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Trichomoniasis infection, chemotherapy, and serology /Macdonald, Etta Mae, January 1947 (has links)
Thesis (Ph. D.)--University of Wisconsin--Madison, 1947. / Typescript. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references.
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Studies on the development of a mouse model of Graves' disease /Barrett, Kerry, January 2003 (has links)
Thesis (M.Sc.)--Memorial University of Newfoundland, 2003. / Bibliography: leaves 121-140. Also available online.
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Neurotoxicity induced by A[beta] 40 and A[beta] 42 in transgenic mouse models of Alzheimer's diseaseShirwany, Najeeb A. January 2009 (has links) (PDF)
Thesis (Ph. D.)--University of Oklahoma. / Bibliography: leaves 145-219.
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Galanin receptor subtypes in rodent modules of mood disordersWardi-Le Maître, Tara, January 2010 (has links)
Diss. (sammanfattning) Stockholm : Karolinska institutet, 2010.
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Genetic, evolutionary and genomic analysis of homocysteine and folate pathway regulationKitami, Toshimori. January 2006 (has links)
Thesis (Ph. D.)--Case Western Reserve University, 2006. / [School of Medicine] Department of Genetics. Includes bibliographical references. Available online via OhioLINK's ETD Center.
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The deafwaddler mouse as a model for human hearing loss /McCullough, Brendan J. January 2005 (has links)
Thesis (Ph. D.)--University of Washington, 2005. / Vita. Includes bibliographical references (leaves 101-112).
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Developing mouse models to understand olfactory deficits in schizophrenia /Clevenger, Amy Christine. January 2005 (has links)
Thesis (Ph.D. in Neuroscience) -- University of Colorado at Denver and Health Sciences Center, 2005. / Typescript. Includes bibliographical references (leaves 145-171).
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Ethanol-dependent developmental toxicity in zebrafish /Reimers, Mark J. January 2005 (has links)
Thesis (Ph.D. in Toxicology) -- University of Colorado at Denver and Health Sciences Center, 2005. / Typescript. Includes bibliographical references (leaves 137-149).
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Human immunodeficiency virus type I (HIV-1) envelope evolution and the relationship to neutralizing antibodies /Blay, Wendy Marie, January 2006 (has links)
Thesis (Ph. D.)--University of Washington, 2006. / Vita. Includes bibliographical references (leaves 115-136).
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Desenvolvimento de um modelo humanizado de camundongo com traço falciforme e expressão de hemoglobina fetal persistente / Development of a humanized mouse model of sickle cell traid with persistent fetal hemoglobin expressionGimenes, Ana Paula, 1970- 26 August 2018 (has links)
Orientador: Marcus Alexandre Finzi Corat / Dissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas / Made available in DSpace on 2018-08-26T05:45:50Z (GMT). No. of bitstreams: 1
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Previous issue date: 2014 / Resumo: A anemia falciforme é uma doença hereditária que acomete milhões de pessoas Promove destruição crônica das células vermelhas (eritrócitos) do sangue, causando anemia, vaso-oclusão, isquemia e consequentes sintomas deintensa dor, susceptibilidade à infecções e, em alguns casos, a morte precoce. Nas últimas décadas, estudos têm mostrado que o aumento dos níveis de hemoglobina fetal (HbF) inibe o processo de falcização das Hemácias melhorando os sintomas de pacientes com anemia falciforme. Neste estudo, produzimos um modelo animal humanizado com traço falciforme e expressão concomitante de HbF persistente, associando as características genéticas dos camundongos transgênicos B-HPFH195 e Berk-SCM . O primeiro é animal transgênico com persistência de hemoglobina fetal, onde aprodução de HbF continua após o nascimento. A segunda linhagem corresponde ao modelo para doença falciforme, Hbatm1Paz Hbbtm1Tow Tg (HBA - HBBS ) 41Paz / J ( Berk - SCM) e mimetiza a doença humana em sua forma mais grave. Nestes animais a reprodução está comprometida, as fêmeas não levam a gestação ao termino e a maioria dos neonatos morrem horas depois do nascimento. Isto ocorre principalmente devido ao fato de que a (HbF) presente no transgene humano destes animais ser trocada pela HbS enquanto o feto ainda esta em gestação. O novo modelo desenvolvido foi analisado clinicamente e histologicamente para a caracterização e apresentou em sua constituição sanguínea hemoglobinas totalmente humanizadas com cadeias ?, ?s e ? persistente porém, ainda mantendo alterações histopatológicas semelhantes aos modelos da doença falciforme. Este novo animal representa um modelo potencial para uso em testes de drogas no aumento de HbF onde os resultados podem ser relevantes para o estudo e tratamento de hemoglobinopatias, bem como para compreender o comportamento das mutações hereditárias para a expressão persistente da cadeia de globina Y / Abstract: Sickle cell disease is a hereditary disease that affects millions of people promotes chronic destruction of red blood cells (erythrocytes), causing anemia, vascular occlusion, ischemia, pain, and susceptibility to infections and in some instances, death premature. In recent decades, studies have shown that increased HbF levels play an important role in improving the symptoms of patients with sickle cell anemia. In this study, we produced and characterized a humanized animal model with sickle cell trait and concomitant expression of persistent HbF, using the genetic characteristics of transgenic mice B - HPFH195 with Berk¿SCM. This model is a transgenic mice model with hereditary persistence of HbF. The second strain constitutes a mouse with sickle cell disease, Hbatm1Paz Hbbtm1Tow Tg ( HBA - HBBs ) 41Paz /J ( Berk - SCM ), an animal model used to study SCD with human hemoglobin S ( HbS ) in its blood. The Berkeley mouse mimics the human disease in severe form, which compromises in its, females do not lead to pregnancy termination and most newborns die hours after birth. This occurs mainly due to the fact that fetal hemoglobin (HbF), present in the human transgene of these animals,is exchanged to HbS while the fetus still in gestation. The new model produced was analyzed clinically and histologically for proper characterization and presents in its constitution humanized blood, hemoglobin chains with ?, ? ?s and persistent, but still maintains histopathological changes similar to models of sickle cell disease. This model may be a potential model for use in drug in testing increase HbF. And results may be relevant for the study and treatment of hemoglobinopathies as well as for understanding the behavior of hereditary mutations for the persistent expression of the Y globin chain / Mestrado / Clinica Medica / Mestra em Clínica Médica
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