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Functional and structural studies on CYP21 mutants in congenital adrenal hyperplasia /Robins, Tiina, January 2005 (has links)
Diss. (sammanfattning) Stockholm : Karol. inst., 2005. / Härtill 5 uppsatser.
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Fibrinogen and susceptibility to myocardial infarction : role of gene-gene and gene-environment interactions /Nastase Mannila, Maria, January 2006 (has links)
Diss. (sammanfattning) Stockholm : Karol. inst., 2006. / Härtill 5 uppsatser.
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Epidemiology of Ross River virus in the south-west of Western Australia and an assessment of genotype involvement in Ross River virus pathogenesis /Prow, Natalie A. January 2006 (has links)
Thesis (Ph.D.)--University of Western Australia, 2006.
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The effect of early dietary amino acid restrictions on serum metabolites in pigs selected for lean growth efficiencyMule, Hazarath Reddy, Chiba, Lee I. January 2005 (has links)
Thesis--Auburn University, 2005. / Abstract. Vita. Includes bibliographic references (p.66-78).
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Plasticity of consumer-prey interactions in the sea chemical signaling, consumer learning, and ecological consequences /Long, Jeremy Dillon. January 2004 (has links) (PDF)
Thesis (Ph. D.)--Biology, Georgia Institute of Technology, 2005. / Hay, Mark, Committee Chair ; Dusenbery, David, Committee Member ; Kubanek, Julia, Committee Member ; Paffenhofer, Gustav-Adolf, Committee Member ; Yen, Jeannette, Committee Member. Includes bibliographical references.
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Genotype by environment interaction estimated by using reaction normsMaricle, Elizabeth Ann. January 2008 (has links)
Thesis (M.S.)--University of Missouri-Columbia, 2008. / The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Title from title screen of research.pdf file (viewed on August 13, 2009) Includes bibliographical references.
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Life history divergence and population structure of New Zealand chinook salmon : a study of contemporary microevolution /Kinnison, M. T. January 1999 (has links)
Thesis (Ph. D.)--University of Washington, 1999. / Vita. Includes bibliographical references (leaves 124-141).
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Cellular events conditioned by the Np gene of Pisum sativum L. in response to reduced UV light, weevil oviposition, and bruchins /Ketter, Ann P. January 1900 (has links)
Thesis (M.S.)--Oregon State University, 2007. / Printout. Includes bibliographical references (leaves 60-64). Also available on the World Wide Web.
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The isolation and genotypic characterisation of Campylobacter jejuni from environmental matrices : a thesis submitted in partial fulfilment of the requirements for the degree of Master of Science in Microbiology in the University of Canterbury /Devane, P. M. L. January 2006 (has links)
Thesis (M. Sc.)--University of Canterbury, 2006. / Typescript (photocopy). Includes bibliographical references (p. 169-200). Also available via the World Wide Web.
