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Dissertations / Theses on the topic 'Autoimmune diseases – Animal models'

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Published: 4 June 2021

Last updated: 31 January 2023

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1

Li, Jinan. "Multifunctional roles of plasmin in inflammation : Studies of animal models on rheumatoid arthritis, multiple sclerosis, wound healing and infection." Doctoral thesis, Umeå : Dept. of medical biochemistry and biophysics, Univ, 2005. http://www.diva-portal.org/umu/theses/abstract.xsql?dbid=422.

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2

Ma, Liang, and 馬亮. "Induction and regulation of autoimmune responses by dendritic cells upon interaction with dying cells in murine models." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B3554756X.

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3

Kezic, Jelena Marie. "A study of the monocyte-derived cell populations of the uveal tract and retina in homeostatic conditions and during the early stages of ocular autoimmune disease." University of Western Australia. School of Anatomy and Human Biology, 2008. http://theses.library.uwa.edu.au/adt-WU2009.0084.

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The eye contains closely related but widely different tissues, offering a unique opportunity to investigate the phenotype and function of monocyte-derived cell populations within functionally unique microenvironments in a single complex organ. The uveal tract and retina contain rich networks of immune cells that reside and traffic through the eye, these cells having been implicated in various ocular inflammatory processes and immune-mediated diseases. One such inflammatory condition is human posterior uveitis, an autoimmune disease mainly affecting the retina. As current treatments for posterior uveitis only serve to slow down disease progression, studies using animal models, namely, experimental autoimmune uveoretinitis (EAU), have focused on determining the key cellular and molecular mediators involved in disease initiation in order to expand the potential for novel therapeutic applications. The overall purpose of experiments in this thesis was to explore monocyte-derived cell populations of the uveal tract and retina, this being achieved by utilising a novel transgenic mouse model. Cx3cr1gfp/gfp transgenic mice on both BALB/c and C57Bl/6 backgrounds contain an enhanced green fluorescent protein (eGFP) encoding cassette knocked into the Cx3cr1 gene, disrupting its expression but facilitating GFP expression under the control of the Cx3cr1 promoter. Heterozygous (Cx3cr1+/gfp) mice were generated by crossing Cx3cr1gfp/gfp mice to wild-type (WT) mice. This transgenic model allowed for the exquisite visualisation of Cx3cr1-bearing monocyte-derived dendritic cells (DC) and macrophages in ocular tissues, whilst also enabling the investigation of a potential role for Cx3cr1 in recruiting monocyte-derived cells to the eye in steady-state and inflammatory conditions.

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4

Marshall, Aiden Christopher James 1976. "The role of Fas and TNFα in experimental autoimmune gastritis." Monash University, Dept. of Pathology and Immunology, 2003. http://arrow.monash.edu.au/hdl/1959.1/9413.

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5

Eppert, Bryan L. "Autoimmune Mechanisms in Cigarette Smoke-Induced Inflammation and Pathology." University of Cincinnati / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1382950967.

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6

Stromnes, Ingunn Margarete. "T cell determinants of central nervous system autoimmune disease /." Thesis, Connect to this title online; UW restricted, 2007. http://hdl.handle.net/1773/8333.

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7

Nordquist, Niklas. "Genetic Studies of Rheumatoid Arthritis using Animal Models." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2001. http://publications.uu.se/theses/91-554-5117-9/.

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8

Raza, Abbas. "Genetic And Functional Approaches To Understanding Autoimmune And Inflammatory Pathologies." ScholarWorks @ UVM, 2020. https://scholarworks.uvm.edu/graddis/1175.

