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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 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
Fournier, 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 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 źródłaYako, Yandiswa. "Bioinformatics-based strategies to identify PFHBII-causing and HCM main locus and/or HCM modifying mutations". Thesis, Stellenbosch : University of Stellenbosch, 2004. http://hdl.handle.net/10019.1/16473.
Pełny tekst źródłaENGLISH ABSTRACT: Progressive familial heart block type II (PFHBII) is an inherited cardiac conduction disorder of unknown aetiology, which has been described in a South African family. The disorder was mapped to a 2.9 centimorgan (cM) locus on chromosome 1q32.2-32.3. Clinically, PFHBII manifests cardiac conduction aberrations, that progress to a disease of the heart muscle, dilated cardiomyopathy (DCM). DCM is also reported as an end phase in hypertrophic cardiomyopathy (HCM), another heart muscle disorder. These cardiomyopathies are genetically heterogeneous with some of the genes reported as causes of both disorders. Therefore, genes identified as causes of HCM and DCM were considered plausible candidates for PFHBII mutation analysis. Additionally, this study provided an opportunity to assess potential modifiers of HCM. HCM exhibits marked phenotypic variability, observed within and between families harbouring the same causative mutation. Genes within the PFHBII locus were selected for PCR-SSCP analysis based on homology to genes previously reported as causing conduction system disorders associated with arrhythmias, DCM and/or HCM. Results were confirmed by direct sequencing and association between the detected variants and HCM parameters was assessed using a quantitative transmission disequilibrium test (QTDT). Eleven plausible candidate genes were selected within the PFHBII locus and two of the genes, PFKFB2 and ATF3, that encode for 6-phosphofructo-2,6-bisphosphatase (PFK-2/FBPase-2) and activating transcription factor 3 (ATF3), respectively, were analysed for PFHBII-causing and HCM main locus and/or HCM modifying mutations. Mutation analysis of PFKFB2 and ATF3 in the PFHBII family revealed no PFHBII causal mutation. PFKFB2 and ATF3 were later localised outside the PFHBII locus, and, therefore, were excluded as PFHBII plausible candidates. Further analysis of the two genes for HCM main locus and/or HCM modifying mutations in the HCM panel identified several sequence variants. QTDT analysis of these variants showed no significant association. Completion of the Human Genome Project (HGP) and annotation of new genes within the PFHBII locus allowed the identification of more PFHBII plausible candidate genes. Identification of causal mutations in plausible PFHBII candidate genes will allow molecular diagnosis of PFHBII pathophysiology. Furthermore, identification of both HCM-modifying and HCM-causing genes will give insight into the phenotypic variability noted among South African HCM-affected individuals and into the molecular cause of the disease among individuals with HCM-like clinical features.
AFRIKAANSE OPSOMMING: Progressiewe familiële hartblok tipe II (PFHBII) is ʼn oorgeërfde hart geleidingsiekte van onbekende etiologie wat in ʼn Suid-Afrikaanse familie beskryf is. Die siekte is ʼn 2.9 sentimorgan (cM) lokus op chromosoom 1q32.2-32.3 gekarteer. Klinies presenteer PFHBII met geleidingsfwykings wat uitloop op gedilateerde kardiomiopatie (DCM). DCM word ook gerapporteer as ʼn endfase in hipertrofiese kardiomiopatie (HCM), ʼn ander hartspiersiekte. Die kardiomiopatieë is geneties heterogeen, met ʼn aantal gene wat as oorsaak van altwee siektetoestande gerapporteer