Дисертації з теми "Genetic Function"
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Shi, Bu-Jun. "Expression and function of cucumoviral genomes." Title page, contents and summary only, 1997. http://web4.library.adelaide.edu.au/theses/09PH/09phs5546.pdf.
Повний текст джерелаObeidat, Ma’en. "Genetic determinants of lung function measures." Thesis, University of Nottingham, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.580163.
Повний текст джерелаYu, Chris 1981. "Characterizing function inlining with genetic programming." Thesis, Massachusetts Institute of Technology, 2004. http://hdl.handle.net/1721.1/33392.
Повний текст джерелаIncludes bibliographical references (leaves 74-75).
Function inlining is a compiler optimization where the function call is replaced by the code from the function itself. Using a form of machine learning called genetic programming, this thesis examines which factors are important in determining which function calls to inline to maximize performance. A number of different heuristics are generated for inlining decisions in the Trimaran compiler, which improve on performance from the current default inlining heuristic. Also, trends in function inlining are examined over the thousands of compilation runs that are completed.
by Chris Yu.
M.Eng.
Golby, Jessica A. "Genetic analysis of Drosophila NSF function /." Thesis, Connect to this title online; UW restricted, 2003. http://hdl.handle.net/1773/10247.
Повний текст джерелаGeorgiou, Marios Andrew. "A molecular genetic analysis of commissureless function." Thesis, King's College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.271968.
Повний текст джерелаBirkett, Paul Brian Lawrie. "Genetic predisposition to schizophrenia and cognitive function." Thesis, King's College London (University of London), 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.431227.
Повний текст джерелаReed, Patricia. "Function of bacteriophage Orf recombinases in genetic exchange." Thesis, Durham University, 2006. http://etheses.dur.ac.uk/4917/.
Повний текст джерелаBuender, Til. "Structural, biochemical and genetic dissection of RPS19 function." Thesis, University of Cambridge, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.609522.
Повний текст джерелаMarcão, Ana Maria Lopes. "Arylsulfatase A : Genetic epidemiology and structure/ function studies." Doctoral thesis, Universidade do Porto. Reitoria, 2003. http://hdl.handle.net/10216/9650.
Повний текст джерелаMarcão, Ana Maria Lopes. "Arylsulfatase A : Genetic epidemiology and structure/ function studies." Tese, Universidade do Porto. Reitoria, 2003. http://hdl.handle.net/10216/9650.
Повний текст джерелаSheehan, Susan. "Exploring the Genetics Regulating Kidney Function." Fogler Library, University of Maine, 2007. http://www.library.umaine.edu/theses/pdf/SheehanS2007.pdf.
Повний текст джерелаTaranova, Olena V. Pevny Larysa. "Genetic analysis of SOX2 function in mouse neural progenitors." Chapel Hill, N.C. : University of North Carolina at Chapel Hill, 2006. http://dc.lib.unc.edu/u?/etd,286.
Повний текст джерелаTitle from electronic title page (viewed Oct. 10, 2007). "... in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the Curriculum in Neurobiology, School of Medicine." Discipline: Neurobiology; Department/School: Medicine.
Gallagher, William. "Somatic genetic analysis of p53 function and cisplatin resistance." Thesis, University of Glasgow, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.321095.
Повний текст джерелаGilmour, Darren T. "Reverse genetic analysis of SPARC function in vertebrate embryogenesis." Thesis, University of Cambridge, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.314018.
Повний текст джерелаde, Marvao Antonio. "Anthropometric and genetic determinants of cardiac morphology and function." Thesis, Imperial College London, 2015. http://hdl.handle.net/10044/1/56050.
Повний текст джерелаPaul, Dirk Stefan. "Maps of open chromatin : from genetic signals to function." Thesis, University of Cambridge, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.607719.
Повний текст джерелаGreetham, Matthew James. "Proteins that function at telomeres : genetic and biochemical investigation." Thesis, University of Newcastle upon Tyne, 2015. http://hdl.handle.net/10443/2882.
