Relevant bibliographies by topics / Genetic risk of disease

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  2. Dissertations / Theses
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Academic literature on the topic 'Genetic risk of disease'

Author: Grafiati
Published: 11 March 2023

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Journal articles on the topic "Genetic risk of disease"

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McDonald, B. A., and C. Linde. "Disease resistance and pathogen population genetic." Plant Protection Science 38, SI 1 - 6th Conf EFPP 2002 (January 1, 2002): 245–48. http://dx.doi.org/10.17221/10375-pps.

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Plant pathologists have seen many boom-and-bust cycles following the deployment of resistant varieties. These cycles result when pathogen populations adapt to the presence of a major resistance gene by evolving a new population that can overcome this resistance gene. The breakdown of genetic resistance is due to the evolution of the local pathogen population because of selection for mutants, recombinants, or immigrants that are better adapted to the resistant cultivar. To understand the process that leads to breakdown of a resistance gene, we need to understand the processes that govern pathogen evolution. Population geneticists have identified five evolutionary forces that interact to affect the evolution of organisms. We ranked these risks and developed a quantitative framework to predict the risk that a pathogen will evolve to overcome major resistance genes. Our hypothesis is that much of the durability of resistance genes is due to the nature of the pathogen population rather than to the nature of the resistance gene. The framework we developed can be used as a hypothesis to test against a large number of plant pathosystems. The underlying principles of the framework can be tested individually or in combination according to the available knowledge of the population genetics for any pathogen. We propose that this framework can be used to design breeding strategies to break the boom-and-bust cycle and lead to durable resistance.
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Roberts, Robert. "Molecular genetics: Cardiac disease and risk-related genes-Genetic risk factors." Clinical Cardiology 18, S4 (September 1995): IV13—IV19. http://dx.doi.org/10.1002/clc.4960181604.

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Alonso, Lorena, Ignasi Morán, Cecilia Salvoro, and David Torrents. "In Search of Complex Disease Risk through Genome Wide Association Studies." Mathematics 9, no. 23 (November 30, 2021): 3083. http://dx.doi.org/10.3390/math9233083.

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The identification and characterisation of genomic changes (variants) that can lead to human diseases is one of the central aims of biomedical research. The generation of catalogues of genetic variants that have an impact on specific diseases is the basis of Personalised Medicine, where diagnoses and treatment protocols are selected according to each patient’s profile. In this context, the study of complex diseases, such as Type 2 diabetes or cardiovascular alterations, is fundamental. However, these diseases result from the combination of multiple genetic and environmental factors, which makes the discovery of causal variants particularly challenging at a statistical and computational level. Genome-Wide Association Studies (GWAS), which are based on the statistical analysis of genetic variant frequencies across non-diseased and diseased individuals, have been successful in finding genetic variants that are associated to specific diseases or phenotypic traits. But GWAS methodology is limited when considering important genetic aspects of the disease and has not yet resulted in meaningful translation to clinical practice. This review presents an outlook on the study of the link between genetics and complex phenotypes. We first present an overview of the past and current statistical methods used in the field. Next, we discuss current practices and their main limitations. Finally, we describe the open challenges that remain and that might benefit greatly from further mathematical developments.
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Bloch, Michael J. "Genetic risk scores and coronary heart disease risk." Journal of the American Society of Hypertension 9, no. 8 (August 2015): 580–81. http://dx.doi.org/10.1016/j.jash.2015.06.010.

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Skrzypa, Marzena, Natalia Potocka, Halina Bartosik-Psujek, and Izabela Zawlik. "Genetic risk factors of Alzheimer’s disease." European Journal of Clinical and Experimental Medicine 17, no. 1 (2019): 57–66. http://dx.doi.org/10.15584/ejcem.2019.1.10.

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Jostins, Luke, and Jeffrey C. Barrett. "Genetic risk prediction in complex disease." Human Molecular Genetics 20, R2 (August 25, 2011): R182—R188. http://dx.doi.org/10.1093/hmg/ddr378.

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Secko, D. "Alzheimer's disease: genetic variables and risk." Canadian Medical Association Journal 172, no. 5 (March 1, 2005): 627. http://dx.doi.org/10.1503/cmaj.050111.

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Billingsley, K. J., S. Bandres-Ciga, S. Saez-Atienzar, and A. B. Singleton. "Genetic risk factors in Parkinson’s disease." Cell and Tissue Research 373, no. 1 (March 13, 2018): 9–20. http://dx.doi.org/10.1007/s00441-018-2817-y.

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Alliey, Ney. "Genetic Variants And Risk Of Disease." European Neuropsychopharmacology 29 (2019): S715—S716. http://dx.doi.org/10.1016/j.euroneuro.2017.06.025.

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Bradshaw, Elizabeth. "CD33 GENETIC RISK IN ALZHEIMER'S DISEASE." Alzheimer's & Dementia 13, no. 7 (July 2017): P1448. http://dx.doi.org/10.1016/j.jalz.2017.07.488.