word. Daarom is alle gene wat geïdentifiseer is as oorsake van DCM en HCM, as moontlike kandidaatgene vir PFHBII mutasieanaliese beskou. Bykomend het hierdie studie die geleentheid gebied om potensiële modifiseerders van HCM te assesseer. HCM toon beduidende fenotipiese variasie binne en tussen families wat dieselfde siekteveroorsakende mutasie het. Gene binne die PFHBII-lokus is geselekteer vir PCR-SSCP-analiese gebaseer op homologie met gene wat voorheen gerapporteer is om betrokke te wees by geleidingsiesisteemsiektes, geassosieerde arritmieë, DCM en/of HCM. Resultate is bevestig deur volgordebepaling. Assosiasie tusssen ontdekte variante en die siekteparameter is bepaal met ʼn kwantitatiewe transmissie disekwilibrium toets (QTDT). Elf moontlike kandidaatgene in die PFHBII-lokus is geselekteer en twee van die gene, PFKFB2 en ATF3, wat kodeer vir 6-fosfofrukto-2,6-bifosfatase (PFK-2/FBPase-2) en aktiveringstranskripsiefaktor 3 (ATF3) respektiewelik, is vir PFHBII-oorsakende en HCMhooflokus en/of HCM-modifiseerende mutasies ondersoek. Mutasie-analiese van PFKFB2 en ATF3 in die PFHBII-familie het nie ʼn siekteveroorsakende mutasie onthul/uitgelig nie. PFKFB2 en ATF3 is later buite die PFHBII-lokus geplaas en dus ook as moontlike PFHBII-kandidate uitgesluit. Verdere ondersoek van díe twee gene vir HCM-hooflokus en/of HCM-modifiserende mutasies in die HCM-paneel het ʼn aantal volgorde variante geïdentifiseer. QTDT-analiese van die variante het geen beduidende assosiasies aangetoon nie. Voltooiing van die Menslike Genoom Projek (HGP) en annotasie van nuwe gene in die PFHBIIlokus het tot die identifikasie van verdere moontlike PFHBII-kandidaatgene gelei. Identifikase van siekte-veroorsaakende mutasies in die moontlike PFHBII-kandidaatgene sal die molekulêre diagnose van PFHBII toelaat en insig in die patofisiologie van die siekte gee. Verder, identifikasie van beide HCM-veroorsakende of HCM-modifiserende gene kan insig gee in die fenotipiese varieerbaarheid wat onder Suid-Afrikaanse HCM-geaffekteerde individue waargeneem word en ook in die molekulêre oorsake van die siekte in individue met HCMsoortige kliniese kenmerke.
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 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 źródłaKuek, 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 źródłaSznajer, Yves. "Etude des manifestations cardiovasculaires chez les patients présentant un syndrome de Noonan porteurs de mutation au sein du gène PTPN11: rôles des gènes de la voie de signalisation des MAP kinases pour les syndromes apparentés". Doctoral thesis, Universite Libre de Bruxelles, 2009. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/210210.
Pełny tekst źródłaAfin d’appréhender les implications possibles du gène PTPN11 dans la survenue des cardiopathies chez les patients porteurs de ces deux syndromes, nous avons conduit une étude chez 272 patients au syndrome de Noonan et une étude chez 19 patients porteurs du syndrome LEOPARD. Parmi la cohorte de patients atteints du syndrome de Noonan, 104 ont été diagnostiqués porteurs d’une mutation du gène (38%). Une prévalence de survenue de cardiopathies affectant les structures droites du cœur se dégage chez les patients identifiés porteurs d’une mutation avec une différence significative pour la SVP, une tendance est relevée pour le canal atrio-ventriculaire et la communication inter-auriculaire de type Ostium Secundum. L’absence de mutation est corrélée avec la survenue de cardiomyopathie hypertrophique et de cardiopathies du cœur gauche. Parmi les patients atteints du syndrome LEOPARD, il n’existe pas de différence statistiquement significative pour les patients porteurs d’une mutation ou non et/ou pour une cardiopathie particulière.