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Our understanding of genetic predisposition to inflammatory and autoimmune diseases has been enhanced by large scale quantitative trait loci (QTL) linkage mapping and genome-wide association studies (GWAS). However, the resolution and interpretation of QTL linkage mapping or GWAS findings are limited. In this work, we complement genetic predictions for several human diseases including multiple sclerosis (MS) and systemic capillary leakage syndrome (SCLS) with genetic and functional data in model organisms to associate genes with phenotypes and diseases. Focusing on MS, an autoimmune inflammatory disease of the central nervous system (CNS), we experimentally tested the effect of three of the GWAS candidate genes (SLAMF1, SLAMF2 and SLAMF7) in the experimental autoimmune encephalomyelitis (EAE) mouse model and found a male-specific locus distal to these loci regulating CNS autoimmune disease. Functional data in mouse suggests this male-specific locus modulates the frequency of immune cells including CD11b+, TCRαβ+CD4+Foxp3+, and TCRαβ+CD8+IL-17+ cells during EAE disease. Orchiectomy experiments demonstrate that this male specific phenotype is dependent on testis but not testosterone (T) or 5α-dihydrotestosterone (DHT). Using a bioinformatic approach, we identified SLAMF8 and SLAMF9 along with other differentially expressed genes in linkage with MS-GWAS predictions whose expression is testis-dependent, but not directly regulated by T or DHT, as potential positional candidates regulating CNS autoimmune disease. Further refinement of this locus is required to identify the causal gene(s) that may be targeted for prevention and/or treatment of MS in men. Using SCLS, an extremely rare disorder of unknown etiology characterized by recurrent episodes of vascular leakage, we identified and modeled this disease in an inbred mouse strain, SJL, using susceptibility to histamine- and infection-triggered vascular leak as the major phenotypic readout. This trait “Histamine hypersensitivity” (Histh/Histh) was mapped to a region on Chr 6. Remarkably, Histh is syntenic to the genomic locus most strongly associated with SCLS in humans (3p25.3). Subsequent studies found that the Histh locus is not unique to SJL but additional mouse strains also exhibit Histh phenotype. Considering GWAS studies in SCLS are limited by the small number of patients, we utilized interval-specific SNP-based association testing among Histh phenotyped mouse strains to predict Histh candidates. Furthermore, to dissect the complexity of Histh QTL, we developed network-based functional prediction methods to rank genes in this locus by predicting functional association with multiple Histh-related processes. The top-ranked genes include Cxcl12, Ret, Cacna1c, and Cntn3, all of which have strong functional associations and are proximal to SNPs segregating with Histh. Lastly, we utilized the power of integrating genetic and functional approaches to understand susceptibility to Bordetella pertussis and pertussis toxin (PTX) induced histamine sensitization (Bphs/Bphs), a sub-phenotype with an established role in autoimmunity. Congenic mapping in mice had earlier linked Bphs to histamine H1 receptor gene (Hrh1/H1R) and demonstrated that H1R differs at three amino acid residues in Bphs-susceptible and -resistant mice. Our subsequent studies identified eight inbred mouse strains that were susceptible to Bphs despite carrying a resistant H1R allele. Genetic analyses mapped the locus complementing Bphs to mouse Chr 6, in linkage disequilibrium with Hrh1; we have designated this Bphs-enhancer (Bphse). Similar to the approaches used for Histh, we utilized interval-specific SNP based association testing and network-based functional enrichment to predict nine candidate loci for Bphse including Atp2b2, Atg7, Pparg, Syn2, Ift122, Raf1, Mkrn2, Timp4 and Gt(ROSA)26Sor. Overall, these studies demonstrate the power of integrating genetic and functional methods in humans and animal models to predict highly plausible loci underlying QTL/GWAS data.

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9

Todd, Derrick James. "Role of the Intestinal Immune System in the Pathogenesis of Autoimmune Diabetes in the BB Rat Model of Type 1 Diabetes Mellitus." eScholarship@UMMS, 2001. https://escholarship.umassmed.edu/gsbs_diss/138.

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The intestine is the largest lymphoid organ in the body, challenged constantly by an enonnous quantity and diversity of antigens. Distinct from peripheral lymphocytes, intestinal lymphocytes have evolved unique mechanisms of tolerance and appear to govern mucosal processes such as "chronic physiologic inflammation" and oral tolerance. Failure of mucosal tolerance has been implicated in the pathogenesis of several diseases, including inflammatory bowel disease, celiac disease, and even autoimmune diabetes. One population of intestinal lymphocytes, intraepithelial lymphocytes (IELs), exists within the intestinal epithelium itself and remains poorly characterized. IELs respond to unique activation signals and appear to be in part responsible for the maintenance of epithelial integrity and mucosal tolerance. Type 1 diabetes is one of the most common chronic childhood illnesses and causes significant morbidity and mortality. Type 1 diabetes mellitus is an autoimmune disease that results from immune-mediated destruction of insulin-producing pancreatic beta cells and is characterized by an absolute insulin deficiency. Several animal models are used to study the immunopathogenesis of type 1 diabetes, including the BB rat and NOD mouse. BBDP rats spontaneously develop autoimmune diabetes mellitus and are severely deficient in peripheral T cells. BBDR rats do not spontaneously develop autoimmune diabetes, have nonnal numbers of peripheral T cells, and can be induced to become diabetic by injections of a cytotoxic anti-ART2a mAb and low doses of poly I:C. The cause of autoimmune diabetes in BB rats and humans is still unknown, but both genetic and environmental factors appear to participate. I hypothesize that one important class of environmental factors--diet and enteromicrobial agents--participates in this pathogenic process through the mediation of the gut immune system. In this dissertation, I report a new method for the isolation of rat IELs that is based on the selective removal of intestinal epithelial cells under conditions that leave the basement membrane undisturbed. The yield of rat IELs using this method is 5-10 fold greater than that reported for other methods. Morphological and phenotypic analyses demonstrate that the purified cell population is comprised of IELs and is not contaminated with lamina propria or Peyer's patch lymphocytes. Phenotypic analysis reveals 5 major subsets of IELs, including populations of γδ T and natural killer (NK) cells present at levels not previously detected. I also report that rat intraepithelial NK (IENK) and peripheral NK cells are similar in morphology, in their ability to lyse NK-sensitive targets, and in their ability to suppress a one-way mixed lymphocyte culture. In contrast, IENK cells differ from splenic NK cells phenotypically, and a substantial fraction of IENK cells appear to spontaneously secrete IL-4 and/or IFN-γ. I conclude that rat IELs harbor a large population of NKR-P1A+ CD3-cells that function as NK cells but display an activated phenotype and unusual cytokine profile that clearly distinguish them from splenic NK cells. Their phenotypic and functional characteristics suggest that these distinctive intraepithelial NK cells may participate in the regulation of mucosal immunity. I next demonstrate that, prior to diabetes, both BBDP and ART2a-depleted BBDR rats have a reduced total number of IELs and exhibit a selective deficiency of IENK cell number and function as compared to control BBDR rats. The deficiency of BBDP rat IELs can be corrected by engraftment of bone marrow from histocompatible WF donors. These results suggest 1) that the peripheral lymphopenia in BBDP rats extends to the IEL compartment, particularly to IENK cells, 2) that in BBDR rats the diabetes-inducing treatment depletes IELs, particularly IENK cells, and 3) that the defect in BBDP rat IELs is intrinsic to hematopoietic cells, not intestinal stromal cells. I also establish that, unlike BBDR and WF rats, BBDP rats are also deficient in γδTCR+IELs, a population of T cells that may play a role in normal mucosal tolerance. In addition, I report preliminary data supporting the hypothesis that systemic autoreactivity may be initiated in the intestine; peripheral autoreactive lymphocyte populations appear to emanate first from mesenteric lymph nodes that drain the intestine, and such cells may initiate a type 2 autoimmune phenomenon driven by IL-4. Collectively, my findings support the hypothesis that a failure of mucosal tolerance in BBDP rats, perhaps secondary to deficiencies in one or more IEL subpopulations, participates in the pathogenesis of autoimmune diabetes in these animals by activating peripheral autoreactive T cells. The nature of the autoimmune response in BB rats (driven by IL-4) appears to be distinct from that of NOD mice. Despite the differences between these two well-accepted animal models of autoimmune diabetes, until more is known about the pathogenesis of type 1 DM in humans, lessons learned from both the BB rat and NOD mouse continue to be of tremendous benefit to our understanding of human disease.