Повний текст джерелаHashimi, Sara Tajyar. "Dissecting genetic regulation of dendritic cell activation and function." Diss., Restricted to subscribing institutions, 2008. http://proquest.umi.com/pqdweb?did=1779835211&sid=4&Fmt=2&clientId=1564&RQT=309&VName=PQD.
Повний текст джерелаMeir, Eli. "Modeling genetic networks to aid in understanding their function /." Thesis, Connect to this title online; UW restricted, 2003. http://hdl.handle.net/1773/5263.
Повний текст джерелаEkaterinaki, Nelly. "Expression and function of TN7 transposition proteins." Thesis, University of Glasgow, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.303343.
Повний текст джерелаAllard, Patrick 1974. "Expression, regulation and function of the stem-loop binding protein during mammalian oogenesis." Thesis, McGill University, 2005. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=85663.
Повний текст джерелаDiril, Muhammed Kasim. "Genetic analysis of stoned B-stonin 2 function in vivo." [S.l.] : [s.n.], 2005. http://webdoc.sub.gwdg.de/diss/2005/diril/diril.pdf.
Повний текст джерелаTan, Elaine May. "Genetic strategies for elucidating neural circuit function in the brain." Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2006. http://wwwlib.umi.com/cr/ucsd/fullcit?p3211372.
Повний текст джерелаTitle from first page of PDF file (viewed June 13, 2006). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references.
Kay, Linda. "Influence of genetic polymorphisms on beta2-adrenoceptor expression and function." Thesis, University of Sheffield, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.489852.
Повний текст джерелаMak, Philip. "An application of genetic algorithms to a function allocation problem." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape7/PQDD_0015/MQ48281.pdf.
Повний текст джерелаPrescher, Finnvid. "Seed orchards - genetic considerations on function, management and seed procurement /." Umeå : Dept. of Forest Genetics and Plant Physiology, Swedish University of Agricultural Sciences, 2007. http://epsilon.slu.se/200775.pdf.
Повний текст джерелаHedner, Margareta. "Olfactory Function : The Influence of Demographic, Cognitive, and Genetic Factors." Doctoral thesis, Stockholms universitet, Psykologiska institutionen, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-85907.
Повний текст джерелаRanlund, S. M. "Biomarkers of brain function in psychosis and their genetic basis." Thesis, University College London (University of London), 2016. http://discovery.ucl.ac.uk/1493030/.
Повний текст джерелаRadhakrishnan, Aparna. "Genetic variation studies of megakaryopoiesis, platelet formation and platelet function." Thesis, University of Cambridge, 2014. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.708102.
Повний текст джерелаStevens, Robin J. "Genetic analysis of synaptogyrin function in the synaptic vesicle cycle." Thesis, Massachusetts Institute of Technology, 2012. http://hdl.handle.net/1721.1/70105.
Повний текст джерелаThis electronic version was submitted by the student author. The certified thesis is available in the Institute Archives and Special Collections.
Cataloged from student-submitted PDF version of thesis.
Includes bibliographical references.
Neuronal communication relies on the continual replenishment of synaptic vesicles that are primed for neurotransmitter release in response to action potentials. A vast array of proteins is required to mediate synaptic vesicle biogenesis, trafficking, docking, exocytosis, and endocytosis. Synaptogyrin and synaptophysin are abundant and evolutionarily conserved synaptic vesicles proteins that were identified over twenty years ago, yet their exact function in the synaptic vesicle cycle remains unknown. To further elucidate the role of these proteins, we have generated and characterized a synaptogyrin null mutant in Drosophila, whose genome encodes a single synaptogyrin isoform and lacks a synaptophysin homolog. Here we demonstrate that Drosophila synaptogyrin is abundantly expressed in neurons, where it localizes to the presynaptic terminal of the larval neuromuscular junction (NMJ). Drosophila lacking synaptogyrin are viable and fertile and have no overt deficits in motor function or courtship behavior. Ultrastructural analysis of mutant larvae revealed an increase in average synaptic vesicle diameter as well as enhanced variability in the size of synaptic vesicles. In addition, the resolution of endocytic cisternae into synaptic vesicles in response to robust exocytosis is defective in synaptogyrin mutants. While basal synaptic transmission at the larval NMJ is unaffected, synaptogyrin mutants do display increased facilitation during high-frequency stimulation, indicating that synaptic vesicle exocytosis is abnormally regulated during strong stimulation conditions. These results suggest that, while not required for neurotransmission, Drosophila synaptogyrin nevertheless modulates synaptic vesicle exo-endocytosis, especially during elevated rates of synaptic vesicle fusion.
by Robin J. Stevens.