Toutes les mutations identifiées du gène PTPN11 sont des mutations ‘faux-sens’. Ce gène appartient à la famille des gènes codant pour une protéine tyrosyl phosphatase, SHP-2, ne possédant pas de récepteur trans-membranaire. Cette phosphatase est impliquée dans la voie de signalisation cellulaire des MAP (‘Mitogen-activated protein’) kinases dont l’expression est ubiquitaire et inclut le coeur. Depuis nos travaux, le concept de syndrome « neuro-cardio-facio-cutané » est établi puisque, à ce jour, 9 gènes (SOS1, RAF1, BRAF, KRAS, NRAS, HRAS, NF1, SPRED1 et SHOC2), tous impliqués dans la voie de signalisation RAS (voie des MAP kinases) sont identifiés. Un spectre phénotypique existe avec des signes communs mais aussi distinctifs chez les patients présentant le syndrome de Noonan, le syndrome LEOPARD, le syndrome de Costello, le syndrome Cardio-Facio-Cutané (CFC), le syndrome « Noonan-NF1 », le syndrome de Legius et le syndrome « Noonan/Multiple Giant Cell Lesion ». Nous rapportons enfin l’observation d’une patiente atteinte du syndrome CFC et porteuse d’une mutation (p.R257Q) au sein du gène BRAF ayant développé une cardiomyopathie hypertrophique.
Ces travaux de cohortes de patients au phénotype du syndrome de Noonan, du syndrome LEOPARD et cette dernière description d’une patiente au syndrome CFC ont permis de participer à la découverte de l’implication d’une voie de signalisation cellulaire dont l’origine génétique est maintenant démontrée. Les résultats de nos travaux réalisés depuis 2002 auront permis, avec les équipes travaillant sur le même sujet, d’orienter les investigations et les nouveaux projets de recherche qui étudient spécifiquement le rôle du gène PTPN11 dans l’embryologie du cœur. Les études des orthologues (zebrafish, murin et Drosophila) porteurs à l’état hétérozygote d’une mutation du gène PTPN11 permettent d’intégrer les anomalies phénotypiques et cardiaques observées. Ces études permettent de postuler les effets cellulaires produits par les mutations chez les patients atteints du syndrome de Noonan et chez les patients atteints du syndrome LEOPARD engendrant in vitro une activation de la phosphatase (effet « gain de fonction ») pour les premiers ou une réduction de l’activité phosphatase (« dominant négatif ») mais engendrant un effet gain de fonction in vivo. Nous discutons les connaissances acquises, les compréhensions obtenues et intégrées et traçons enfin les perspectives offertes par ces travaux.
Doctorat en Sciences médicales
info:eu-repo/semantics/nonPublished
Rondelet, Benoît. "Médiation humorale de l'hypertension artérielle pulmonaire dans un modèle de cardiopathie congénitale à shunt systémo-pulmonaire chez le porcelet en croissance". Doctoral thesis, Universite Libre de Bruxelles, 2008. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/210373.
Pełny tekst źródłaPennington, Catherine Margaret. "Genetic aspects of human prion diseases". Thesis, University of Edinburgh, 2013. http://hdl.handle.net/1842/24216.
Pełny tekst źródłaGuo, Youling, i 郭友玲. "Genetic and genomic mapping of common diseases". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hub.hku.hk/bib/B50533861.
Pełny tekst źródłapublished_or_final_version
Psychiatry
Doctoral
Doctor of Philosophy
Lau, Kin-chong, i 劉健莊. "Microarray-based investigations of genetic diseases". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B45894760.
Pełny tekst źródłaRoscioli, Tony Clinical School Prince of Wales Hospital Faculty of Medicine UNSW. "The genetic basis of veno-occlusive disease with immunodeficiency syndrome". Awarded by:University of New South Wales. Clinical School - Prince of Wales Hospital, 2007. http://handle.unsw.edu.au/1959.4/40599.
Pełny tekst źródłaWong, Hoi-man Emily, i 黃凱敏. "Genome-wide association analyses on complex diseases: from single-nucleotide polymorphism to copy numbervariation". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2013. http://hub.hku.hk/bib/B50534099.