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

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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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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 découvertes qui émergent des études d'association pangénomique (GWAS) qui permettent de tester l’association de variation génétique au risque de contracter une maladie commune. Les GWAS ont considérablement amélioré notre connaissance de l'architecture génétique des maladies cardio-Vasculaires, à ce jour plus de 50 variations génétiques sont formellement associées à des maladies cardio-Vasculaires, de même plus de 200 marqueurs génétiques seraient associés à des facteurs de risque cardiovasculaire traditionnels (p. ex. le taux sanguin des lipides, la pression artérielle, l’indice de masse corporelle et le diabète de type 2). Le succès remarquable de ces études d’association, qui a permis l’identification de nombreux bio-Marqueurs, a conduit à une réévaluation des données génétiques dans le but de définir des informations cliniquement utiles pour limiter et mieux prédire les risques de maladies, grâce à une application plus efficace des stratégies de prévention. Dans cette thèse, nous examinons tout d'abord une nouvelle approche pour étudier l'architecture génétique de l'hypertension artérielle (HTA; facteur de risque majeur des maladies cardiovasculaires prématurées), puis nous avons constitué plusieurs modèles pour prédire le risque de développer une maladie coronarienne (MC; type le plus commun de MCV), enfin nous avons déterminé une base génétique commune du principal prédicteur de complications cliniques des maladies coronariennes – l'athérosclérose subclinique - afin d'ajouter une valeur pronostique supplémentaire en plus des scores de risque traditionnels à différents âges. Nous avons estimé l'héritabilité de la première mesure de la pression artérielle systolique (PAS) à ~25%/~45% et à ~30%/~37% pour la pression artérielle diastolique (PAD) chez les sujets d’origine Européenne (N = 8901) et d’origine Africaine (N = 2860) faisant respectivement partie de la cohorte Atherosclerosis Risk in Communities (ARIC), en accord avec les études antérieures. Par ailleurs, nous avons développé un moyen de combiner un score de risque génétique (SRC) – somme des effets génétiques parmi un ensemble de marqueurs – avec une évaluation indépendante du risque clinique, en utilisant un système d'équations log-Linéaire. Nous avons employé cet outil à la prédiction de la maladie coronarienne (MC) dans la cohorte ARIC. L'ajout d'un score de risque génétique (SRG) à un score de risque clinique (SRC) améliore à la fois la discrimination et l'étalonnage des maladies coronariennes dans la cohorte ARIC, et révèle par la même comment cette information génétique influence l'évaluation des risques ainsi que l’approche clinique. Enfin, parmi 1561 cas et 5068 contrôles (de la présence ou non de calcifications coronaires), faisant partie de plusieurs ensembles de données cliniques et génétiques disponibles via la base de données NCBI de Génotypes et Phénotypes (dbGAP), nous avons constaté qu’une augmentation d'un écart-Type dans le score de risque génétique de 49 bio-Marqueurs de MC est associée à 28 % d’augmentation de risque de développer une athérosclérose coronarienne subclinique diagnostiquée à un stade avancé (p=1.43x10-16). Cette augmentation du risque est significative dans chaque catégorie d'âge (de 15 ans en 15 ans) (0,01 > p > 9.4x10-7) et a été remarquablement similaire dans toutes les catégories d'âge (test d'hétérogénéité p = 0.98). (...)
Complex diseases such as cardiovascular disease (CVD) are influenced by both genetic and environmental factors. Estimation of an individual’s cardiovascular risk usually involves measurement of risk factors correlated with risk of CVD (e.g. age, sex, smoking, blood pressure, and total cholesterol). Lately, several biomarkers have been evaluated for their ability to improve prediction of cardiovascular disease beyond traditional risk factors. The interest in novel loci is propelled notably by emerging discoveries from the advent of genome-Wide association studies (GWAS) of genetic variants associated with risk for common diseases. GWAS has greatly enhanced our knowledge of the genetic architecture of cardiovascular disease, yielding over 50 variants confirmed to be associated with CVD to date, as well as over 200 associated with traditional cardiovascular risk factors (e.g. lipids, blood pressure, body mass index, and type 2 diabetes mellitus). This recent and continuing success in discovering increasing numbers of robustly associated genetic markers has led to reassessment of whether genetic data can provide clinically useful information by refining risk prediction and moderating disease risk through a more efficient application of prevention strategies. In this thesis, we first address novel approach to survey the genetic architecture of hypertension (i.e. major risk factor for premature CVD), then construct risk prediction models for coronary artery disease (CAD; i.e. most common type of CVD) and finally establish a common genetic basis of the strongest predictor of clinical complications of CAD, subclinical atherosclerosis, to add incremental prognostic value above traditional risk scores across a range of ages. We show that, for first visit measurements, the heritability is ~25%/~45% and ~30%/~37% for systolic (SBP) and diastolic blood pressure (DBP) in European (N=8,901) and African (N=2,860) ancestry individuals from the Atherosclerosis Risk in Communities (ARIC) cohort, respectively, in accord with prior studies. Then we present a means to combine a polygenic risk score - genetic effects among an ensemble of markers - with an independent assessment of clinical risk using a log-Link function. We apply the method to the prediction of coronary heart disease (CHD) in the ARIC cohort. The addition of a genetic risk score (GRS) to a clinical risk score (CRS) improves both discrimination and calibration for CHD in ARIC and subsequently reveal how this genetic information influences risk assessment and thus potentially clinical management. Finally, Among 1561 cases and 5068 controls, from several clinical and genetic datasets available through the NCBI's database of Genotypes and Phenotypes (dbGAP), we found a one SD increase in the genetic risk score of 49 CAD SNPs was associated with a 28% increased risk of having advanced subclinical coronary atherosclerosis (p = 1.43 x 10-16). This increase in risk was significant in every 15-Year age stratum (.01 > p > 9.4 x 10-7) and was remarkably similar across all age strata (p test of heterogeneity = 0.98). We obtained near identical results and levels of significance when we restricted the genetic risk score to 32 SNPs not associated with traditional risk factors. Accordingly, common variation largely recapitulates the known heritability of blood pressure traits. The vast majority of this heritability varies by chromosome, depending on its length, and is largely concentrated in intronic and intergenic regions of the genome but widely distributed across the common allele frequency spectrum. Respectively, our proposed method to combine genetic information at established susceptibility loci with a nongenetic risk prediction tool facilitates the standardized incorporation of a GRS in risk assessment. (...)