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10

Gómez, Morago Alba. "Estudio de los mecanismos terapéuticos en la inducción de tolerancia inmunológica en un modelo animal de esclerosis múltiple." Doctoral thesis, Universitat de Barcelona, 2016. http://hdl.handle.net/10803/386466.

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La terapia génica puede ser una herramienta para inducir tolerancia inmunológica de forma experimental. Nuestro trabajo anterior mostró que la transferencia de células de médula ósea que habían sido transducidas con un autoantígeno (MOG40-55) en ratones con encefalomielitis autoinmune experimental (EAE) mejoró el pronóstico de los animales. En este trabajo, hemos tratado de identificar la subpoblación de células de médula ósea transducidas que fue la principal responsable del efecto terapéutico observado. Se encontró que en los cultivos de transducción de células de médula ósea se generaban células mieloides supresoras de los dos subtipos descritos, tanto granulocíticos (CD11b+ Gr-1high) como monocíticos (CD11b+ Gr-1low), y que las células transducidas con mayor eficacia consistieron en gran medida de estos tipos de células. Tanto las células de médula ósea como las dos subpoblaciones de células mieloides supresoras presentaron una capacidad de inhibir la proliferación de células T inducidas por un antígeno in vitro. Curiosamente, a pesar de la constatación de que células CD11b+ Gr-1low transducidas fueron inmunosupresora in vitro y tenían actividades de la arginasa y de la óxido nítrico sintasa, sólo la subpoblación de células CD11b+ Gr-1high transducidas con el antígeno tenía un efecto terapéutico en ratones con EAE establecida. Por último, se observó un mayor porcentaje de células T reguladoras en los bazos de ratones tratados con la población de médula ósea total transducida con MOG y las células CD11b+ Gr-1high lo que sugiere un papel para las células T reguladoras en la mediación del efecto terapéutico.
Gene therapy can be used to experimentally induce immune tolerance. Our previous work showed that transferring bone marrow cells that had been transduced with an autoantigen (MOG40-55) into mice with experimental autoinmune encephalomyelitis improved the animals’ prognosis. In this work, we sought to identify the cell subpopulation in the transduced bone marrow that was primarily responsible for the observed therapeutic effect. We found that both granulocyte-like (CD11b+ Gr-1hi) and monocyte-like (CD11b+ Gr-1lo) myeloid-derived suppressor cells were generated during the standard 4-day retroviral transduction of bone marrow cultures and that the effectively transduced cells largely consisted of these cell types. Both of the myeloid cell subtypes inhibited antigen-induced T cell proliferation in vitro, and they were significantly more suppressive than their sham-transduced controls. Interestingly, despite the finding that transduced CD11b+ Gr-1lo cells were immunosuppressive in vitro and exhibited arginase and nitric oxide synthase activities, only the antigen-transduced CD11b+ Gr-1hi cell subpopulation had a therapeutic effect in mice with the experimentally induced disease. Finally, we observed higher percentages of T regulatory cells in the spleens of mice treated with MOG-expressing total bone marrow population and CD11b+ Gr-1hi cells, which suggests a role for these T regulatory cells in mediating the therapeutic effect.

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11

Thomas, Kurt Florian Patrick. "Animal models of retroviral neurological diseases." Thesis, McGill University, 1995. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=39882.

