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Dissertations / Theses on the topic 'Triple transgenic mice model'

Author: Grafiati

Published: 4 June 2021

Last updated: 12 February 2022

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1

So, Chi-leung. "Transgenic mouse model of human chondrodysplasia /." Hong Kong : University of Hong Kong, 1997. http://sunzi.lib.hku.hk/hkuto/record.jsp?B19161347.

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2

蘇志良 and Chi-leung So. "Transgenic mouse model of human chondrodysplasia." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1997. http://hub.hku.hk/bib/B31237678.

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3

衛永剛 and Wing-kong Wai. "Abnormal chondrocyte differentiation: a transgenic model." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1998. http://hub.hku.hk/bib/B31237800.

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4

Wai, Wing-kong. "Abnormal chondrocyte differentiation : a transgenic model /." Hong Kong : University of Hong Kong, 1998. http://sunzi.lib.hku.hk/hkuto/record.jsp?B19656439.

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5

Makinen, Kimmo. "Spontaneous model of experimental autoimmune uveoretinitis : IRBP-HEL transgenic mice." Thesis, University of Aberdeen, 2006. http://digitool.abdn.ac.uk/R?func=search-advanced-go&find_code1=WSN&request1=AAIU490269.

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To generate a spontaneous EAU model, transgenic mice expressing membrane-bound hen egg lysozyme (HEL) under control of the IRBP promoter were generated. The mice expressed HEL in the photoreceptors, and in the thymus as measured by immunofluorescent confocal microscopy and real-time RT-PCR, respectively. When crossed with the 3A9 TCR-transgenic mice whose CD4+ T cells are HEL-specific, double-transgenic mice developed spontaneous EAU with 100% incidence and an onset age of 22 days post-partum. The ocular inflammation was multifocal and affected the posterior segment of the eye, and led to comp

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6

Siu, Kwan-yin. "The development and characterization of a knockout model for secretin." Click to view the E-thesis via HKUTO, 2008. http://sunzi.lib.hku.hk/hkuto/record/B40887674.

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7

Chung, Chi-kin Samuel. "The development and characterization of a gene-knockout mouse model for secretin receptor /." View the Table of Contents & Abstract, 2005. http://sunzi.lib.hku.hk/hkuto/record/B31491121.

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8

Siu, Kwan-yin, and 蕭君言. "The development and characterization of a knockout model for secretin." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2008. http://hub.hku.hk/bib/B40887674.

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9

Tsang, Kwok-yeung. "Molecular pathogenesis of abnormal chondrocyte differentiation in a transgenic mouse model /." View the Table of Contents & Abstract, 2006. http://sunzi.lib.hku.hk/hkuto/record/B35132796.

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10

楊重文 and Chung-man Yeung. "Studies on the tissue specificity of the glucose-dependent insulinotropic polypeptide promoter by a transgenic mouse model." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1997. http://hub.hku.hk/bib/B31220204.

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11

Yeung, Chung-man. "Studies on the tissue specificity of the glucose-dependent insulinotropic polypeptide promoter by a transgenic mouse model /." Hong Kong : University of Hong Kong, 1997. http://sunzi.lib.hku.hk/hkuto/record.jsp?B19098947.

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12

Cheng, Yin-wo. "Molecular basis for the increased osteoblast activity in a mouse model with hyperostosis." Click to view the E-thesis via HKUTO, 2005. http://sunzi.lib.hku.hk/hkuto/record/B34612981.

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13

Chung, Chi-kin Samuel, and 鍾志堅. "The development and characterization of a gene-knockout mouse model for secretin receptor." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B45014759.

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14

Phan, Tri Giang. "The SW hel model for studying B cell responses in tolerance and immunity." Connect to full text, 2004. http://hdl.handle.net/2123/626.

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Thesis (Ph. D.)--University of Sydney, 2005.<br>Title from title screen (viewed 22 May 2008). Submitted in fulfilment of the requirements for the degree of Doctor of Philosophy to the Discipline of Experimental Medicine, Faculty of Medicine. Degree awarded 2005; thesis submitted 2004. Includes bibliographical references. Also available in print form.