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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 Cancer Prevention Study II Nutrition Cohort. Across all analyses, PD cases were identified via biennial questionnaires and confirmed through medical record review by neurologists specializing in movement disorders. In our first two aims, we used Cox proportional hazards models to calculate relative risks of PD according to cumulative average intakes of foods and nutrients of interest. In aim 1, we found no associations between intake of vitamin E, vitamin C, or carotenoids and risk of PD. In our second aim, we found that low fat dairy intake was associated with increased PD risk, and that this association appeared to be driven by an increased risk of PD associated with skim and low-fat milk intake. The results of a meta-analysis including previously conducted prospective investigations of milk intake and PD risk suggested a relative risk of PD comparing extreme milk intake levels of 1.80 (95% CI 1.44-2.25). In our third aim, although a large body of research suggests that higher urate levels could be protective against PD risk and progression, we found that genetic variants in the SLC2A9 gene that influence circulating urate levels were not associated with risk of PD. Our analyses suggest that while antioxidant vitamins are unlikely to alter PD risk, dairy products may represent an important modifiable PD risk factor. Whether dairy products also alter rates of PD progression or conversion from premotor PD to clinical PD are important, answerable questions. Finally, the results of our third analysis suggest that genetic variants associated with plasma urate levels are not associated with PD risk; however, larger studies are needed to confirm these results.
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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 any coding variants in XPNPEP2, which encodes membrane-bound APP, subsequent linkage analysis of APP activity in eight families provided a maximum LOD score (3.75) for this locus. Sequencing of additional cases identified a splice variant (314_431del) and a non-coding polymorphism (rs3788853) in this locus, which cosegregate with low plasma APP activity. The latter accounts for the linkage signal and is associated with AE-ACEi (P = 0.036). In addition, we identified other potential loci for APP activity and demonstrated that certain ACEi (Captopril and Enalapril) non-specifically inhibit APP activity. Furthermore, we detected polymorphisms associated with reduced APP and ACE activities among females with estrogen-dependent inherited angioedema.
We also conducted a genetic investigation of depression among CAD patients to identify common susceptibility loci which might explain the correlation between these diseases. Our candidate gene association study identified a polymorphism (rs216873) in the von Willebrand factor gene that was significantly associated (P = 7.4 x 10-5) with elevated depressive symptoms in our CAD cohort. These results suggest that risk factors for atherosclerosis also underlie susceptibility to depression among CAD patients.
This dissertation contributes to the field of genetics and pharmacogenomics of CAD. A better understanding of the toxic effects of CAD drugs will assist in the development of safer and more effective treatments. In addition, our results may facilitate clinical assays to identify individuals who are susceptible to angioedema prior to ACEi or estrogen therapy. Finally, our genetic investigation of depression in CAD patients reveals a novel drug target (VWF) for treatment of depression in cardiac cases.
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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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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 trigger, accelerate, or exacerbate the disease process. Among the risk factors for CAD, hyperhomocysteinemia has been recognized for its relation to atherosclerotic alterations in the vessels. In addition, gene polymorphisms in methylene - tetrahydrofolate reductase (MTHFR), methionine synthase reductase (MTRR), methionine synthase (MS), and cystathionine ß - synthase (CßS), which are involved in homocysteine metabolism, have been identified as a result of advances in genetic research related to cardiovascular pathophysiology. In particular, the results of recent salient studies have provided evidence of significant association of these genetic polymorphisms and CAD in Japanese and part of European populations but not in the United States, Australian, and part of European populations. This disparity may explain the variation of prevalence of CAD among different populations. Potential gene - environment interactions may elevate homocysteine levels and increase the risk of CAD. This discussion includes the pathogenesis of hyperhomocysteinemia, definitions of normal and elevated homocysteine levels, the physiological background of homocysteine metabolism, polymorphisms of genes involved in homocysteine metabolism from the perspective of CAD risk, and implications for nursing practice based on emerging information regarding hyperhomocysteinemia as a risk factor for CAD. Findings from these recent studies are important for nurses, clinicians, and researchers to be able to incorporate cardiovascular genetic information in their practice and research and provide more adequate care to reduce the risk for CAD and improve patient outcomes.
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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. These findings suggest that brains from AD patients have defective antimicrobial immune defences and individual genetic makeup, such as positivity for the APOE ε4 and IRF7 A alleles, further decreases brain immune efficiency. Chronic stress at different stages of life, including intrauterine life, has a negative impact on AD pathology and prenatal stress (PNS) is an important programming factor in brain development and function. The second part of this thesis shows that experimental animal research has the advantage of enabling strict control of environmental factors, such as PNS exposure, that might have a role in AD-related behaviour and neuropathology. Long-term cognitive consequences of PNS in AD mice and the PNS-early neurobiological effects in wild type animals were investigated. As these, mouse represented a useful model to suggest that PNS affects the onset of AD cognitive deficit in a sex-dependent manner and that the impairment of fetal neurodevelopment might influence adult mental health and brain ageing. In conclusion, the presented study gives new perspectives for prevention and treatment of the ageing-associated cognitive decline and AD. Protecting women from chronic stress during pregnancy, on the one side, and maintenance of efficient immune responses during ageing, on the other one, might slowdown neurodegenerative mechanisms associated with senile dementia and positively influence both prevalence and incidence of AD.