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The neuropathogenicity of two retroviruses was investigated. The human immunodeficiency virus, in addition to its profound effect on the immune system, also causes degenerative changes in the brain, the spinal cord and peripheral nerves. In order to elucidate how it affects the nervous system, transgenic mice were generated that express the entire HIV genome in neurons in the anterior thalamus and in the anterior horn of the spinal cord, and examined clinically, neuropsychologically, electrophysiologically and histologically. Animals developed a neurological syndrome characterized by hypoactivity and weakness, and by axonal degeneration in peripheral nerves. These results provide evidence for a role of HIV in affecting both the central and peripheral nervous systems.
In a second project, pathological effects associated with a disease determining region contained in the gp70 envelope protein of the Cas-Br-E murine leukemia virus, were investigated. In infected mice, this virus causes hind limb paralysis and a spongiform myeloencephalopathy with gliosis and neuronal loss. Stably transfected fibroblasts that express gp70 were injected into the brains of mice, and the animals were examined for histopathological changes attributable to the effects of gp70. While gp70 protein was detected at the implantation site, this was not accompanied by any specific histological changes. These data suggest that the intracerebral expression of the neuropathogenic gp70 protein alone is not sufficient to cause disease, and lend indirect support to a model according to which gp70 causes disease by altering the cytokine profile of infected mononuclear cells in the central nervous system.

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12

Newton, Sonja Grace. "The response to heat shock protein 60 in autoimmune models." Thesis, Imperial College London, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.324991.

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13

Vingsbo, Lundberg Carina. "Chronic autoimmune arthritis in rats pathogenesis and genetic factors /." Lund : Lund University, 1997. http://catalog.hathitrust.org/api/volumes/oclc/68945081.html.

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14

Ma, Liang. "Induction and regulation of autoimmune responses by dendritic cells upon interaction with dying cells in murine models." Click to view the E-thesis via HKUTO, 2005. http://sunzi.lib.hku.hk/hkuto/record/B3554756X.

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15

Steffen, Johannes [Verfasser]. "Analysis of animal models of neurodegenerative diseases with protein deposits / Johannes Steffen." Magdeburg : Universitätsbibliothek, 2016. http://d-nb.info/1084697238/34.

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16

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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17

Liu, Po-Ching. "Molecular genetic investigation of animal models for human neuronal ceroid lipofuscinoses /." free to MU campus, to others for purchase, 1997. http://wwwlib.umi.com/cr/mo/fullcit?p9841169.

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18

Lui, Sing-leung, and 雷聲亮. "Therapeutic potential of rapamycin in renal parenchymal diseases: insights from murine models of lupusnephritis, adriamycin nephropathy and renal ischemia reperfusioninjury." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2008. http://hub.hku.hk/bib/B41291013.

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19

Hansson, Helene. "Methodological aspects on anti-nuclear antibody determination in canine autoimmunity and in vitro studies of antigen-specific cellular responses /." Uppsala : Swedish Univ. of Agricultural Sciences (Sveriges lantbruksuniv.), 1999. http://epsilon.slu.se/avh/1999/91-576-5439-5.pdf.

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20

Yang, Cuihong, and 楊翠紅. "Regulation of autoimmune responses by dendritic cells and regulatory Tcells in murine models of systemic lupus erythematosus." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B39707362.

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21

Wilder, 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.

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22

Kanju, Patrick M. Suppiramaniam Vishnu. "Synaptic glutamate receptor dysfunction in tissue and animal models of Alzheimer's disease." Auburn, Ala., 2005. http://repo.lib.auburn.edu/2005%20Summer/doctoral/KANJU_PATRICK_11.pdf.

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23

Lam, Kai-yee, and 林佳儀. "A study on the role of probiotic lactobacillus rhamnosus GG on gastricmucosal damages in rats." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2006. http://hub.hku.hk/bib/B37340050.

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24

Takemura, Ai. "Effects of exposure to mild hyperbaric oxygen on metabolism-related diseases in animal models." Kyoto University, 2019. http://hdl.handle.net/2433/242722.

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Kyoto University (京都大学)
0048
新制・課程博士
博士(人間・環境学)
甲第21845号
人博第874号
新制||人||210(附属図書館)
2018||人博||874(吉田南総合図書館)
京都大学大学院人間・環境学研究科共生人間学専攻
(主査)教授石原昭彦, 教授久代恵介, 教授神﨑素樹
学位規則第4条第1項該当

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25

Jacobson, Magdalena. "Enteric diseases in pigs from weaning to slaughter /." Uppsala : Dept. of Large Animal Clinical Sciences, Swedish Univ. of Agricultural Sciences, 2003. http://epsilon.slu.se/v158.pdf.

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26

Schubert, David. "Arthritisinduktion durch Immunität gegen ein systemisch exprimiertes Autoantigen." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2005. http://dx.doi.org/10.18452/15271.