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15

Letronne, Florent. "ADAM30 et métabolisme de l'APP : implication dans le développement physiopathologique de la maladie d'Alzheimer." Thesis, Lille 2, 2014. http://www.theses.fr/2014LIL2S062/document.

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L’accumulation cérébrale progressive de peptides amyloïdes générés à partir du clivage du précurseur du peptide amyloïde (APP) par les sécrétases est un mécanisme central de la maladie d’Alzheimer. C’est pourquoi, améliorer la compréhension de la régulation et de l’homéostasie du métabolisme de l’APP est devenu primordial. Partant de ce constat, nous avons supposé qu’une partie de la réponse pourrait être apportée par la caractérisation de nouveaux acteurs du métabolisme de l’APP. De part leurs rôles cruciaux dans le cerveau (développement, plasticité et réparations) et dans le métabolisme de

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16

Golovan, Serguei Petrovich. "Transgenic mice expressing AppA phytase as a model demonstrating reduced pollution in monogastric animals." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2002. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/NQ65822.pdf.

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17

Tsang, Kwok-yeung, and 曾國揚. "Molecular pathogenesis of abnormal chondrocyte differentiation in a transgenic mouse model." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2006. http://hub.hku.hk/bib/B4501551X.

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18

Mak, King-lun Kingston. "A transgenic mouse model to study the role of epidermal growth factor (EGF) in hair and skin development." Click to view the E-thesis via HKUTO, 2002. http://sunzi.lib.hku.hk/hkuto/record/B42576787.

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19

Terryberry, Melissa S. Lorson Christian Garcia Michael L. "A study of readthrough therapy for spinal muscular atrophy in a transgenic mouse model." Diss., Columbia, Mo. : University of Missouri--Columbia, 2009. http://hdl.handle.net/10355/6600.

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Title from PDF of title page (University of Missouri--Columbia, viewed on Feb 19, 2010). The entire thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file; a non-technical public abstract appears in the public.pdf file. Thesis advisor: Dr. Christian Lorson and Dr. Michael Garcia. Includes bibliographical references.

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20

Li, Wan-Fen. "Development of a mouse model to study the role of paraoxonase (PON1) in organophosphate detoxication /." Thesis, Connect to this title online; UW restricted, 1999. http://hdl.handle.net/1773/8447.

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21

Taguchi, Tomoyuki. "α-Synuclein BAC transgenic mice exhibit RBD-like behaviour and hyposmia: a prodromal Parkinson’s disease model". Doctoral thesis, Kyoto University, 2021. http://hdl.handle.net/2433/263550.

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22

Kellogg, Sara Leilani. "Behavioral and Histological Effects of Traumatic Brain Injury on Alzheimer's Disease Transgenic Mice." Scholar Commons, 2012. http://scholarcommons.usf.edu/etd/4097.

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The main objective of this study was to elucidate the possible mechanistic link between traumatic brain injury (TBI) and Alzheimer's disease (AD) using an animal model. We examined behavioral and histological effects of TBI in pre-symptomatic AD-transgenic mice (C57B6/SJL/SwissWebster/B6D2F1). In previous studies, these mice displayed AD-like behavioral deficits by 15-17 months of age and AD-like neuropathology as early as six months of age. To clarify the effects of TBI on these mice, the present study began when they were about three months of age and the study ended when they were about fiv

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23

Burns, Andrew J. "Fear conditioning as a measuring tool for cognitive deficits related to amyloid burden coupled with iron, zinc, and copper in the transgenic Tg2576 mouse model for alzheimer's disease." Fairfax, VA : George Mason University, 2008. http://hdl.handle.net/1920/3004.

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Thesis (M.A.)--George Mason University, 2008.<br>Vita: p. 68. Thesis director: Jane M. Flinn. Submitted in partial fulfillment of the requirements for the degree of Master of Arts in Psychology. Title from PDF t.p. (viewed June 30, 2008). Includes bibliographical references (p. 62-67). Also issued in print.