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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 associated with Parkinson’s disease. Variants in SMPD1, LRRK2 or CHCHD10, previously detected in other populations, were not detected, suggesting that they are rare or even absent in the Finnish population. Patients with Huntington’s disease were investigated for HTT gene haplotypes as well as whether these haplotypes alter the stability of the elongated CAG repeat. Haplogroup A was less common in Finns than in other European populations, whereas it was significantly more common in patients with Huntington’s disease than in the general population. Certain HTT haplotypes as well as the parental gender were found to affect the repeat instability. We found that compound heterozygous mutations in POLG1 were causative of Parkinson’s disease, rare length variants in POLG1 were associated with Parkinson’s disease and GBA p.L444P was significantly more frequent in patients than in the controls, which suggests that these mutations are associated with the development of Parkinson’s disease. The low prevalence of Huntington’s disease in Finland correlates with the low frequency of the disease-associated HTT haplogroup A. Paternal inheritance combined with haplotype A1 increased the risk of repeat expansion. Movement disorders in Finland were found to share some of the same genetic risk factors found in other European populations, but some other recognized genetic variants could not be detected
Tiivistelmä Parkinsonin tauti ja Huntingtonin tauti ovat hermostoa rappeuttavia eteneviä liikehäiriösairauksia, jotka tyypillisesti ilmenevät aikuisiällä. Tässä tutkimuksessa selvitettiin näiden kahden liikehäiriösairauden geneettisiä riskitekijöitä suomalaisilla potilailla. Tutkimme potilaita, joilla oli varhain alkava Parkinsonin tauti tai myöhään alkava Parkinsonin tauti sekä väestökontrolleja. GBA-geenin p.L444P mutaation havaittiin lisäävän Parkinsonin taudin riskiä. Kaksi Parkinsonin tautia sairastavaa potilasta oli yhdistelmäheterotsygootteja haitallisten POLG1-geenin varianttien suhteen ja harvinaiset POLG1 CAG toistojaksovariantit assosioituivat Parkinsonin tautiin. Tutkittuja variantteja SMPD1-, LRRK2- ja CHCHD10-geeneissä ei löydetty tästä aineistosta lainkaan, mikä viittaa siihen, että ne puuttuvat suomalaisesta väestöstä tai ovat harvinaisia. Huntingtonin tautia sairastavilta potilailta tutkittiin HTT-geenin haploryhmiä ja niiden vaikutusta Huntingtonin tautia aiheuttavan pidentyneen toistojakson epästabiiliuteen. Haploryhmä A oli suomalaisessa väestössä harvinainen verrattuna eurooppalaiseen väestöön ja se oli huomattavasti yleisempi Huntingtonin tautipotilailla kuin väestössä. Toistojakson epästabiiliuteen vaikuttivat tietyt HTT-geenin haplotyypit samoin kuin sen vanhemman sukupuoli, jolta pidentynyt toistojakso periytyy. POLG1 yhdistelmäheterotsygoottien katsottiin aiheuttavat Parkinsonin tautia ja harvinaisten POLG1 CAG toistojaksovarianttien todettiin assosioituvan Parkinsonin tautiin Suomessa. GBA p.L444P mutaatio merkittävästi yleisempi Parkinsonin tautipotilailla kuin kontrolleilla, mikä viittaa siihen, että se on Parkinsonin taudin riskitekijä. Huntingtonin tautiin assosioituvan haploryhmä A:n matala frekvenssi selittää taudin vähäistä esiintyvyyttä Suomessa. Paternaalinen periytyminen ja haplotyyppi A1 lisäsivät HTT-geenin toistojakson pidentymisen riskiä. Liikehäiriösairauksilla todettiin Suomessa osittain samanlaisia riskitekijöitä kuin muualla Euroopassa, mutta kaikkia tutkittuja variantteja emme havainneet
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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 identified in Caucasians using genome-wide association approach. In order to have a better understanding on the genetic components of LOAD in Chinese as well as identify other potential genetic risk factors for Chinese ethnic population, we conducted a case-control study using candidate gene association approach. In view of increasing evidence on the neural protective effects of sex steroid hormones both in vivo and in vitro, we hypothesized variations on sex steroid metabolic pathway genes were associated with LOAD. Four candidate genes (ESR1, ESR2, CYP19A1, CYP11A1) were evaluated based on 462 cases and 350 non-demented controls. Apart from consistent result for APOE, polymorphisms in ESR2 and CYP11A1 were found to be significantly associated with the disease. When stratification according to gender, marginally significant associations were detected for ESR1 and ESR2 variants in men while CYP11A1 variants relevant to LOAD risk were detected exclusively in women. Additionally, genotypic and phenotypic correlation analysis revealed CYP19A1 was significantly relevant to serum 17-estradiol (E2) levels in 689 subgroup participants, especially in 400 LOAD patients of subgroup. Further gene-level analyses based on whole sample confirmed above disease association for ESR2 and CYP11A1 and pathway-level analyses highlighted the impact of sex steroid metabolic pathway on disease predisposition. The independent follow-up study for CR1, CLU and PICALM previously reported by genome-wide association study (GWAS) in Caucasians was conducted in the same Chinese cohort. Similar to the Caucasian cohort, polymorphisms in CR1 and CLU were found to be significantly different between cases and non-demented controls. However, significant disease association for PICAML was detected only in the APOE ε4 (-) subgroup of our Chinese cohort. In conclusions, genetic abnormalities were founded in Chinese LOAD patients. In addition to confirmation disease susceptibility for APOE, CR1, CLU and PICALM, we were first to report the associations between several sex steroid metabolic pathway genes and LOAD. This valuable genetic information obtained from Chinese patients may lead to the development of novel diagnostic strategies and therapeutic interventions in LOAD.
published_or_final_version
Biochemistry
Doctoral
Doctor of Philosophy
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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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Books on the topic "Genetic risk of disease"