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Ungefähr 1% der Bevölkerung der westlichen Welt leidet an rheumatoider Arthritis (RA). In einem T-Zellrezeptor transgenen Mausmodell, dem K/BxN Modell, wird die ubiquitär exprimierte Glukose-6-phosphat Isomerase (G6PI) von autoreaktiven T- und B-Zellen erkannt. Diese Mäuse entwickeln spontan eine antikörpervermittelte Arthritis, die viele Gemeinsamkeiten mit der humanen RA aufweist. In dieser Arbeit wurde untersucht, ob die Immunisierung mit G6PI eine Arthritis auch in nicht-transgenen Mäuse induzieren kann. Die Immunisierung mit heterologer humaner G6PI führte zur Entwicklung einer peripheren symmetrischen Polyarthritis in über 95% der DBA/1 Mäuse. Damit konnte zum ersten Mal gezeigt werden, dass eine Immunreaktion gegen ein systemisches exprimiertes Antigen zur einer organspezifischen Erkrankung in normalen nicht-transgenen Mäusen führt. Die Tiere entwickeln nach 9 Tagen eine Arthritis, die bis Tag 15 ihr Maximum erreicht hat und dann langsam abnimmt. Histologisch ist die Arthritis durch eine frühe Synovitis charakterisiert, gefolgt von massiven Erosionen des Knorpel und Knochens und anschließenden Reparaturprozessen, inklusive Fibrose. Obwohl die Tiere hohe Antikörpertiter entwickeln, kann die Arthritis nicht durch aufgereinigte Antikörper kranker Mäuse transferiert werden. Trotzdem spielen Antikörper eine große Rolle, da FcR-gamma-Kette defiziente Mäuse eine Arthritis mit geringer Inzidenz und mildem Verlauf entwickeln. Die Depletion der CD4 positiven Zellen verhindert die Entwicklung der Arthritis völlig, und eine Depletion während der Erkrankung führt zur schnellen Heilung. Daneben ist für die Entwicklung der Arthritis auch das Komplementsystem und TNF-alpha entscheidend, was durch Depletion von C5 bzw. durch Blockade von TNF-alpha gezeigt wurde. Zusätzlich wurde die Rolle der G6PI bei der Pathogenese der RA im Menschen untersucht. RA-Patienten zeigten keine erhöhte Frequenz von CD4 positiven T-Zellen, die nach Restimulation mit G6PI TNF-alpha oder IFN-gamma produzierten. Außerdem konnten keine erhöhten anti-G6PI Titer in Patienten mit RA oder anderen rheumatischen Erkrankungen detektiert werden.
About 1% of the of the population of the western world suffers from rheumatoid arthritis (RA). In a T-cell receptor transgenic mouse model, the K/BxN model, the ubiquitously expressed glucose-6-phosphate isomerase (G6PI) is recognized by autoreactive T- and B-cells. These mice do develop an antibody dependent arthritis which show a lot of features of human RA. In this study it was examined whether arthritis could be induced in normal non-transgenic mice by immunization with G6PI. Immunization with heterologous human G6PI induces a symmetric polyarthritis in over 95% of DBA/1 mice. Therewith showing for the first time that an immune reaction against an systemic expressed antigen will lead to the development of an organ specific disease in normal non-transgenic mice. The mice develop arthritis 9d after immunization, reach their maximum at d15 and then arthritis slowly resolve. Histologically, the disease is characterized by early synovitis followed by massive cartilage destruction and erosions of the bones and later repair processes including fibrosis. Although antibody titers in the mice are high, transfer of purified anti-G6PI antibodies of sick mice alone do not transfer disease. Anyway, antibodies seem to play a major role since FcR-gamma-chain deficient mice develop disease with a much lower frequency and reduced severity. Depletion of CD4 positive T cells completely prevents disease and depletion during disease leads to an rapid resolution of arthritis. Aside this, complement and TNF-alpha is critical for the development of arthritis, which could shown by depletion of C5 and blockade of TNF-alpha. In addition, the role of G6PI in the pathogenesis of RA in humans was examined. RA patients do not show a higher frequency of CD4 positive T-cells which produce TNF-alpha and IFN-gamma after restimulation with G6PI. Furthermore, no elevated anti-G6PI titers could be detected in RA patients and in patients with other rheumatic diseases.

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27

Stevens, Kim Barbra. "Risk-based decision making tools for highly pathogenic avian influenza virus (H5N1) in domestic poultry in Asia : a comparison of spatial-modelling methods." Thesis, Royal Veterinary College (University of London), 2016. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.701672.

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28

Hulbig, Veronica A. "Developing a Model for Bacterial Kidney Disease in the Zebrafish, Danio rerio." Fogler Library, University of Maine, 2010. http://www.library.umaine.edu/theses/pdf/HulbigVA2010.pdf.

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29

Pringle, Nadine Alex. "Characterization of a glycated gelatin model to explore the therapeutic properties of macrofungi in diabetic wound healing: an in vitro study." Thesis, Nelson Mandela Metropolitan University, 2017. http://hdl.handle.net/10948/11992.

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Diabetic wounds frequently undergo impaired and prolonged wound healing due to a multitude of factors including hypoxia, impaired angiogenesis, hyperglycaemia, formation of ROS and AGEs, and infection - all of which may lead to cellular dysfunction. To date, however, treatment options for individuals suffering from impaired diabetic wound healing are limited, non-specific, and generally unsuccessful. The search for new and effective treatment strategies is severely hampered by the availability of adequately characterized screening models which comprehensively mimic the complexity of the diabetic wound healing process. In order to explore natural products as potential therapeutics to treat diabetic wounds and to encourage more research on this topic, this study sought out to develop and characterize a more convenient and cost effective in vitro screening assay which mimics the effects of protein glycation on the healing process of diabetic wounds. As proof of principal, this model was subsequently used to screen the potential of five wild mushroom species (P. tinctorius, R. capensis, B. badius, P. ostreatus and G. lucidum) as suitable diabetic wound healing therapies. The glycated gelatin model developed during this study was found to suitably mimic the diabetic state as it successfully simulated the major cellular dysfunctions in macrophages (NO production, phagocytosis, macrophage polarization, NF-ĸB translocation and COX-2 expression) and fibroblasts (proliferation and migration) documented during diabetic wound healing. Together these findings provide confidence that the model may serve as a valuable tool to study the poorly understood mechanisms which characterize cellular dysfunction in response to AGE accumulation and also to aid the identification of novel therapeutic agents to treat this pathology. Screening a number of mushroom extracts revealed that the ethanol extracts of R. capensis and P. ostreatus had the greatest potential for attenuating chronic inflammation due to their ability to promote macrophage phagocytosis, increased M2 activation (R. capensis) and decreased M1 activation (P. ostreatus) as well as reduced COX-2 expression while the water extract of G. lucidum proved to be the most promising candidate for stimulating fibroplasia as it was the most successful at promoting both fibroblast proliferation and migration. Different mushroom species were thus shown to promote different stages of the wound healing process providing sufficient evidence to support further studies related to the use of macrofungi as therapeutic agents in the search for more cost-effective and efficient treatment strategies for impaired diabetic wound healing.

