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McCaskie, Pamela Ann. "Multiple-imputation approaches to haplotypic analysis of population-based data with applications to cardiovascular disease". University of Western Australia. School of Population Health, 2008. http://theses.library.uwa.edu.au/adt-WU2008.0160.
Pełny tekst źródłaFournier, Caroline. "Genetic investigation of vascular diseases in the French-Canadian population". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0030/MQ64355.pdf.
Pełny tekst źródłaMakubalo, Zola. "Mutation screening of candidate genes and the development of polymorphic markers residing on chromosome 19q13.3, the progressive familial heart block I gene search area". Thesis, Stellenbosch : Stellenbosch University, 2000. http://hdl.handle.net/10019.1/51838.
Pełny tekst źródłaENGLISH ABSTRACT: Progressive familial heart block type I (PFHBI) is a cardiac ventricular conduction disorder of unknown cause associated with risk of sudden death, which has been described in several South African families. Clinically, PFHBI is characterised by right bundle branch block on ECG, which may progress to complete heart block, necessitating pacemaker implantation. The disease shows an autosomal dominant pattern of inheritance with evidence of genetic anticipation. Using genetic linkage analysis, the PFHBI-causative gene was mapped to a 10 eentimorgan (cM) gene-rich area of chromosome (C) 19q13.3, which has, subsequently, been reduced to 7cM by fine mapping with polymorphic dinucleotide (CA)n short tandem repeat (STR) markers. Several attractive candidate genes, including muscle glycogen synthase (GSY 1) and histidine-rich calcium binding protein (HRC), lie within this region. The aim of the present study was two-fold: 1) to identify and characterise tetranucleotide (AAAT)n STRs within the PFHBI critical region that could be developed as polymorphic markers for use in genetic fine mapping and 2) to screen selected regions of GSY 1and HRC, positional candidate genes, for the presence ofPFHBI-causing mutation(s). Cosmids harbouring CI9q13.3 insert DNA were screened for the presence of (AAAT)n STRs by dot blot and Southern blot hybridisation using a radiolabelled (AAAT)lO oligonucleotide probe. To characterise the harboured (AAAT)n STRs, the positively hybridising fragments identified by Southern blot were sub-cloned, sequenced and primers designed from the unique repeat-flanking sequences. These primers were used to genotype the (AAAT)n repeat locus to assess its polymorphic nature in a panel of unrelated individuals. Alternatively, vectorette PCR, a rapid method of identifying repeat sequences and obtaining the flanking sequences in large inserts, was employed to develop polymorphic markers from the positively hybridising clones. Selected exons of GSY1 and HRC were screened for the presence of potentially disease-causing mutations by PCR-SSCP analysis and direct sequencing, respectively, in PFHBI-affected and unaffected family members. Of the available cosmid clones that gave strong signals on dot blot and Southern blot hybridisation, three, 29395, 24493 and 20381, were located within the critical PFHBI area and were used for marker development. An interrupted (AAAT)n repeat motif (n less than 5) was identified in cosmid 29395, however, the repeat locus was not polymorphic in the tested population. No (AAAT)n motif, single or repeated was observed in the partial sequence of the sub-cloned fragment of cosmid 24493. Using vectorette peR, no repeated (AAAT)n motif was identified on sequencing the generated products in either cosmid 24493 or 2038l. However, diffuse single AAAT motifs were detected in both cosmids. Exons 4, 5, 11, 12 and 16 of GSY 1, containing domains that are conserved across species, and the conserved eterminus- encoding exons 2-6 of HRC were selected for screening for potential PFHBI-causing mutation(s). However, no sequence variations were detected. The interrupted (AAAT)n repeat identified in cosmid 29395 was not polymorphic, which confirmed reports that complex repeats, especially those containing AAAT motifs of less than 6 repeats, are not polymorphic. One possible explanation for the absence of a repeated AAAT motif in cosmids 24493 and 20381, which both gave positive hybridisation signals, is that the low annealing temperature of the AfT -rich repeat-anchored primers used in vectorette peR may have resulted in transient annealing to the diffuse single AAAT motifs detected on sequencing. The screened regions of candidate genes GSYI and HRC were excluded from carrying the disease-causing mutation(s). The availability of new sequence data generated by the Human Genome Project will influence future strategies to identify the PFHBI gene. Electronic searches will allow identification of STR sequences for development of polymorphic markers and gene annotation will allow selection of new candidate genes for mutation screening.
