositions, people at risk could be screened earlier before the disease onset. I used information from genome wide association studies (GWASs) approach to characterize some of the genetic polymorphisms that increase the risk of CAD in large case-control studies. From
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23

Perdigão, Catarina. "The impact of the genetic risk factor BIN1 to Alzheimer’s disease development." Doctoral thesis, Universidade Nova de Lisboa. Instituto de Tecnologia Quimica e Biológica António Xavier, 2021. http://hdl.handle.net/10362/132008.

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" Alzheimer’s disease (AD) was identified more than a century ago. Yet, there is still no cure and the mechanisms behind the most common form of AD (late-onset, LOAD) are still an open question. BIN1 was the second gene most frequently associated with LOAD. Bin1 depletion has been linked with AD earliest pathomechanisms: increased beta-amyloid (Aβ) accumulation, endosomal abnormalities, and synaptic defects. Sequencing of BIN1 genomic locus identified regulatory and coding variants of BIN1, indicating that Bin1 correct levels and function are essential for a healthy bra
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24

Eckart, Kerstin. "Identification and Functional Characterization of Genetic Risk Factors in Alzheimer´s Disease." Diss., lmu, 2009. http://nbn-resolving.de/urn:nbn:de:bvb:19-102595.

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25

Clark, Graeme Richard. "The role of genetic risk factors on the phenotype of Parkinson's Disease." Thesis, University of Newcastle upon Tyne, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.489728.

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Parkinson's disease (PD) is the second most comInon neurodegenerative disease after Alzheimer's disease (AD), and effects approximately 1% of the over 50 population. PD can be clinically characterised by the so called 'cardinal features', which include resting tremor rigidity, bradykinesia and postural instability. Many PD patients later develop non-motor symptoms, including depression, psychosis, anxiety, insomnia and dementia. Previous studies have focussed on dementia in PD, with co-prevalence rates of between 10-80% being reported, the most consistent estimates being 25-30%. Also, PD patie
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26

Chan, Daniel Kam Yin School of Physiology &amp Pharmacology UNSW. "Genetic and environmental risk factors for Parkinson's disease in Chinese and Australians." Awarded by:University of New South Wales. School of Physiology & Pharmacology, 2000. http://handle.unsw.edu.au/1959.4/17795.

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The aim of this work was to study the environmental and genetic factors for Parkinson???s disease (PD) in Chinese and Australian. Using a case-control method, environmental factors for PD were studied in a Chinese population (n=528) in Hong Kong. Current smoking (OR=0.437; p=0.013) and infrequent tea drinking (OR=1.51; p=0.02) were found to be protective factors, whereas family history and pesticide exposure during farming in females were found to be risk factors in the univariate analysis. In the multivariate analysis, current smoking reached borderline significance at the 5% level and the va
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27

Heslop, Claire Louise. "Emerging environmental, molecular, and genetic risk factors in stable coronary artery disease." Thesis, University of British Columbia, 2009. http://hdl.handle.net/2429/11244.

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Both environmental and inherited risk factors make significant contributions to coronary artery disease, however susceptibility and age of disease onset for individuals with similar risk profiles varies widely. Novel biomarkers may yet be found which could improve detection of high-risk individuals, and highlight new areas of research for treatment discovery. This thesis explores risk factors for coronary artery disease and cardiovascular mortality. The first study investigates one specific environmental variable—neighbourhood socioeconomic status—in a cohort of patients who underwent selectiv
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28

Wang, Lisa Yuan [Verfasser], and Manu [Akademischer Betreuer] Sharma. "Genetic Risk Factors of Parkinson's disease / Lisa Yuan Wang ; Betreuer: Manu Sharma." Tübingen : Universitätsbibliothek Tübingen, 2018. http://d-nb.info/1168634261/34.

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29

Liolitsa, Danae. "Genetic risk factors in Alzheiner's disease : a hypothesis-based candidate gene approach." Thesis, King's College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.252104.

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30

Patel, Bipen Dahyabhai. "Environmental and genetic risk factors for the development of obstructive airways disease." Thesis, University of Cambridge, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.613675.

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31

Erqou, Sebhat. "Lipoprotein(a) and the risk of vascular disease." Thesis, University of Cambridge, 2010. https://www.repository.cam.ac.uk/handle/1810/225182.