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24

麥經綸 and King-lun Kingston Mak. "A transgenic mouse model to study the role of epidermal growthfactor (EGF) in hair and skin development." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2002. http://hub.hku.hk/bib/B42576787.

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25

Chokalingam, Kumar. "Transgenic Mouse Model: Examination of Healing, Development and Mechanical Response of Cells." University of Cincinnati / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1259076989.

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26

Andersson, Patrik. "Functional role of a constitutively active dioxin/Ah receptor in a transgenic mouse model /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-469-0/.

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27

Yamakado, Hodaka. "α-synuclein BAC transgenic mice as a model for Parkinson's disease manifested decreased anxiety-like behavior and hyperlocomotion". Kyoto University, 2012. http://hdl.handle.net/2433/159387.

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28

Ng, Hang-pong. "Development of murine model of autoimmune thyroiditis induced with homologous thyroid peroxidase and evaluation of immune tolerance in a transgenic mice that overexpress mTPO in the thymus." Click to view the E-thesis via HKUTO, 2005. http://sunzi.lib.hku.hk/hkuto/record/B35772554.

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29

Hessein, Hassona Mohamed Darwish. "The Role of Profilin1 Gene in the Development of Cardiovascular Diseases: Insights From Profilin1 Transgenic Mouse Model." The Ohio State University, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=osu1292209565.

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30

Ahmad, Fahmida. "Modelling heterogeneity of triple-negative breast cancer in mice to uncover and target signaling essentiality." Thesis, Aix-Marseille, 2020. http://www.theses.fr/2020AIXM0225.

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Le cancer du sein triple négatif (TNBC) est un sous-type de cancer du sein très agressif et hétérogénène qui ne bénéficie actuellement d'aucun traitement efficace. Le but de mon projet de Thèse était d'explorer les mécanismes qui conduisent au TNBC pour concevoir de nouvelles approches thérapeutiques.Dans notre équipe, nous avons généré un modèle de souris unique (souris MMTV-R26Met) dans lesquelles le récepteur tyrosine kinase MET est faiblement augmenté. Elles développent spontanément et exclusivement des TNBC. Ce modèle récapitule la formation de métastases pulmonaires, la résistance aux ag

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31

Chu, Kit-hang, and 朱傑亨. "Study of abnormal inner ear development in Waardenburg-Shah syndrome using a Sox10-GEP mutant mouse model." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hdl.handle.net/10722/206530.

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Sox10 is a high mobility group (HMG) domain transcription factor which is an important regulator for neural crest development. SOX10 mutations have been identified in Waardenburg-Shah syndrome type 4 (WS4) patients who suffer from sensorineural deafness. However, the mechanisms underlying the hearing defect of SOX10-mediated WS4 are unclear. The aim of this study is to elucidate the function of Sox10 during mouse inner ear development using a mutant mouse model, in order to reveal the underlying basis for SOX10 mutation associated sensorineural deafness in WS4 patients. The mammalian inner

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32

Morcinek, Kerstin [Verfasser]. "Brainstem of the P301L tau transgenic pR5 model : pattern of tau hyperphosphorylation and neurotransmitter markers in senescent mice / Kerstin Morcinek." Köln : Deutsche Zentralbibliothek für Medizin, 2013. http://d-nb.info/1037403789/34.

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33

Schleif, William. "Effects of Long-Term Administration of Caffeine in a Mouse Model for Alzheimer’s Disease." Scholar Commons, 2005. https://scholarcommons.usf.edu/etd/854.