AFRIKAANSE OPSOMMING: Sien volteks vir opsomming
Kuek, Conchita Maria. "Hereditary haemochromatosis and the C282Y genotype : implications in diagnosis and disease". University of Western Australia. School of Surgery and Pathology, 2003. http://theses.library.uwa.edu.au/adt-WU2004.0024.
Pełny tekst źródłaPocathikorn, Anothai. "Low density lipoprotein receptor-related protein (LRP) and its mRNA : influence of genetic polymorphisms, a fat load and statin therapy". University of Western Australia. School of Surgery and Pathology, 2006. http://theses.library.uwa.edu.au/adt-WU2006.0117.
Pełny tekst źródłaZdravkovic, Slobodan. "Coronary heart disease in Swedish twins : quantitative genetic studies /". Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-771-5/.
Pełny tekst źródłaMeng, Weihua. "Investigation of the genetic basis of coronary heart disease". Thesis, Queen's University Belfast, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.501377.
Pełny tekst źródłaDunn, Jeremy. "Genetic influences on the premature development of coronary heart disease". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/mq24837.pdf.
Pełny tekst źródłaNet, J. B. van der. "Towards genetic prediction of coronary heart disease in familial hypercholesterolemia". [S.l.] : Rotterdam : [The Author] ; Erasmus University [Host], 2009. http://hdl.handle.net/1765/14566.
Pełny tekst źródłaSarwar, 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.
Pełny tekst źródłaZhang, Qiuping. "Genetic variants of lipid transport genes, dyslipidaemia and coronary heart disease". Thesis, Queen Mary, University of London, 1997. http://qmro.qmul.ac.uk/xmlui/handle/123456789/1642.
Pełny tekst źródłaAshton, Emma Louise, i emma ashton@deakin edu au. "Effects of dietary constituents on coronary heart disease risk factors". Deakin University. School of Biological and Chemical Sciences, 2000. http://tux.lib.deakin.edu.au./adt-VDU/public/adt-VDU20061207.153511.
Pełny tekst źródłaBjörnstedt, Bennermo Marie. "On the genetic variation of interleukin-6 in health and coronary heart disesase /". Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-253-5/.
Pełny tekst źródłaAbdul-Majid, Hariyati Shahrima. "Psychological aspects of recovery from coronary heart disease among patients in Malaysia". Thesis, University of Surrey, 2001. http://epubs.surrey.ac.uk/843015/.
Pełny tekst źródłaLluís, 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.