Ph.D.
Soler, Artigas María. "Genetic epidemiology of lung function and chronic obstructive pulmonary disease." Thesis, University of Leicester, 2015. http://hdl.handle.net/2381/31980.
Повний текст джерелаGuo, Ruijian. "Genetic and environmental components of sperm function in Drosophila melanogaster." Technische Universität Dresden, 2019. https://tud.qucosa.de/id/qucosa%3A37772.
Повний текст джерелаKlejnot, John Timothy. "Molecular genetic studies of cryptochrome 2 function in Arabidopsis thaliana." Diss., Restricted to subscribing institutions, 2008. http://proquest.umi.com/pqdweb?did=1666130271&sid=3&Fmt=2&clientId=1564&RQT=309&VName=PQD.
Повний текст джерелаTaylor, Michael Robert. "Genetic and biochemical analysis of zebrafish with visual function defects /." Thesis, Connect to this title online; UW restricted, 2002. http://hdl.handle.net/1773/9242.
Повний текст джерелаMa, Yong. "Genetic and biochemical analysis of dispatched function in hedgehog signaling." Available to US Hopkins community, 2003. http://wwwlib.umi.com/dissertations/dlnow/3080721.
Повний текст джерелаKim, Changhyeon. "Development of a Genetic Transformation System of Raspberry Cultivars for Gene Function Analysis." Thesis, North Dakota State University, 2018. https://hdl.handle.net/10365/29223.
Повний текст джерелаWan, Wen. "Semi-Parametric Techniques for Multi-Response Optimization." Diss., Virginia Tech, 2007. http://hdl.handle.net/10919/29425.
Повний текст джерелаPh. D.
Lee, Kin-shing, and 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.
Повний текст джерелаpublished_or_final_version
Biochemistry
Doctoral
Doctor of Philosophy
Chen, Shen Liang. "Function of transcription cofactors in terminal muscle differentiation /." St. Lucia, Qld, 2001. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe16099.pdf.
Повний текст джерелаBlevins, Todd Lucas. "Molecular genetic analysis of siRNA biogenesis and function in Arabidopsis thaliana /." [S.l.] : [s.n.], 2009. http://edoc.unibas.ch/diss/DissB_8814.
Повний текст джерелаEriksson, Jonas. "Genetic and Genomic Studies in Chicken : Assigning Function to Vertebrate Genes." Doctoral thesis, Uppsala universitet, Institutionen för medicinsk biokemi och mikrobiologi, 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-162597.
Повний текст джерелаZhan, Yougen 1968. "Proteomics and genetic studies of dystroglycan function in the nervous system." Thesis, McGill University, 2006. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=102771.
Повний текст джерелаUsing proteomics I found that beta-DG is directly associated with the GTPase dynamin 1 in the retina and in the brain together with alpha-DG and Grb2, and immunohistochemically beta-DG was colocalized with dynamin 1 in the outer plexiform layer where photoreceptor terminals are localized. Moreover, loss of DG in differentiated DG-null embryonic stem cells significantly increases dynamin-mediated transferrin-uptake and re-expression of DG in null cells by infection with an adenovirus containing DG reduced transferrin uptake to levels seen in wild-type cells. This result implies that one of mechanisms in muscular dystrophy might be the altered synaptic vesicle endocytosis, especially in the retina where synaptic transmission defect has been known for decades.