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Petrakis, Peter L. Alcoholism, and inherited disease. Rockville, Md: U.S. Dept. of Health and Human Services, Public Health Service, Alcohol, Drug Abuse, and Mental Health Administration, National Institute on Alcohol Abuse and Alcoholism, 1985.

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J, Alberts Mark, ed. Genetics of cerebrovascular disease. Armonk, NY: Futura Pub. Co., 1999.

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Uri, Goldbourt, De Faire Ulf, and Berg Kåre, eds. Genetic factors in coronary heart disease. Dordrecht: Kluwer Academic, 1994.

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Kåre, Berg, ed. Genetic approaches of coronary heart disease and hypertension. Berlin: Springer-Verlag, 1991.

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Gormley, Myra Vanderpool. Family diseases: Are you at risk? Baltimore, MD: Genealogical Pub. Co., 1989.

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Ueland, Per Magne, and Rima Rozen. MTHFR polymorphisms and disease. Georgetown, Tex: Landes Bioscience, 2005.

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Magne, Ueland Per, and Rozen Rima, eds. MTHFR polymorphisms and disease. Georgetown, Tex: Landes Bioscience/ Eurekah.com, 2005.

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Mapping fate: A memoir of family, risk, and genetic research. New York: Times Books, 1995.

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Wexler, Alice. Mapping fate: A memoir of family, risk, and genetic research. Berkeley: University of California Press, 1995.

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Genetic susceptibility to cancer. Boston: Kluwer Academic, 1998.

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Book chapters on the topic "Genetic risk of disease"

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Böger, Carsten A., and Peter R. Mertens. "Genetic Risk Factors for Diabetic Nephropathy." In Diabetes and Kidney Disease, 29–44. Oxford, UK: Wiley-Blackwell, 2012. http://dx.doi.org/10.1002/9781118494073.ch3.

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Marigorta, Urko M. "Genetic Risk Prediction in IBD." In Molecular Genetics of Inflammatory Bowel Disease, 141–56. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-28703-0_7.

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Combarros, Onofre. "Genetic Risk Factors for Alzheimer’s Disease." In Neurodegenerative Diseases, 49–64. London: Springer London, 2014. http://dx.doi.org/10.1007/978-1-4471-6380-0_4.

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Berg, K. "Genetic Risk Factors for Atherosclerotic Disease." In Human Genetics, 326–35. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-71635-5_40.

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Tsang, Kin-Lun, Zhe-Hui Feng, Hong Jiang, Shu-Leong Ho, and David B. Ramsden. "Genetic Risk Factors in Parkinson’s Disease." In Mapping the Progress of Alzheimer’s and Parkinson’s Disease, 251–57. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-0-306-47593-1_42.

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Khan, Mosin S., Iqra Farooq, Sunia Faiz, Suhail S. Lone, Sabhiya Majid, and Waseem Qureshi. "Cytokine Polymorphisms and Their Role in Modulating Cancer Risk." In Genetic Polymorphism and Disease, 459–75. Boca Raton: CRC Press, 2022. http://dx.doi.org/10.1201/9781003246244-21.

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Hollingworth, Paul, and Julie Williams. "Genetic Risk Factors for Dementia." In The Handbook of Alzheimer's Disease and Other Dementias, 195–234. Oxford, UK: Wiley-Blackwell, 2011. http://dx.doi.org/10.1002/9781444344110.ch6.

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Dallongeville, Jean. "Apolipoprotein E Polymorphism and Atherosclerosis Risk." In Genetic factors in coronary heart disease, 289–97. Dordrecht: Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-011-1130-0_19.