Pełny tekst źródłaL’expansió principal pel que fa al descobriment de variants genètiques associades amb malalties complexes s’ha dut a terme durant la última dècada. Aquesta expansió ha estat acompanyada, i d’alguna forma motivada, pel desig d’usar aquesta informació per millorar la capacitat de predicció d’aquelles malalties on hi és present un cert component familiar però en les que no es coneixien les variants que conferien un major risc de patir la malaltia, entre elles la cardiopatia isquèmica (CI). La present tesis doctoral està estructurada en dues línies d’investigació que avaluen el possible rol d’un gen candidat en la susceptibilitat de la CI i també avalua la millora en la capacitat de predicció d’un esdeveniment coronari de les eines usades habitualment en la pràctica clínica mitjançant la inclusió d’informació genètica. Més concretament, la primera línea d’investigació es centra en la contribució de la variació genètica en un dels gens més estudiats en relació amb CI: el gen que codifica pel receptor d’estrogens alfa (ESR1). En aquesta línea hem proveït un sòlid meta-anàlisis entre la variant més àmpliament estudiada d’aquest gen i risc coronari i també hem explorat el paper de la majoria de les variants comunes descrites en aquest gen i risc de CI. Mitjançant cap dels anàlisis hem trobat evidència d’associació entre les variants genètiques en aquest gen i el risc de CI. No obstant això, i encara que podem acceptar que les variants genètiques comunes d’aquest gen no estan associades amb esdeveniments coronaris, no podem descartar que altres tipus de variació en aquest gen (com per exemple variació epigenètica) pugui estar modificant la susceptibilitat a patir un esdeveniment coronari, ni tampoc que altres elements de la mateixa cadena de senyalització estiguin associats amb la malaltia. En la segona línea d’investigació, hem explorat el possible paper de les variants genètiques, obtingudes mitjançant estudis d’associació global del genoma (GWAS), en la millora de la capacitat de predicció a 10 anys dels esdeveniments coronaris, mitjançant la seva addició en les funcions de risc cardiovascular clàssiques. Hem seguit les recomanacions proposades per la American Heart Association per l’avaluació en la pràctica clínica de nous biomarcadors, i hem demostrat que, tot i que la magnitud de l’associació d’aquestes variants és modesta, hi ha una tendència cap a la millora de la capacitat de predicció de les funcions de risc.
Jain, Ravi. "Intelligent techniques for the diagnosis of coronary artery disease /". Title page, contents and abstract only, 1998. http://web4.library.adelaide.edu.au/theses/09PH/09phj248.pdf.
Pełny tekst źródłaHo, Lai-yi Ada, i 何麗儀. "Does social support influence coronary heart disease prognosis?: a meta-analysis". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B39724116.
Pełny tekst źródłaPatel, Riyaz. "Beyond genome wide discovery : an exploration of novel genetic variants for coronary heart disease". Thesis, Cardiff University, 2012. http://orca.cf.ac.uk/38470/.
Pełny tekst źródłaKarackattu, Sharon Liz. "Genetic approaches to studying coronary heart disease in SR-BI/apoE double knockout mice". Thesis, Massachusetts Institute of Technology, 2006. http://hdl.handle.net/1721.1/34279.
Pełny tekst źródła"February 2006."
Includes bibliographical references.
Coronary heart disease (CHD) is a major healthcare concern in both developed and developing nations. The principal cause of CHD is atherosclerosis, the buildup of fatty deposits in vessel walls. SR-BI/apoE double knockout (dKO) mice are a novel mouse model of human CHD, exhibiting spontaneous coronary occlusive atherosclerosis, myocardial infarction, cardiac dysfunction and premature death. This model represents a unique system in which to study the two principal underlying mechanisms of atherosclerosis and CHD, inflammation and lipoprotein lipid metabolism. The first part of this thesis demonstrates that B- and T-lymphocytes do not play a significant role in development or progression of atherosclerosis or CHD in SR-BI/apoE dKO mice. More importantly, this study eliminates B- and T-lymphocyte-driven immunoglobulin-mediated inflammation as a significant mechanism instigating or exacerbating myocardial injury in dKO mice. Strikingly, the mice generated for this study also demonstrate that genetic background influences both average lifespan and lifespan variability of dKO mice. The second study investigates alterations in lipoprotein metabolism on CHD and demonstrates that hepatic lipase deficiency, despite raising plasma cholesterol levels, retards development of both aortic and coronary occlusive atherosclerosis in dKO mice.
(cont.) This reduction in atherosclerosis is associated with delayed onset and/or progression of hypertrophy, myocardial infarction and cardiac dysfunction as well as a 37% extension in lifespan. Both of these studies, along with others, suggest SR-BI/apoE dKO mice experience atherosclerotic coronary-occlusion-induced ischemic heart disease and that they may be a valuable tool in which to investigate the etiology of as well as influences of genetic, environmental and pharmacologic manipulations on CHD.
by Sharon Liz Karackattu.