Muscular dystrophies show not only impaired retinal synaptic transmission and several DG-related congenital muscular dystrophies also display retinal structural defects. To further understand the roles of DG in the retina, I used Drosophila eye as a model and demonstrated for the first time that DG is required cell-autonomously for photoreceptor morphogenesis in the developing visual system. Deficiency of DG in the eye causes severe disruption of retinal structure, aberrant lens formation and abolition of electroretinogram in the adult fly eye. These adult defects appear derived from autonomous photoreceptor cell (PRC) defects in the early pupa including size arrest, loss of polarity and progressive degeneration. All defects in the eye, however, can be reversed by re-expression of wild type DG in DG-deficient PRCs, suggesting DG functions cell-autonomously in PRCs and non-autonomously for lens. In the 3rd instar larvae DG is present in the apical tips and the basal membranes of PRCs, two polarized locations opposing the extracellular matrix. At the pupal stage it continues to mainly distribute at the apical rhabdomere and basal membrane of PRCs. Over-expression of DG leads to larger ommatidia but the PRC number remains unchanged, suggesting that DG is both necessary for and sufficient to promote PRC expansion. By rescue experiments, I demonstrated that the extracellular DG alone could not rescue DG-deficient eye defects, whereas the intracellular DG can substantially ameliorate PRC degeneration and structural defects while some PRCs remain disorganized, a sign of disrupted PRC planar polarity in absence of the extracellular DG. Therefore, our data suggest that the degeneration and planar polarity disruption in DG-deficient PRCs are two independent processes that appear to require the respective function of intracellular and extracellular DG. In summary, our experiments demonstrated several novel findings and provided the basis for future investigations on DG function and the molecular mechanisms of nervous system defects in muscular dystrophies.
Harpham, Colin. "Development of a novel radial basis function network using genetic algorithms." Thesis, University of Derby, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.411390.
Повний текст джерелаKelly, David Christopher. "Genetic approaches to the study of epithelial function in Drosophila melanogaster." Thesis, University of Glasgow, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.321066.
Повний текст джерелаWhitlock, Rajenda. "The consequences of genetic impoverishment for plant community structure and function." Thesis, University of Sheffield, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.419639.
Повний текст джерелаYeang, Han Xian Aw. "Modulation of dendritic cell function by molecular, pharmacological and genetic approaches." Thesis, University of Liverpool, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.548801.
Повний текст джерелаWarmke, Jeffrey Wayne. "Genetic analysis of myosin light chain-2 function in Drosophila melanogaster /." The Ohio State University, 1990. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487677267730356.
Повний текст джерелаWang, Ying. "Genetic dissection of adaptor molecules in lymphocyte development, homeostasis and function." Aix-Marseille 2, 2006. http://www.theses.fr/2006AIX22035.
Повний текст джерелаL’adaptateur transmembranaire LAT (Linker for Activation of T cells) constitue une plateforme moléculaire assurant le recrutement de nombreuses protéines impliquées dans la transduction des signaux médiés par le TCR. Les souris homozygotes pour une mutation ponctuelle de la tyrosine 136 du domaine intracytoplasmique de LAT présentent un défaut dans le développement des lymphocytes T. En outre, elles développent progressivement une lymphoprolifération T CD4+ polyclonale qui est associée à une éosinophilie tissulaire et à une maturation massive des cellules B en plasmocytes sécrétant des niveaux élevés d’IgG1 et d’IgE. Pour disséquer les mécanismes cellulaires et moléculaires associés au développement de cette pathologie, nous avons mis en oeuvre un système de transfert adoptif à court terme et à long terme dans des hôtes présentant une immunodéficience sélective en lymphocytes T. Nous avons montré que les cellules T CD4+ des souris mutantes LATY136F présentent une homéostasie similaire à celle