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Caracterização molecular de elementos VanA em enterococos com genótico e fenótipo discrepantes relativos à resistência aos glicopeptídeos / Molecular characterization of the VanA element in enterococci with incongruent genotype and phenotypes relative to glycopeptide resistance.Priscila Moraes Henrique 06 March 2007 (has links)
Enterococos resistentes aos glicopeptídeos representam, atualmente, importantes patógenos causadores de infecção nosocomial, sendo isolados em várias regiões do mundo, inclusive no Brasil. Dos fenótipos de resistência descritos até o momento, VanA e VanB são os mais encontrados. O fenótipo VanA é caracterizado por linhagens resistentes a altos níveis de vancomicina e teicoplanina, enquanto VanB é representado por linhagens com altos níveis de resistência à vancomicina, mas com sensibilidade à teicoplanina. O fenótipo VanA é codificado por um grupamento de genes (vanRSHAXYZ) localizados em um elemento genético móvel denominado Tn1546 ou elemento VanA, freqüentemente inserido em plasmídeo conjugativo. Quatro linhagens de enterococos resistentes à vancomicina e sensíveis à teicoplanina que apresentaram genótipo vanA e fenótipo VanB foram estudadas com objetivo de se determinar qual o mecanismo responsável por esta incongruência. A identificação das espécies foi realizada por multiplex PCR, sendo três linhagens identificadas como Enterococcus faecalis e uma linhagem Enterococcus faecium. Todas confirmaram a presença do gene vanA por PCR e, no entanto, apresentaram sensibilidade à teicoplanina, determinada por Etest, condizente com o fenótipo VanB. Reações de Long-PCR e overlapping PCR foram realizadas para amplificação e caracterização do elemento VanA. O elemento VanA das linhagens de E. faecalis mostrou deleção da extremidade direita, correspondente à perda dos genes vanY e vanZ. Na linhagem de E. faecium foi detectada a inserção da ISEfa5 na região intergênica vanXY, como reportado em estudo prévio. A tipagem molecular das linhagens foi realizada pelo perfil de PFGE após macrorestrição do DNA com enzima SmaI e indicou que duas linhagens de E. faecalis pertenciam ao mesmo clone, enquanto a outra era geneticamente não relacionada. Estudos de hibridação com sonda para localização do gene vanA indicaram que este gene estava associado a um plasmídeo de 70Kb. Para verificar a presença de eventuais mutações no gene vanS, relatadas em alguns estudos como causa da perda da sensibilidade à teicoplanina, os elementos VanA das linhagens foram seqüenciados, contudo nenhuma mutação foi encontrada. Os experimentos de clonagem para analisar a possível presença de uma região promotora entre os genes vanY e vanZ indicaram a viii não existência de um promotor nesta região. A presença de elemento VanA com a mesma característica, sendo carreado por plasmídeos de mesmo tamanho em linhagens de E. faecalis com perfil de PFGE diferentes, sugere que este elemento foi transferido horizontalmente. O estudo molecular deste elemento de resistência gerou informações sobre a epidemiologia e eventos genéticos no elemento VanA que estão ocorrendo nas linhagens de VRE isoladas no Brasil. / Vancomycin-resistant enterococci (VRE) have emerged worldwide including in Brazil as important nosocomial pathogens. The most prevalent phenotypes described among glycopeptide resistant enterococci are VanA and VanB. VanA phenotype is characterized by induced high-level resistance both to vancomycin and teicoplanin, whereas VanB resistant strains show inducible resistance to vancomycin and retained susceptibility to teicoplanin. The vanA gene cluster (vanRSHAXYZ) is located in a mobile genetic element called Tn1546 or VanA element, which is often carried by conjugative plasmids. Four VRE showing VanB phenotype and vanA genotype isolated in a Brazilian hospital were investigated to better understand the molecular mechanisms underlying this incongruence. Multiplex PCR was performed for species identification. Three strains were identified as Enterococcus faecalis and the fourth as Enterococcus faecium. All VRE strains harboured gene vanA but showed VanB phenotype as determined by the Etest. Long PCR and PCR amplification of internal regions were employed for Tn1546 structural analysis. Three E. faecalis showed deletion of vanYZ genes corresponding to the inverted repeated right terminal of Tn1546 and E. faecium showed insertion of an IS element, ISEFa5, between vanX and vanY genes, as previously reported. These genetic rearrangements were associated to loss of resistance to teicoplanin. PFGE performed after SmaI digestion of DNA revealed that two E. faecalis were genetically related but the third one was unrelated. Plasmid analysis followed by Southern blotting and hybridization with vanA probe were performed for localization of VanA element. Results indicated that E. faecalis isolates showed the same structure of VanA element and plasmid profile with vanA located into plasmid. Thus, horizontal dissemination of this genetic element was suggested. VanA elements in all isolates were sequenced to detect point mutations in vanS, previously observed in VanB phenotype-vanA-genotype VRE isolates. However, no mutation was found. Assays to detect the presence of a promoter between vanX and vanY genes were negative for this region. Molecular characterization of these VRE furnished additional important information about VanA element epidemiological and evolutionary events in Brazilian isolates.
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