Ph.D.
Robinson, Simon David. "Environmental, genetic and inflammatory factors modifying endothelial function in patients with coronary heart disease". Thesis, University of Edinburgh, 2007. http://hdl.handle.net/1842/29340.
Pełny tekst źródłaHill, John Stuart. "Genetic and environmental factors affecting the incidence of coronary artery disease in heterozygous familial hypercholesterolemia". Thesis, University of British Columbia, 1990. http://hdl.handle.net/2429/28810.
Pełny tekst źródłaMedicine, Faculty of
Pathology and Laboratory Medicine, Department of
Graduate
Jenneke, Cindy A. N. "The effect of dietary patterns on risk factors for CHD : a comparative study of students residing at the Adventist International Institute of Advanced Studies in the Philippines". Thesis, Link to online version, 2006. http://hdl.handle.net/10019/554.
Pełny tekst źródłaLoung, Le Anh. "Genetic variations in the interleukin-6(IL-6) gene : implication in coronary heart disease (CHD)". Thesis, University College London (University of London), 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.406589.
Pełny tekst źródłaBuri, Robert J. (Robert John). "The Role of Anger/Hostility on Physiological and Behavioral Risk Factors for Coronary Heart Disease". Thesis, University of North Texas, 1995. https://digital.library.unt.edu/ark:/67531/metadc278222/.
Pełny tekst źródłaWarner, Anke Sigrid. "The expression, regulation and effects of inducible nitric oxide synthase in hibernating myocardium". Title page, contents and summary only, 2002. http://web4.library.adelaide.edu.au/theses/09PH/09phw279.pdf.
Pełny tekst źródłaEl, Rayess Mohamed Aghar. "Genetic variation in the PECAM-1 gene and its role in atherosclerosis and coronary heart disease". Thesis, University College London (University of London), 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.404401.
Pełny tekst źródłaNaqvi, Habib. "Coronary heart disease : Lay representations of genetics, genetic testing and the decision to pursue predictive genetic testing amongst South Asians". Thesis, University of the West of England, Bristol, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.522563.
Pełny tekst źródłaSaleheen, Danish. "Genetic determinants of major lipids and myocardial infarction in Pakistan". Thesis, University of Cambridge, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.609033.
Pełny tekst źródłaPepe, Salvatore. "The influence of dietary fatty acids on cardiac function /". Title page, table of contents and abstract only, 1991. http://web4.library.adelaide.edu.au/theses/09PH/09php4201.pdf.
Pełny tekst źródłaRajput-Williams, Jayshri. "Genetic variation at the apolipoprotein B gene and associations with coronary heart disease and its risk factors". Thesis, Queen Mary, University of London, 1996. http://qmro.qmul.ac.uk/xmlui/handle/123456789/1681.
Pełny tekst źródłaWilliams, Angela B. "Incidence and implications of atypical exercise blood pressure responses in adults without diagnosed coronary heart disease". Thesis, Virginia Tech, 1985. http://hdl.handle.net/10919/45657.
Pełny tekst źródłaMaster of Science
Abbott, Janice Melodie. "Psychological, cardiovascular and haematological aspects of the Type A behaviour pattern in relation to coronary heart disease". Thesis, University of Central Lancashire, 1988. http://clok.uclan.ac.uk/20137/.
Pełny tekst źródła吳湘舒 i Xiangshu Wu. "Illness perception and coping among older adults with coronary heart disease: a study at acute convalescentstage". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2002. http://hub.hku.hk/bib/B31243794.
Pełny tekst źródłaPocathikorn, Anothai. "Low density lipoprotein receptor-related protein (LRP) and its mRNA : influence of genetic polymorphisms, a fat load and statin therapy /". Connect to this title, 2005. http://theses.library.uwa.edu.au/adt-WU2006.0117.