Pełny tekst źródłapublished_or_final_version
Psychiatry
Doctoral
Doctor of Philosophy
Nitoiu, Daniela. "Insights into molecular and functional mechanisms behind inherited heart and skin disorders". Thesis, Queen Mary, University of London, 2015. http://qmro.qmul.ac.uk/xmlui/handle/123456789/8911.
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 źródłaHo, Wai-hung Daniel, i 何偉雄. "Genetic study of lumber disc degeneration". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B42841215.
Pełny tekst źródłaAl-Abri, Mohammed Ali. "Genetic variability of health disorders in Ontario Holstein cows". Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=112310.
Pełny tekst źródłaKao, Yu-ping Patrick, i 高宇平. "Genetic association studies of lumbar disc degeneration (LDD)". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B45154430.
Pełny tekst źródłaLee, Kin-shing, i 李鍵成. "In vivo study of asporin function in cartilage tissues". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2014. http://hdl.handle.net/10722/207898.
Pełny tekst źródłapublished_or_final_version
Biochemistry
Doctoral
Doctor of Philosophy
Tam, Chun-yee, i 譚雋怡. "Dissecting the physiological role of the novel lupus-associated C-type lectin-like protein CLEC16A". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2014. http://hdl.handle.net/10722/206749.
Pełny tekst źródłapublished_or_final_version
Medicine
Doctoral
Doctor of Philosophy
Roy, Mélanie. "Identification and characterization of differentially expressed genes in response to Escherichia coli and Staphylococcus aureus in bovine mammary epithelial cells and mammary gland". Thesis, McGill University, 2006. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=98785.
Pełny tekst źródłaJenner, Kris Harlan. "The study of inherited diseases using recombinant DNA technology". Thesis, University of Oxford, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.670385.
Pełny tekst źródłaBroderick, Daniel J. "Mitral valve prolapse syndrome : a proposed treatment through respiratory rebalancing". Virtual Press, 1996. http://liblink.bsu.edu/uhtbin/catkey/1027110.
Pełny tekst źródłaDepartment of Counseling Psychology and Guidance Services
Jagoda, Allison M. "Prevalence of abnormal heart rate acceleration at the onset of exercise in an asymptomatmic, self-referred adult population". CardinalScholar 1.0, 2010. http://liblink.bsu.edu/uhtbin/catkey/1567413.
Pełny tekst źródłaSchool of Physical Education, Sport, and Exercise Science
Jim, Jin-to, i 詹展韜. "Genetics and molecular characterization of degenerative disc disease". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B35720189.
Pełny tekst źródłaWong, Tik-wun Lina, i 黃荻媛. "Construction of an infectious PRRSV cDNA clone and its use as a vectorfor foreign gene expression". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B44251841.
Pełny tekst źródłaHerman, Kazibwe. "Barriers experienced by parents/caregivers of children with clubfoot deformity attending specific clinics in Uganda". Thesis, University of the Western Cape, 2006. http://etd.uwc.ac.za/index.php?module=etd&action=viewtitle&id=gen8Srv25Nme4_9901_1194348551.
Pełny tekst źródłaClubfoot is the most common congenital structural deformity that leads to physical impairments in children in many poor developing countries. Inadequately treated or neglected clubfoot has been found to be a common cause of ohysical disability globally among children and young growing adults. Many children are referred to the clinics for treatment but some parents do not comply with the treatment regimen whcih requires attending for consecutive treatment sessions. The purpose of this study was to investigate barriers to treatment attendance parents/caregivers of children with clubfoot encounter in complying with clubfoot treatment during the plaster csting phase in Uganda.
Sheehan, Susan. "Exploring the Genetics Regulating Kidney Function". Fogler Library, University of Maine, 2007. http://www.library.umaine.edu/theses/pdf/SheehanS2007.pdf.