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A recent epidemiological study suggested that higher caffeine intake reduces the risk of Alzheimer's disease (AD). Caffeine, a widely consumed stimulatory drug, is a non-selective adenosine receptor antagonist that has been shown to increase plasma adenosine levels in rodents. To determine any long-term protective effects of caffeine in a controlled longitudinal study, caffeine was added to the drinking water of APPsw transgenic (Tg) mice between 4 and 9 1/2 months of age, with behavioral testing done during the last 6 weeks of treatment. The average daily intake of caffeine per mouse (1.5 mg)

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34

Costa, David Antonio. "Promoting and preventing alzheimer's disease in a transgenic mouse model : apolipoprotein e and environmental enrichment /." [Tampa, Fla.] : University of South Florida, 2005. http://purl.fcla.edu/fcla/etd/SFE0001179.

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35

Noristani, Harun. "Altered serotonergic neurotransmission as a main player in the pathophysiology of Alzheimer's disease : structural and ultrastructural studies in a triple transgenic mouse model of the disease." Thesis, University of Manchester, 2012. https://www.research.manchester.ac.uk/portal/en/theses/altered-serotonergic-neurotransmission-as-a-main-player-in-the-pathophysiology-of-alzheimers-disease-structural-and-ultrastructural-studies-in-a-triple-transgenic-mouse-model-of-the-disease(65e84f4d-05ad-43d5-ace2-b8eab4a7a985).html.

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Alzheimer´s disease (AD) is an age-related, irreversible and progressive neurodegenerative pathology that deteriorates cognitive function including learning and memory. AD is characterised neuropathologically by the presence of neuritic plaques (Aβ), neurofibrillary tangles (NFTs), synaptic loss and neuronal death. AD affects specific brain regions involved in mnestic function such as the neocortex and the hippocampus. The dorsal (DR) and the median raphe (MR) nuclei give rise to serotonergic (5-HT) projections that innervate multiple brain regions including the cortex and the hippocampus, pla

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36

Ru, Zhitao. "Creating and use of an new experimental preclinical HLA transgenic mice model to mapping HLA-restricted T cells epitopes for polyepitopes vaccine design." Phd thesis, Université Paris Sud - Paris XI, 2012. http://tel.archives-ouvertes.fr/tel-00714984.

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A new homozygous humanized HLA transgenic mouse strain, HLA-A2.1+/+HLA-DP4+/+hCD4+/+mCD4-/-IAβ-/-β2m-/- (HLA-A2/DP4), was obtained by crossing the HLA transgenic HLA-A2.1+/+β2m-/-(A2) mice and HLA transgenic HLA-DP4+/+hCD4+/+mCD4-/-IAβ-/-(DP4) mice. In HLA-A2/DP4 mice, HLA-A2 restricted or HLA-DP4 restricted T cell responses against HBs antigen of hepatitis B virus after immunization with the HBsAg vaccine are similar to those induced in A2 mice, in DP4 mice, in HBV-infected or HBsAg-vaccinated humans. These results show that cellular responses induced in HLA-A2/DP4 mice faithfully mimic human

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37

Ng, Hang-pong, and 伍恆邦. "Development of murine model of autoimmune thyroiditis induced with homologous thyroid peroxidase and evaluation of immune tolerance in atransgenic mice that overexpress mTPO in the thymus." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B35772554.

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38

Li, Chaoyun [Verfasser], and Hermann [Akademischer Betreuer] Schlüsener. "Comparison of protective effects of four polyphenols on neuropathology and behavior of APP/PS1-21 transgenic mice, a model of Alzheimer’s disease / Chaoyun Li ; Betreuer: Hermann Schlüsener." Tübingen : Universitätsbibliothek Tübingen, 2014. http://d-nb.info/1196878277/34.

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39

Dreykluft, Angela [Verfasser], and Heinz [Akademischer Betreuer] Wiendl. "The PD-1/B7-H1 Pathway in a Transgenic Mouse Model for Spontaneous Autoimmune Neuroinflammation : Immunological Studies on Devic B7-H1-/- Mice / Angela Dreykluft. Betreuer: Heinz Wiendl." Würzburg : Universitätsbibliothek der Universität Würzburg, 2013. http://d-nb.info/1042899444/34.