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30

Chan, Arthur Ho-Yin. "Image-guided high intensity focused ultrasound treatment for uterine leiomyomata /." Thesis, Connect to this title online; UW restricted, 2003. http://hdl.handle.net/1773/8068.

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31

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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Ha, Hong Clinical School St Vincent's Hospital Faculty of Medicine UNSW. "Role of T cells and cytokines in the induction of tolerance to renal tubular antigen in active Heymann nephritis." Awarded by:University of New South Wales. Clinical School - St Vincent's Hospital, 2007. http://handle.unsw.edu.au/1959.4/40871.

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Idiopathic Membranous nephropathy (MN) is a common cause of nephrotic syndrome in humans, and many patients progress to end-stage kidney disease. The best available animal model of MN is active Heymann nephritis (HN) in which rats are immunized with renal tubular antigen (RTA) in complete Freund's adjuvant (CFA). Rats develop heavy proteinuria, a key measure of glomerular damage, and the disease is histologically identical to human MN. It has been thought that HN is mediated by antibody-based mechanisms. More recent evidence demonstrates a critical role for cytotoxic T cells. This thesis aims to further examine the role of T cell responses in active HN. First, the effect of the anti-CD3 monocIonal antibody (mAb) G4.18 was investigated. Anti-CD3 given 4 weeks after immunization prevented the development of proteinuria, delayed anti-RTA antibody responses, and reduced glomerular infiltration of CD8+ T cells and macrophages, but did not affect glomerular deposition of IgG or complement. Increased mRNA expression of the Th2 cytokines IL-4 and IL-5 was detected in draining lymph nodes. These findings suggest that immune deviation to a Th2 response reduces glomerular injury in HN. Second, the role of CD4+ T cells in immune tolerance was examined. Rats were given RTA in incomplete Freund's adjnvant (lFA) to induce tolerance to RTA, and three weeks later were immunized with RTA in CFA. Anti-CD4 mAb therapy at the time of RTA1IFA treatment had no effect on subsequent proteinuria or anti-RTA autibodies. Third, the role of IL-4 in this model of immune tolerance was examined. Anti-IL-4 mAb therapy blocked the induction of tolerance, and led to the development of proteinuria. Finally, the effect of treatment with IL-4 and IL-5 was examined. Treatment with these cytokines separately or together after immunization blocked the development of proteinuria, without a consistent effect on anti-RTA antibodies. These results demonstrate a central role for T cell regulation in HN, and show that immune deviation to a Th2 response is protective against glomerular injury. The findings may have implications in the future for focused therapeutic intervention in human idiopathic MN.

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Fu, Shing-yan Karen, and 符誠欣. "Cigarette smoke-induced inflammatory changes in rat heart in vivo." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hub.hku.hk/bib/B48333864.

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Cigarette smoke (CS) is a well-established risk factor to cardiovascular health and the most preventable cause of death. Countless studies have demonstrated its harm to health and many more studies investigating its pathogenic mechanisms. While the CS-induced pathogenic mechanism of cardiovascular dysfunction has been mainly attributed to a combination of oxidative imbalance, vascular endothelial dysfunction, inflammation and modification of lipid profile, the focus of the current study was on the mediators of inflammation and the activation of signal pathways. In this study, we investigated the effects of CS on the pro-inflammatory/anti-inflammatory status in the heart and to elucidate the activation of specific signaling pathways in an in vivo rat model. Male Sprague-Dawley rats were divided into groups of CS exposure and sham air (SA) and exposed to 1 hour of respective CS and SA exposure daily for 56 days. The rats were then sacrificed and the ventricular homogenates were examined. Cardiac pro- inflammatory and anti-inflammatory mediators such as C-reactive protein (CRP), interleukin (IL)-6, cytokine-induced neutrophil chemoattractant (CINC-1), transforming growth factor (TGF)-β1, vascular endothelial growth factor (VEGF) and IL-10 were measured by enzyme-linked immunosorbent assay (ELISA) and the activation of specific signaling pathways was determined by Western blot analysis. CS caused suppression of cardiac CRP, IL-6, TGF-β1, and IL-10 and elevation of VEGF, revealing the imbalance of pro-inflammatory/anti-inflammatory status. Nuclear factor-κB (NF-κB) was also activated along with the activation of extracellular-regulated kinase (ERK) and c-Jun NH2-terminal kinase (JNK) but not p38 mitogen-activated protein kinase (MAPK) after 56 days of CS exposure. These data suggests the presence of a local adaptive mechanistic response to modulate cardiac pro-inflammatory/anti-inflammatory status via NF-κB/MAPK pathways after exposure to CS. These findings shed insight into the mechanistic pathways of CVD progression, allowing possible identification of selected mediators as biomarkers that could benefit early detection of CVD arisen from cigarette smoking.
published_or_final_version
Pharmacology and Pharmacy
Master
Master of Medical Sciences

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MacLeod, Ian. "A Drosophila model of familial encephalopathy with neuroserpin inclusion bodies." Thesis, University of Cambridge, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.611439.