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Song, Yiqing, Cuilin Zhang, Lu Wang, Qi Dai, and Simin Liu. "Magnesium Intake, Genetic Variants, and Diabetes Risk." In Magnesium in Human Health and Disease, 103–18. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-62703-044-1_6.

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Workman, Heather. "Overview of Cerebrovascular Disease and Stroke Risk Factors." In Genetic Counseling for Adult Neurogenetic Disease, 133–41. Boston, MA: Springer US, 2014. http://dx.doi.org/10.1007/978-1-4899-7482-2_10.

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Conference papers on the topic "Genetic risk of disease"

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Hunter, David J. "Prediction of disease risk using common genetic variants." In AACR International Conference: Molecular Diagnostics in Cancer Therapeutic Development– Sep 27-30, 2010; Denver, CO. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/diag-10-pl5-2.

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Mishra, Sushruta, Brojo Kishore Mishra, and Hrudaya Kumar Tripathy. "A neuro-genetic model to predict hepatitis disease risk." In 2015 IEEE International Conference on Computational Intelligence and Computing Research (ICCIC). IEEE, 2015. http://dx.doi.org/10.1109/iccic.2015.7435719.

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Kurtović-Kozarić, Amina. "GENETICS OF CARDIOMYOPATHY." In International Scientific Symposium “Diagnostics in Cardiology and Grown-Up Congenital Heart Disease (GUCH)”. Academy of Sciences and Arts of Bosnia and Herzegovina, 2021. http://dx.doi.org/10.5644/pi2021.199.01.

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Heart failure is a leading cause of morbidity and mortality. Around 4% of patients with heart failure carry a pathogenic genetic aberration that causes cardiomyopathy and subsequently leads to heart failure. There are five types of primary genetic cardiomyopathies that can give rise to heart failure: hypertrophic cardiomyopathy (HCM), dilated cardiomyopathy, arrhythmogenic cardiomyopathy (ACM), restrictive cardiomyopathy (RCM), and left ventricular noncompaction (LVNC). If genetic cardiomyopathy is suspected, genomic/genetic testing is recommended because it provides the underlying cause for the diagnosis, prognostic parameters, and possibility to test family members at risk. Testing should be conducted as part of a multidisciplinary approach by a team of adult or paediatric cardiologists, geneticists, and genetic counsellors. Here we will discuss 1) different genomic testing approaches and the management of variants of uncertain significance, 2) management of patients with suspected genetic cardiomyopathy in a multidisciplinary team, and 3) the associations between genotypes and phenotypes of most commonly mutated genes such as MYH7, TNNT2, TPM1, MYBPC3, TTN, and others. In conclusion, genetic testing of patients with cardiomyopathies helps with proper diagnosis, prognosis, treatment, and identification of relatives at risk.
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Francis-Lyon, Patricia, Shashank Belvadi, and Fu-Yuan Cheng. "Detection and characterization of interactions of genetic risk factors in disease." In Python in Science Conference. SciPy, 2013. http://dx.doi.org/10.25080/majora-8b375195-007.

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Snyder, J., A. Weston, and E. Demchuk. "332. Molecular Basis of Genetic Risk Assessment in Chronic Beryllium Disease." In AIHce 2004. AIHA, 2004. http://dx.doi.org/10.3320/1.2758364.

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Xu, Yu, Chonghao Wang, Zeming Li, Yunpeng Cai, Ouzhou Young, Aiping Lyu, and Lu Zhang. "A machine learning model for disease risk prediction by integrating genetic and non-genetic factors." In 2022 IEEE International Conference on Bioinformatics and Biomedicine (BIBM). IEEE, 2022. http://dx.doi.org/10.1109/bibm55620.2022.9994925.

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Dijkstra, Akkelies, Marike Boezen, Joanna Smolonska, Pieter Zanen, Ciska Wijmenga, Harry Groen, Jorgen Vestbo, and Dirkje Postma. "Genetic Risk Factors For Chronic Mucus Hypersecretion In Chronic Obstructive Pulmonary Disease." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a5865.

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Bidstrup Leffers, Henrik Christian, David Westergaard, Karina Banasik, and Søren Jacobsen. "P90 Genetic risk, smoking and the development of systemic autoimmune rheumatic disease." In 12th European Lupus Meeting. Lupus Foundation of America, 2020. http://dx.doi.org/10.1136/lupus-2020-eurolupus.134.

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Rezende, Rubens Barbosa, and Larissa Teodoro. "Presence of genetic polymorphisms may impact on predisposition to Parkinson’s disease." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.004.