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40

D'Amico, Davide 1983. "Fear memories in TgNTRK3 mice, a model of panic disorder : definition of mechanism and search for new therapeutic targets." Doctoral thesis, Universitat Pompeu Fabra, 2013. http://hdl.handle.net/10803/292366.

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Estudios genéticos en pacientes sugieren que el gen del receptor tirosina quinasa de la neurotrofina de tipo 3 (NTRK3) podría contribuir en la patología del trastorno de pánico (PAND), un trastorno de ansiedad caracterizado por alteración y exageración del miedo. En esta tesis, proponemos que PAND podría estar relacionado con procesos anormales de aprendizaje asociativo, subyacentes a una alteración en la regulación del funcionamiento del circuito del miedo hipocampo - amígdala – corteza prefrontal media. Hemos estudiado esta hipótesis utilizando el único modelo genético de ratón validado de

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41

Griffitts, Jeffrey Daniel. "In vivo detection of alterations in fatty acyl species unsaturation in a mouse hepatocarcinogenesis model." Oklahoma City : [s.n.], 2008.

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42

Das, Krishna [Verfasser], and Stefan [Akademischer Betreuer] Eichmüller. "Generation of a transplantable murine tumor model expressing the human breast cancer associated tumor antigen NY-BR-1 in HLA-DRB1*0401-transgenic mice / Krishna Das ; Betreuer: Stefan Eichmüller." Heidelberg : Universitätsbibliothek Heidelberg, 2017. http://d-nb.info/1178009513/34.

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43

Das, Krishna [Verfasser], and Stefan B. [Akademischer Betreuer] Eichmüller. "Generation of a transplantable murine tumor model expressing the human breast cancer associated tumor antigen NY-BR-1 in HLA-DRB1*0401-transgenic mice / Krishna Das ; Betreuer: Stefan Eichmüller." Heidelberg : Universitätsbibliothek Heidelberg, 2017. http://d-nb.info/1178009513/34.

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44

Peshdary, Vian. "Genetic Ablation of the Platelet Activating Factor Receptor Does Not Impair Learning and Memory in Wild-Type Mice or Alter Amyloid Plaque Number in a Transgenic Model of Alzheimer’s Disease." Thesis, Université d'Ottawa / University of Ottawa, 2012. http://hdl.handle.net/10393/20627.

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We have recently established that aberrant alkylacylglycerophosphocholine metabolism results in the increased tissue concentration of platelet activating factors (PAFs) in the temporal cortex of Alzheimer Disease (AD) patients and in TgCRND8 mice over-expressing mutant human amyloid precursor protein. PAF lipids activate a G-protein coupled receptor (PAFR) reported to be expressed by microglia and subsets of neurons in rat. It is not known whether this same expression pattern is recapitulated in mice however, as the expression has only been inferred by use of pharmacological PAFR antagonists,

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45

Petkova, Mina. "Generation and characterization of a dmdegfp reporter mouse as a tool to investigate dystrophin expression." Thesis, Paris 6, 2016. http://www.theses.fr/2016PA066090/document.

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La dystrophine est une protéine cytoplasmique qui lie physiquement le cytosquelette à la matrice extracellulaire par le biais du complexe dystrophine-protéines associées (DAPC), assurant ainsi la stabilité du sarcolemme. Des mutations dans le gène DMD codant pour la dystrophine, conduisant à l’absence de la protéine, sont à l’origine de la dystrophie musculaire de Duchenne qui est une maladie liée au chromosome X. Pour mes travaux de thèse, j’ai généré et caractérisé un nouveau modèle de souris transgéniques rapportrices, dénommé DmdEGFP, qui exprime une protéine dystrophine endogène fusionnée

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46

Hottier, Mouton Laura. "Développement de l’imagerie IRM de diffusion pour la caractérisation des atteintes neuropathologiques induites par les radiations ionisantes chez un modèle murin." Thesis, université Paris-Saclay, 2020. http://www.theses.fr/2020UPASS062.