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Lu, Song, and 鲁嵩. "Phenotype analysis of Pdss2 conditional knockout mouse." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B45552381.

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Armstrong, Richard James Ernest. "Cell replacement therapy through transplantation of expanded neural precursor cells : experiments in animal models of Parkinson's and Huntington's diseases." Thesis, University of Cambridge, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.431572.

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Childers, Martin K. "Contraction-induced muscle damage in dogs with golden retriever muscular dystrophy." free to MU campus, others may purchase free online, 2002. http://wwwlib.umi.com/cr/mo/preview?3074385.

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Klöting, Nora. "Phenotypic and genetic analysis in animal models and humans with type 1 diabetes or metabolic syndrome: unraveling complex mammalian diseases." [S.l.] : [s.n.], 2004. http://deposit.ddb.de/cgi-bin/dokserv?idn=974087254.

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Ibrahim, Rouba [Verfasser], and Holger [Akademischer Betreuer] Garn. "Investigating the efficacy of transcription factor-specific DNAzymes in animal models of inflammatory skin diseases / Rouba Ibrahim. Betreuer: Holger Garn." Marburg : Philipps-Universität Marburg, 2016. http://d-nb.info/1097530418/34.

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Bobé, Pierre. "La gestation : un modele d'etude de la regulation de la reponse immunitaire." Paris 7, 1987. http://www.theses.fr/1987PA077192.

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Erdely, Aaron. "Progression of chronic renal disease in several animal models possible role of decreased renal nitric oxide production as a primary causative factor /." Morgantown, W. Va. : [West Virginia University Libraries], 2002. http://etd.wvu.edu/templates/showETD.cfm?recnum=2740.

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Kitto, Michael Ryan. "Biconditional discrimination learning in rats with 192 IgG-saporin lesions of the nucleus basalis magnocellularis." CSUSB ScholarWorks, 2006. https://scholarworks.lib.csusb.edu/etd-project/3002.

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The experiment tested the hypothesis that 192 IgG-saporin lesions of the nucleus basalis magnocellularis (NBM) in rats would impair performance in a biconditional visual discrimination task, which requires configural association learning. Experiment used 22 male Long-Evan rats (Harlan Sprague-Dawley). Behavioral testing was conducted in two identical T-mazes. Rats were randomly assigned to either a bilateral 192 IgG-saporin lesion group (n = 10) or to a control group (n = 12). Results support the hypothesis that NBM is critically involved in configural but not simple association learning and suggest that NBM may be involved more generally in cognitive flexibility.

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Halpern, Melissa Dale. "The in vivo and in vitro effects of diethyldithiocarbamate on autoimmune New Zealand Black/White F₁ hybrid, MRL/Mp-lpr/lpr and related and normal murine strains." Diss., The University of Arizona, 1989. http://hdl.handle.net/10150/184940.

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New Zealand Black/White F₁ hybrid (NZB/W) and MRL/Mp-lpr/lpr (MRL/lpr) mice spontaneously develop a Systemic Lupus Erythematosus-like autoimmune disease. While the primary immunologic defect in the NZB/W is due to B cells, in the MRL/lpr it is a result of T cell abnormalities. Diethyldithiocarbamate (DTC), an agent suggested to enhance T cell function, was used to treat both strains. Weekly treatment of NZB/W mice with 25 mg/kg DTC had no significant effect upon survival or autoantibody levels but did induce changes in cell surface antigen expression. MRL/lpr mice treated with DTC displayed normalization of cell surface antigen expression (particularly increased expression of Lyt-2, macrophage markers and Lyt-2⁺/L3T4⁺ thymocytes), decreased lymphoproliferation and thymic atrophy, decreased serum autoantibody levels and kidney deposition of C3 and IgM, restored responses to mitogens and significantly prolonged survival. To determine both the influence of MRL background and lpr genes and to better understand on what cell populations DTC effects, changes in cell surface antigen expression were examined in DTC treated MRL-+/+, Balb/c, and Balb/lpr strains. The only consistent similarities observed between all strains tested were DTC induced changes in Mac-1 splenocyte surface antigen expression. In vitro studies showed DTC to have variable effects upon the mitogenic responses of lymphoid cells to phytohemagluttinin, but DTC alone stimulated both MRL/lpr and Balb/lpr lymphocytes. DTC stimulated the null cell population that predominates in lpr gene-bearing mice, but all observed in vitro effects of DTC were dependent upon the adherent cell population included in culture. DTC had no apparent direct effects upon adherent cells alone however. These studies have shown that DTC is capable of positive effects upon one autoimmune murine strain, the MRL/lpr, but not the NZB/W. DTC appears to affect macrophages, but other cell populations are required to obtain full activity of this compound. The variable effects of DTC emphasize the need to define the immunopathology of individual patients with autoimmune disease before initiating treatment with immunomodulative therapy.