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Background: Lipoprotein(a) [Lp(a)] is composed of a low density-lipoprotein (LDL) particle and a glycoprotein molecule known as apolipoprotein(a) [apo(a)]. Apo(a) exists in several differently-sized isoforms and is responsible for the unique properties of Lp(a). Although Lp(a) has been known for the past 40 years its relationship with coronary heart disease (CHD) has not been characterized in sufficient detail. Whether Lp(a) causes CHD is not clear. Furthermore, the role of apo(a) isoform variation and other sources of Lp(a) heterogeneity (e.g., level of oxidized phospholipids) in Lp(a)-diseas
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32

Naguib, M. "Late paraphrenia : phenomenology, classification and risk factors implicated in its causation." Thesis, King's College London (University of London), 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.325085.

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33

Kennedy, Amy. "Genetic Markers, Birth Characteristics, and Childhood Leukemia Risk." FIU Digital Commons, 2013. http://digitalcommons.fiu.edu/etd/992.

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The cause for childhood acute lymphoblastic leukemia (ALL) remains unknown, but male gender is a risk factor, and among ethnicities, Hispanics have the highest risk. In this dissertation, we explored correlations among genetic polymorphisms, birth characteristics, and the risk of childhood ALL in a multi-ethnic sample in 161 cases and 231 controls recruited contemporaneously (2007-2012) in Houston, TX. We first examined three lymphoma risk markers, since lymphoma and ALL both stem from lymphoid cells. Of these, rs2395185 showed a risk association in non-Hispanic White males (OR=2.8, P=0.02; Pi
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34

Fuller, Melissa Suzanne. "Primary Care Providers Believe Patient-Generated Family History Will Increase Ability to Assess Patient Risk." University of Cincinnati / OhioLINK, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1218051698.

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35

Bradley, India. "Clinical Practices of Neurologists Related to Predictive Testing of Presymptomatic Patients At Risk for Huntington Disease." University of Cincinnati / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1406900839.

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36

Lluís, Ganella Carla 1984. "Genetic factors associated with coronary heart disease and analysis of their predictive capacity." Doctoral thesis, Universitat Pompeu Fabra, 2012. http://hdl.handle.net/10803/84185.

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The main expansion of the discovery of genetic variants associated with complex diseases has occurred during the last decade. This expansion has been accompanied, and in some sense motivated, by the desire to use this information to improve the predictive capacity of many diseases with an unidentified familial component, including coronary heart disease (CHD), with the aim of translating this genetic knowledge into clinical practice. This doctoral thesis is structured in two lines of investigation that address distinct aspects of this issue, first to evaluate the possible role of genetic varia
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37

Wanby, Pär W. "On certain genetic and metabolic risk factors for carotid stenosis and stroke /." Linköping : Kalmar : Linköping University ; Department of Internal Medicine, County Hospital of Kalmar, 2006. http://www.bibl.liu.se/liupubl/disp/disp2006/med942s.pdf.

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38

Antoine, Darlène. "Functional Regulation at the 9p21.3 Genetic Risk Locus in Coronary Artery Disease (CAD)." Thesis, Université d'Ottawa / University of Ottawa, 2015. http://hdl.handle.net/10393/33148.

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The first genetic CAD risk locus to be identified by genome-wide association studies, single nucleotide polymorphisms (SNPs) at 9p21.3 predispose to increased risk of CAD. By bioinformatics scan analysis of the 9p21.3 locus; we interrogated the 59 linked SNPs over the 53,202bp to identify putative transcription factor-binding consensus sequences. We hypothesize that some genetic polymorphisms at the 9p21.3 locus are functional and will disrupt specific regulatory sequences within enhancers. Here, I investigated how polymorphisms affect TEAD-dependent regulation at the 9p21.3 locus, and also ho
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39

Reitz, Christiane. "Genetic and vascular risk factors for cognitive decline and cerebral small-vessel disease." [S.l.] : [The Author], 2006. http://hdl.handle.net/1765/13309.

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40

Carter, Sarah. "The potential value and regulation of genetic tests for complex disease risk factors." Thesis, University College London (University of London), 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.433791.

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41

Assimes, Themistocles L., and Robert Roberts. "Genetics: Implications for Prevention and Management of Coronary Artery Disease." ELSEVIER SCIENCE INC, 2016. http://hdl.handle.net/10150/623131.