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Introduction: Parkinson’s disease (PD) is characterized by the degeneration and loss of dopaminergic neurons in the black substantia and the formation of Lewy bodies, thus being considered a neurodegenerative disease. Thus, the objective was to understand the impact of polymorphisms in the predisposition to PD. Methods: It’s a narrative review of literature in the PubMed and SciELO databases, using the descriptors: “Polymorphism, Single Nucleotide” and “Parkinson disease”, registered in DeCS/MeSH, and using the Boolean operator AND. The inclusion criteria were: complete articles and made available free of charge, published in English, Spanish and Portuguese, between 2016 and January 2021. Results: After the research, 167 publications were found and seven were included. The data from the first study indicate that the rs33949390 of the LRRK2 gene helps in predisposition to PD in Asian populations, mainly Chinese. The second study indicated that the NFE2L2 rs6721961 allele was linked to a reduced risk of PD. The third study found that the GSK3B rs1732170, STK11 rs8111699, SNCA rs356219 and FCHSD1 rs456998 polymorphisms were linked to a high risk of PD. The fourth study found that the SNCA variants rs7684318, rs356220, rs356203 and rs2736990 were linked to the disease and were at high risk of developing PD in the Mexican population. The fifth and sixth study are meta-analyzes, the fifth confirming the lower allele rs11558538 of HNMT is associated with a reduced risk of developing PD. And the sixth assumes a possible link between CCDC62 rs12817488 and the risk of PD in the Chinese population. Conclusion: However, the analyzed data indicate that the polymorphisms contributed to the susceptibility to PD, however further studies related to the polymorphisms and their relationship to PD are still needed for more ethnic groups, and thus early diagnosis is possible.
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Evans, Jacquelyn M., Heidi G. Parker, Jocelyn Plassais, Gerard R. Rutteman, and Elaine A. Ostrander. "Abstract 829: Genetic risk factors for histiocytic sarcoma in a canine disease model." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-829.

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Reports on the topic "Genetic risk of disease"

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Krauss, Ronald. CRADA Final Report: Genetic Testing for Evaluation of Heart Disease Risk. Office of Scientific and Technical Information (OSTI), January 2002. http://dx.doi.org/10.2172/1157021.

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Wang, Ying yuan, Zechang Chen, Luxin Zhang, Shuangyi Chen, Zhuomiao Ye, Tingting Xu, and Yingying Zhang c. A systematic review and network meta-analysis: Role of SNPs in predicting breast carcinoma risk. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, February 2022. http://dx.doi.org/10.37766/inplasy2022.2.0092.

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Review question / Objective: P: Breast cancer patient; I: Single nucleotide polymorphisms associated with breast cancer risk; C: Healthy person; O: By comparing the proportion of SNP mutations in the tumor group and the control group, the effect of BREAST cancer risk-related SNP was investigated; S: Case-control study. Condition being studied: Breast cancer (BC) is one of the most common cancers among women, and its morbidity and mortality have continued to increase worldwide in recent years, reflecting the strong invasiveness and metastasis characteristics of this cancer. BC is a complex disease that involves a sequence of genetic, epigenetic, and phenotypic changes. Polymorphisms of genes involved in multiple biological pathways have been identified as potential risks of BC. These genetic polymorphisms further lead to differences in disease susceptibility and severity among individuals. The development of accurate molecular diagnoses and biological indicators of prognosis are crucial for individualized and precise treatment of BC patients.
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Cao, Xianling, Xuanyou Zhou, Naixin Xu, Songchang Chang, and Chenming Xu. Association of IL-4 and IL-10 Polymorphisms with Preterm Birth Susceptibility: A Systematic Review and Meta-Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, April 2022. http://dx.doi.org/10.37766/inplasy2022.4.0044.

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Review question / Objective: The aim of our systematic review and meta-analysis was to summarize the effects of IL-4 and IL-10 gene polymorphism and clarify their possible association with PTB. Condition being studied: World Health Organization (WHO) defines preterm birth (PTB) as babies born alive before 37 weeks of pregnancy are completed. The new estimates show that the prevalence of PTB during 2014 ranged from 8.7% to13.4% of all live births, about 15 million preterm babies born each year. Besides, PTB is the leading cause of death worldwide for children below 5 years of age. Babies born preterm are at an increased risk of short-term and long-term complications attributed to immaturity of multiple organ systems, such as cerebral palsy, intellectual disabilities, vision and hearing impairments, and impaired cognitive development. PTB has become a worldwide public health problem, but its etiology remains unclear. Accumulating evidence shows that PTB is a syndrome that can be attributed to a variety of pathological processes(5). Inflammatory diseases and genetic background are known risk factors for PTB, many studies had shown that genetic variations in proinflammatory cytokines such as tumor necrosis factor-α (TNF-α) and interleukin-1 α (IL-1 α) are associated with increased risk of PTB, but the relationship between genetic polymorphism in anti-inflammatory cytokines and risk of PTB remains controversial.
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Zhao, Bingyu, Saul Burdman, Ronald Walcott, and Gregory E. Welbaum. Control of Bacterial Fruit Blotch of Cucurbits Using the Maize Non-Host Disease Resistance Gene Rxo1. United States Department of Agriculture, September 2013. http://dx.doi.org/10.32747/2013.7699843.bard.