Pełny tekst źródłaEsslinger, Krista. "Dietary outcomes of a school-based trial to reduce risk factors for coronary heart disease". Thesis, McGill University, 2000. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=31227.
Pełny tekst źródłaCoe, Ellen Moster. "The correlation between changes in conicity index and changes in other risk factors for coronary heart disease at baseline and after a six- month intervention program". Virtual Press, 1995. http://liblink.bsu.edu/uhtbin/catkey/941352.
Pełny tekst źródłaDepartment of Family and Consumer Sciences
Bruce, Sharon Diane. "Development of rate related exercise-induced myocardial ischemia and risk of selected coronary diesease endpoints". Thesis, This resource online, 1993. http://scholar.lib.vt.edu/theses/available/etd-11102009-020132/.
Pełny tekst źródłaWideman, Laurie. "Postprandial lipemia in abdominally obese and non-obese males". Virtual Press, 1993. http://liblink.bsu.edu/uhtbin/catkey/845959.
Pełny tekst źródłaSchool of Physical Education
Erqou, Sebhat. "Lipoprotein(a) and the risk of vascular disease". Thesis, University of Cambridge, 2010. https://www.repository.cam.ac.uk/handle/1810/225182.
Pełny tekst źródłaLai, Josanna Yuk-Lin. "Is keeping in or letting out anger good for your heart?" Thesis, University of British Columbia, 1990. http://hdl.handle.net/2429/30099.
Pełny tekst źródłaArts, Faculty of
Psychology, Department of
Graduate
Chan, Kin-wang, i 陳健宏. "Study of the in vivo role of TSPYL2 in transgenic mice". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B38225049.
Pełny tekst źródła何耀 i Yao He. "A case-control study on passive smoking and coronary heart disease in never-smoking women in Xi'an, China". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1997. http://hub.hku.hk/bib/B31235839.
Pełny tekst źródłaZhian, Samaneh. "Molecular Genetic Analysis of CRELD1 in Patients with Heterotaxy Disorder". PDXScholar, 2011. https://pdxscholar.library.pdx.edu/open_access_etds/410.
Pełny tekst źródłaHarshfield, Eric Leigh. "Genomics of lipid metabolism : identification of genetic determinants of lipid metabolites and the effect of perturbations of lipid levels on coronary heart disease risk factors". Thesis, University of Cambridge, 2018. https://www.repository.cam.ac.uk/handle/1810/277818.
Pełny tekst źródłaStrath, Scott J. "The effect of a light-moderate versus hard exercise intensity on health and fitness benefits". Virtual Press, 1998. http://liblink.bsu.edu/uhtbin/catkey/1115726.
Pełny tekst źródłaSchool of Physical Education
Ward, Clay Herold. "Psychological aspects and potential pathogenic processes of achievement striving associated with the Type A personality". Diss., Virginia Polytechnic Institute and State University, 1986. http://hdl.handle.net/10919/82607.
Pełny tekst źródłaPh. D.
Hong, Ki-Ho. "The development of a normative reference standard for maximal oxygen con[s]umption using the Ball State University-Adult Physical Fitness Program cohort". Virtual Press, 2005. http://liblink.bsu.edu/uhtbin/catkey/1319542.
Pełny tekst źródłaSchool of Physical Education, Sport, and Exercise Science
Horner, Katrina E. "The effect of increasing physical activity on health benefits in sedentary women". Virtual Press, 1997. http://liblink.bsu.edu/uhtbin/catkey/1041902.
Pełny tekst źródłaSchool of Physical Education
Frewen, Sharon H. "The design and evaluation of a short-term group psychotherapy model for survivors of a first myocardial infarction". Thesis, Rhodes University, 2005. http://hdl.handle.net/10962/d1015041.
Pełny tekst źródłaHarper, Christopher Scott. "Family-Supportive Supervisory Behaviors as a Moderator of the Relationship between Job Strain and Workers' Blood Pressure". PDXScholar, 2011. https://pdxscholar.library.pdx.edu/open_access_etds/198.
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