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Le diagnostic ou le traitement d’une pathologie par l’emploi de rayonnements ionisants peut causer l’apparition de conséquences néfastes et irréversibles pour le cerveau notamment au cours de son développement. D’autant plus, si on considère certains facteurs génétiques modulant la radiosensibilité des individus exposés. Il devient alors nécessaire de développer des marqueurs d’imagerie sensibles aux atteintes cérébrales de l’irradiation à la fois aux fortes et aux faibles doses. Cette thèse a permis de développer une approche non-invasive, par IRM anatomique et de diffusion, p

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47

Köhler, Stefan. "Das humane CD4 Molekül als Zielstruktur zur therapeutischen Beeinflussung zellulärer Immunantworten in einem transgenen Tiermodell." Doctoral thesis, Universitätsbibliothek Leipzig, 2015. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-171261.

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In einem komplexen tierexperimentellen Ansatz wurde das Potenzial der anti huCD4-Antikörper MAX16H5 und MAX12F6 zur Modulierung zellvermittelter Immun-reaktionen in vivo untersucht. Dafür kam ein mehrfach transgenes Mausmodell zur Anwendung, in dem das humane Zielmolekül und dessen physiologischer Ligand als Transgene exprimiert waren. Als T-Zell vermittelte Immunreaktion wurde eine Kon-taktreaktion (delayed type hypersensitivity, DTH) gegen DNFB etabliert und validiert. An der DTH wurde untersucht, ob und wie die verschiedenen Antikörper die Sen-sibilisierungs- und die Auslösungsphase beeinfl

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48

Tee, Boon-Lead, and 鄭文立. "Weight, behavior, metabolism and amyloid pathology in triple transgenic Alzheimer’s mice." Thesis, 2017. http://ndltd.ncl.edu.tw/handle/q9rtyd.

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碩士<br>國立臺灣大學<br>臨床醫學研究所<br>105<br>Background: Alzheimer’s disease (AD) is a neurodegenerative disease well recognized for its cognitive decline features. Yet increasing evidence has indicated that AD also developed noncognitive symptoms such as body weight alterations, sleep and psychiatric symptoms. Furthermore, researches suggest that these noncognitive symptoms occurs early in the clinical course of AD and may even precede the cognitive deterioration of AD. Candidate brain regions responsible for these noncognitive symptoms includes hypothalamus and amygdala. Typical AD pathology mainly com

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49

Su, Yi-Chen, and 蘇易辰. "The Protective Effects of Edible Folic Acid and Medicinal Folinic Acid on Late-Stage Triple-Transgenic Alzheimer's Old Mice Hearts." Thesis, 2015. http://ndltd.ncl.edu.tw/handle/59825918692849063223.

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碩士<br>亞洲大學<br>保健營養生技學系<br>103<br>PART I Alzheimer’s disease and cardiovascular disease share some risk factors. Many experimental and clinical studies showed the involvement of cardiovascular disease-related pathways in Alzheimer’s disease. Persons with Alzheimer’s disease also displayed a higher risk of incident ischemic heart disease. In this study, we apply triple-transgenic late-stage Alzheimer's (AD) mice to examine the heart function changes, in order to explore the relationship between Alzheimer's disease and Cardiovascular diseases. The triple-transgenic late-stage Alzheimer's

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50

Cheng, Ling-Yi, and 鄭令宜. "Establishment of a hepatitis B virus infected animal model in HLA-A2 transgenic mice." Thesis, 2012. http://ndltd.ncl.edu.tw/handle/89963519519945468134.

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碩士<br>國立陽明大學<br>臨床醫學研究所<br>100<br>There are nearly 350 million people worldwide chronically infected with hepatitis B virus (HBV). Chronic HBV infection is a major cause of cirrhosis and hepatocellular carcinoma (HCC). HBV is a noncytopathic virus and the pathogeneses of its chronic complications are immune-mediated. To test the efficacy of the newly developed antiviral therapies of HBV, it is necessary to establish an animal model to evaluate the immune responses to the treatment. Mice are easy to handle and may be the most suitable animal model for immunological studies of HBV infection. How

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