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An exciting new era has dawned for the prevention and management of CAD utilizing genetic risk variants. The recent identification of over 60 susceptibility loci for coronary artery disease (CAD) confirm not only the importance of established risk factors, but also the existence of many novel causal pathways that are expected to improve our understanding of the genetic basis of CAD and facilitate the development of new therapeutic agents over time. Concurrently, Mendelian randomization studies have provided intriguing insights on the causal relationship between CAD-related traits, and highlig
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42

Porter, Tenielle L. S. "Genetic determinants of rates of cognitive decline in preclinical Alzheimer’s Disease." Thesis, Edith Cowan University, Research Online, Perth, Western Australia, 2018. https://ro.ecu.edu.au/theses/2114.

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In 2015 the number of people worldwide living with Dementia was 46.8 million, with approximately 50-75% of these cases being clinically defined as Alzheimer’s disease (AD). Despite extensive efforts, clinical trials have so far failed to yield a treatment that successfully addresses the underlying cause of AD. This lack of treatment has been suggested, in part, to be a result of late stage of intervention in current clinical trial design. For this reason, greater focus has been placed on preclinical trials and in turn both the identification of individuals at-risk for AD and, amongst these, th
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43

Hartman, Mikael. "Risk and prognosis of breast cancer among women at high risk of the disease /." Stockholm : Karolinska institutet, 2007. http://diss.kib.ki.se/2007/978-91-7357-303-0/.

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44

Bombard, Yvonne. "The nature and extent of genetic discrimination among persons at risk for Huntington disease." Thesis, University of British Columbia, 2008. http://hdl.handle.net/2429/7525.

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Huntington disease (HD), the “Dancing Mania” of the Middle Ages, has always been a particular target of social stigma and discrimination. With the discovery of a polymorphic DNA marker linked to HD in 1983, individuals at-risk for HD were able to learn whether or not they had inherited the causative HD mutation and possibly escape its stigma and discrimination. For those who had inherited the HD mutation increased discrimination became a real possibility. Genetic discrimination (GD) refers to the differential treatment of asymptomatic individuals or their family based on genetic differences. I
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45

Munz, Matthias [Verfasser]. "Identification of genetic risk factors predisposing to the inflammatory oral disease periodontitis / Matthias Munz." Berlin : Freie Universität Berlin, 2019. http://d-nb.info/1187244384/34.

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46

Karimiani, Ehsan Ghayoor. "Defining disease risk groups through the quantification of genetic heterogeneity across single leukaemia cells." Thesis, University of Manchester, 2012. http://www.manchester.ac.uk/escholar/uk-ac-man-scw:163858.

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Chronic myeloid leukaemia (CML) is typified by the BCR-ABL fusion gene. Primitive CML cells are less responsive to treatment and have high BCR-ABL mRNA and protein expression. BCR-ABL may also be required for cell adhesion, which may possess increased resistance. Previous studies have analysed bulk cell populations but the significance of BCR-ABL expression heterogeneity at the single cell level is unknown. In this study, the K562 CML cell line was used. Surface-adherent (K562/Adh) and non-adherent (K562/NonAdh) cell populations from standard suspensions were generated through 4 months of pass
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47

Bellis, Claire. "Use of the Isolated Norfolk Island Population for Cardiovascular Disease Risk Trait Genetic Analysis." Thesis, Griffith University, 2009. http://hdl.handle.net/10072/368099.

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Cardiovascular disease (CVD) is a major public health issue and a disorder that accounts for over half of all deaths in Western countries. Many important risk factors for cardiovascular disease have been identified, with environmental factors, such as diet, smoking, bodyweight, blood pressure, lipid levels and exercise involvement, have shown to be important in cardiovascular predisposition. However, CVD and its associated risk traits display both environmental and genetic components. A family history has been shown to one of the most important risk factors for disease development, emphasising
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48

Guyatt, Anna Louise. "Complex genetic loci and their association with disease risk traits in population-based cohorts." Thesis, University of Bristol, 2017. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.742995.

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49

So, Hon-cheong, and 蘇漢昌. "Genetic architecture and risk prediction of complex diseases." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B4452805X.

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50

Nishio, Kazuko, Sakurako Nakamura, Yoshitaka Sekido, Toshimitsu Niwa, and Nobuyuki Hamajima. "Associations between Disease Risk and Eight Polymorphisms Adopted for Genotype Announcements at Nagoya University Hospital." Nagoya University School of Medicine, 2004. http://hdl.handle.net/2237/5404.

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