des cellules wt en début de reconstitution. En revanche, 8 semaines après reconstitution, les cellules T CD4+ desLATY136F induisent une pathologie lymphoproliférative qui reproduit en tout point celle observée initialement dans les souris LATY136F. Ainsi, les souris reconstituées présentent-elles une accumulation massive de cellules T CD4+ et de lymphocytes B dans les organes lymphoïdes secondaires, une ypergammaglobulinémie IgG1 et IgE et une éosinophilie marquée dans de nombreux tissus. Ceci démontre que les lymphocytes T sont nécessaires et suffisants pour induire la pathologie LATY136F. Par comparaison des reconstitutions réalisées dans des hôtes déficients en CD3 et exprimant ou non les molécules d’histocompatibilité de classe II, nous avons établi que les lymphocytes T CD4+ LATY136F conservent, en l’absence de molécules d’histocompatibilité de classe II, leur capacité à proliférer et à stimuler la maturation des lymphocytes B en plasmocytes sécrétant des IgG1 et des IgE -avec une efficacité néanmoins deux fois moindre-. Ces résultats suggèrent que la lymphoprolifération des cellules T CD4+ dans les souris mutantes LATY136F et que la coopération T/B associée qui conduit à des concentrations sériques considérables d’IgE et IgG1 sont, pour une large part, indépendants des moléculesd’histocompatibilité de classe II. Ce comportement largement indépendant du TCR et pouvant à ce titre être qualifié de comportement autistique vis-à-vis des molécules de classe II apparaît comme une propriété unique des cellules T CD4+ portant la mutation LATY136F. NTAL (Non T cell Activation Linker, également appelé LAB) est un adaptateur transmembranaire récemment identifié qui possède des similarités structurales avec LAT. NTAL est fortement exprimé dans les cellules B, les cellules NK et les mastocytes. NTAL est rapidement phosphorylé par les kinases de la famille Src (Lck ou Fyn) et de la famille Syk (Zap-70 ou Syk) après engagement du récepteur des cellules B (BCR) ou des récepteurs au fragment Fc des immunoglobulines de type FcγRI et FcεRI. Les principales protéines identifiées comme associées à la molécule NTAL phosphorylée sont Grb2, SOS1, C-Cbl, Gab1. La suppression de l’expression de NTAL dans une lignée B conduit à une diminution des flux calciques et de l’activation des molécules Erk, ce qui suggère que NTAL participe à l’induction des flux calciques et à l’activation de la voie Ras-MAPKassociées à la stimulation du BCR. Pour identifier les rôles respectifs de NTAL et de LAT dans le développement et la fonction des lymphocytes B, des souris déficientes pour Ntal ont été générées et croisées avec des souris déficientes pour LAT. L’ analyse de ces souris a montré que les cellules B se développent avec la même efficacité dans les souris doublement déficientes Lat-/-Ntal-/-, dans les souris déficientes dans l’un de ces deux gènes et dans les souris wild-type, ce qui démontre que NTAL n’est pas indispensable pour le développement des lymphocytes B. L’agrégation des récepteurs des cellules B induit, par ailleurs, des niveaux de prolifération et des niveaux de flux calciques légèrement augmentés dans les souris déficientes pour Ntal. L’analyse des réponses humorales T dépendantes et T indépendantes a montré que les souris déficientes pour Ntal possèdent, en outre, des niveaux augmentés d’anticorps naturels et des réponses humorales légèrement amplifiées en réponse à des antigènes T dépendants. Des titres normaux d’immunoglobulines sériques spécifiques sont observés en réponse à des antigènes T indépendants. Enfin, bien que NTAL soit également exprimé dans les plasmocytes, son absence n’affecte pas l’hypergammaglobulinémie E et G1 sedéveloppant dans les souris porteuses de la mutation LATY136F. NTAL ne constitue donc pas dans les lymphocytes B l’équivalent fonctionnel de LAT dans les lymphocytes T
Trebble, Peter. "Glucocorticoid receptor function : new insights from genetic and chemical biology approaches." Thesis, University of Manchester, 2013. https://www.research.manchester.ac.uk/portal/en/theses/glucocorticoid-receptor-function-new-insights-from-genetic-and-chemical-biology-approaches(b55c612b-eda1-4908-a0df-ec916f03ade2).html.
Повний текст джерелаMa, Jiya. "A Genetic Algorithm for Solar Boat." Thesis, Högskolan Dalarna, Datateknik, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:du-3488.
Повний текст джерела