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The specific objectives of this BARD proposal were: (1) To determine whether Rxol can recognize AacavrRxo1 to trigger BFB disease resistance in stable transgenic watermelon plants. (2) To determine the distribution of Aac-avrRxo1 in a global population of Aae and to characterize the biological function of Aac-avrRxo1. (3) To characterize other TIS effectors of Aae and to identify plant R gene(s) that can recognize conserved TIS effectors of this pathogen. Background to the topic: Bacterial fruit blotch (BFB) of cucurbits, caused by Acidovorax avenae subsp. citrulli (Aae), is a devastating disease that affects watermelon (Citrullus lanatus) and melon (Cucumis melo) production worldwide, including both Israel and USA. Two major groups of Aae strains have been classified based on their virulence on host plants, genetics and biochemical properties. Thus far, no effective resistance genes have been identified from cucurbit germplasm. In this project, we assessed the applicability of a non-host disease resistance gene, Rxol, to control BFB in watermelon. We also tried to identify Aae type III secreted (TIS) effectors that can be used as molecular probes to identify novel disease resistance genes in both cucurbits and Nieotianatabaeum. Major conclusions, solutions, achievements: We generated five independent transgenic watermelon (cv. Sugar Babay) plants expressing the Rxol gene. The transgenic plants were evaluated with Aae strains AAC001 and M6 under growth chamber conditions. All transgenic plants were found to be susceptible to both Aae strains. It is possible that watermelon is missing other signaling components that are required for Rxol-mediated disease resistance. In order to screen for novel BFB resistance genes, we inoculated two Aae strains on 60 Nieotiana species. Our disease assay revealed Nicotiana tabaeum is completely resistant to Aae, while its wild relative N. benthamiana is susceptible to Aae. We further demonstrated that Nieotiana benthamiana can be used as a surrogate host for studying the mechanisms of pathogenesis of Aae. We cloned 11 TIS effector genes including the avrRxolhomologues from the genomes of 22 Aae strains collected worldwide. Sequencing analysis revealed that functional avrRxol is conserved in group" but not group I Aae strains. Three effector genes- Aave_1548, Aave_2166 and Aave_2708- possessed the ability to trigger an HR response in N. tabacum when they were transiently expressed by Agrobaeterium. We conclude that N. tabacum carries at least three different non-host resistance genes that can specifically recognize AaeTIS effectors to trigger non-host resistance. Screening 522 cucurbits genotypes with two Aae strains led us to identify two germplasm (P1536473 and P1273650) that are partially resistant to Aae. Interestingly, transient expression of the TIS effector, Aave_1548, in the two germplasms also triggered HR-Iike cell death, which suggests the two lines may carry disease resistance genes that can recognize Aave_1548. Importantly, we also demonstrated that this effector contributes to the virulence of the bacterium in susceptible plants. Therefore, R genes that recognize effector Aave1548 have great potential for breeding for BFB resistance. To better understand the genome diversity of Aae strains, we generated a draft genome sequence of the Israeli Aae strain, M6 (Group I) using Iliumina technology. Comparative analysis of whole genomes of AAC001, and M6 allowed us to identify several effectors genes that differentiate groups I and II. Implications, both scientific and agricultural: The diversity of TIS effectors in group I and II strains of Aae suggests that a subset of effectors could contribute to the host range of group I and II Aae strains. Analysis of these key effectors in a larger Aae population may allow us to predict which cucurbit hosts may be at risk to BFB. Additionally, isolation of tobacco and cucurbit Rgenes that can recognize Aae type III effectors may offer new genetic resources for controlling BFB.
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Reecy, James M., and Matt Schneider. Heritability of Genetic Resistance to Bovine Respiratory Disease. Ames: Iowa State University, Digital Repository, 2006. http://dx.doi.org/10.31274/farmprogressreports-180814-757.

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Mengak, Michael T. Wildlife Translocation. U.S. Department of Agriculture, Animal and Plant Health Inspection Service, July 2018. http://dx.doi.org/10.32747/2018.7210105.ws.

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Many people enjoy wildlife. Nationwide, Americans spend over $144 billion annually on fishing, hunting, and wildlife-watching activities. However, wildlife is not always welcome in or near homes, buildings, or other property and can cause significant damage or health and safety issues. Many people who experience a wildlife conflict prefer to resolve the issue without harming the offending animal. Of the many options available (i.e., habitat modification, exclusion, repellents) for addressing nuisance wildlife problems, translocation—capturing and moving—of the offending animal is often perceived to be effective. However, trapping and translocating wild animals is rarely legal nor is it considered a viable solution by wildlife professionals for resolving most nuisance wildlife problems. Reasons to avoid translocating nuisance wildlife include legal restrictions, disease concerns, liability issues associated with injuries or damage caused by a translocated animal, stress to the animal, homing behavior, and risk of death to the animal. Translocation is appropriate in some situations such as re-establishing endangered species, enhancing genetic diversity, and stocking species in formerly occupied habitats. The main focus of this publication, however, is to address nuisance wildlife issues that may be commonly encountered by homeowners and nuisance wildlife control professionals.
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Gelmann, Edward P. Genetic Risk Factor for Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, January 2005. http://dx.doi.org/10.21236/ada434784.

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Gelmann, Edward P. Genetic Risk Factor for Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, January 2003. http://dx.doi.org/10.21236/ada414867.

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Gardner, Murray B. Genetic Immunization for Lentiviral Immunodeficiency Virus Infection and Disease. Fort Belvoir, VA: Defense Technical Information Center, October 1998. http://dx.doi.org/10.21236/ada361721.

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Sonia Vallabh & Eric Minikel, Sonia Vallabh &. Eric Minikel. Can anle138b delay the onset of genetic prion disease? Experiment, May 2013. http://dx.doi.org/10.18258/0558.

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