Pełny tekst źródłaPurdum, Michael B. "The Effects of Positive Emotion, Negative Emotion, Flourishing, and Languishing on Cardiovascular Risk". Thesis, University of North Texas, 2010. https://digital.library.unt.edu/ark:/67531/metadc30503/.
Pełny tekst źródłaMasilamani, Twinkle Jasmine. "Identification of genetic markers associated with Marek's disease resistance in chickens". Thesis, McGill University, 2003. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=19691.
Pełny tekst źródłaWilder, Steven P. "Computational analysis of susceptibility genes for diabetes and cardiovascular diseases in animal models". Thesis, University of Oxford, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.670109.
Pełny tekst źródłaGudmundsdottir, Hafrun. "Coping strategies and causal attributions following myocardial infarction : a longitudinal study". Thesis, University of St Andrews, 1996. http://hdl.handle.net/10023/13534.
Pełny tekst źródłaYuen, Man-fung, i 袁孟峰. "Role of hepatitis B virus genotypes B and C on chronic liver disease in the Chinese". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2004. http://hub.hku.hk/bib/B33710089.
Pełny tekst źródłaSilver, Karlee Linnea. "Genotypic and phenotypic approaches to pathways involved in humoral autoimmunity". Thesis, University of Oxford, 2006. http://ora.ox.ac.uk/objects/uuid:1a18398f-942a-49a4-bd2e-a8ec4b4f647f.
Pełny tekst źródłaLau, Hoi-lun, i 劉海倫. "Genetic and environmental determinants of bone mineral density in Southern Chinese". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B31930633.
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
Mells, George Frank Gannaway. "Investigation of the genetic basis of primary biliary cirrhosis : the PBC genetics study". Thesis, University of Cambridge, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.648610.
Pełny tekst źródłaWilliams, Kevin John. "Biological and genetic studies of wheat resistance to Heterodera avenae". Title page, summary and contents only, 1994. http://web4.library.adelaide.edu.au/theses/09PH/09phw7238.pdf.
Pełny tekst źródłaHollis-Moffatt, Jade Elissa, i n/a. "Fine mapping and characterisation of an autoimmune diabetes locus, insulin dependent diabetes 21, (Idd21) on mouse chromosome-18". University of Otago. Department of Biochemistry, 2006. http://adt.otago.ac.nz./public/adt-NZDU20070130.151657.
Pełny tekst źródłaZhu, Quan. "Role of CDP in MMTV transcriptional regulation and tumorigenesis". Access restricted to users with UT Austin EID, 2001. http://wwwlib.umi.com/cr/utexas/fullcit?p3037038.
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
Li, Yick-yeung, i 李亦揚. "Molecular and phylogenetic analysis of porcine reproductive and respiratory syndrome virus (PRRSV) and porcine circovirus type 2(PCV2)". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2003. http://hub.hku.hk/bib/B29297102.
Pełny tekst źródła李震威 i Chun-wai Davy Lee. "RET receptor tyrosine kinase in developing, adult and polycystic kidneys". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2000. http://hub.hku.hk/bib/B31241931.
Pełny tekst źródłaTse, Wing-on, i 謝永安. "Hepatic oxidative stress in COX-1 knockout mice". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2006. http://hub.hku.hk/bib/B4501095X.
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
Agenbag, Gloudi. "Molecular genetic analysis of familial breast cancer in South Africa". Thesis, Link to the online version, 2005. http://hdl.handle.net/10019/953.
Pełny tekst źródłaLam, To-kam, i 林吐金. "In vivo study of asporin polymorphic variants in chondrogenesis and degenerative disc disease (DDD)". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B42182591.
Pełny tekst źródłaRoss, Ian Lindsay. "Mechanisms of biocontrol of Gaeumannomyces graminis var. tritici by Pseudomonas corrugata strain 2140 : genetic and biochemical aspects". Title page, table of contents and summary only, 1996. http://web4.library.adelaide.edu.au/theses/09PH/09phr824.pdf.
Pełny tekst źródła