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Koontz, Thadeus B. "MCMV induced cerebellar maldevelopment." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2007. https://www.mhsl.uab.edu/dt/2007p/koontz.pdf.

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Lau, Ho-fai, and 劉浩輝. "In vivo DTI study of rodent brains during early postnatal development and injuries." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2008. http://hub.hku.hk/bib/B41290641.

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Ho, Tsun-bond Horace, and 何存邦. "Generation of Na+-coupled dicarboxylate cotransporter (NaDC-1) deficient mice for the study of NaDC-1's role in caloric restrictionand renal ischemia/reperfusion injury." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B38575231.

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Parsons, Sven David Charles. "Natural animal model systems to study tuberculosis." Thesis, Stellenbosch : University of Stellenbosch, 2010. http://hdl.handle.net/10019.1/4505.

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Thesis (PhD (Molecular Biology and Human Genetics))--University of Stellenbosch, 2010.
ENGLISH ABSTRACT: The growing global epidemic of human tuberculosis (TB) results in 8 million new cases of this disease and 2 million deaths annually. Control thereof will require greater insight into the biology of the causative organism, Mycobacterium tuberculosis, and into the pathogenesis of the disease. This will benefit the design of new vaccines and diagnostic assays which may reduce the degree of both disease transmission and progression. Animal models have played a vital role in the understanding of the aetiology, pathogenesis, and treatment of TB. Much of such insight has been obtained from experimental infection models, and the development of new vaccines, for example, is dependant on these. Nonetheless, studies utilising naturally occurring TB in animals, such as those which have investigated the use of interferon-gamma release assays (IGRA) for its diagnosis, have contributed substantially to the body of knowledge in this field. However, there are few such examples, and this study sought to identify and investigate naturally occuring animal TB in South Africa as an opportunity to gain further insight into this disease. During the course of this study, the dassie bacillus, a distinctly less virulent variant of M. tuberculosis, was isolated from a rock hyrax from the Western Cape Province of South Africa. This has provided new insight into the widespread occurrence of this organism in rock hyrax populations, and has given impetus to further exploring the nature of the difference in virulence between these pathogens. Also investigated was M. tuberculosis infection in dogs in contact with human TB patients. In so doing, the first reported case of canine TB in South Africa was described, v a novel canine IGRA was developed, and a high level of M. tuberculosis infection in these animals was identified. This supports human data reflecting high levels of transmission of this pathogen during the course of human disease. Additionally, the fact that infected companion animals may progress to disease and potentially act as a source of human infection was highlighted. However, an attempt to adapt a flow cytometric assay to study cell-mediated immune responses during canine TB revealed the limitations of such studies in species in which the immune system remains poorly characterised. The use of IGRAs to diagnose TB was further explored by adapting a human assay, the QuantiFERON-TB Gold (In-Tube Method), for use in non-human primates. These studies have shown that such an adaption allows for the sensitive detection of TB in baboons (Papio ursinus) and rhesus macaques (Macaca mulatta) and may be suitable for adaption for use in other species. However, they have also evidenced the limitation of this assay to specifically detect infection by M. tuberculosis. Finally, to contextualise the occurrence of the mycobacterial infections described above, and other similar examples, these have been reviewed as an opinion piece. Together, these investigations confirm that animal models will continue to make important contributions to the study of TB. More specifically, they highlight the opportunities that naturally occuring animal TB provides for the discovery of novel insights into this disease.
AFRIKAANSE OPSOMMING: Wêreldwye tuberkulose (TB) epidemie veroorsaak agt miljoen nuwe gevalle en twee miljoen sterftes jaarliks. Ingryping by die beheer hiervan vereis begrip van die biologie van die mikroörganisme Mycobacterium tuberculosis, die oorsaak van TB, asook van die patogenese van die siekte self. Hierdie kennis kan lei tot ontwerp van nuwe entstowwe en diagnostiese toetse wat gevolglik beide die oordrag- en vordering van die siekte mag bekamp. Dieremodelle speel lankal 'n rol in ons begrip van die etiologie-, patogenese- en behandeling van TB. Insig is grotendeels verkry vanaf eksperimentele infeksiemodelle, en ontwikkeling van entstowwe, onder andere, is afhanklik van soortgelyke modelle. Desnieteenstaande, studies wat natuurlike TB voorkoms in diere ondersoek, byvoorbeeld dié wat op die ontwikkeling van interferon-gamma vrystellingstoetse (IGVT) fokus, het merkwaardige bydrae gemaak tot kennis en begrip in hierdie studieveld. Daar is slegs enkele soortgelyke voorbeelde. Om hierdie rede is die huidige studie uitgevoer waarbinne natuulike diere-TB geïdentifiseer en ondersoek is in Suid-Afrika om verdere kennis en insig te win aangaande TB. Die "dassie bacillus", bekend om beduidend minder virulent te wees as M. tuberculosis, is tydens hierdie studie geïsoleer vanuit 'n klipdassie (Procavia capensis) in die Wes-Kaapse provinsie, Suid-Afrika. Insig in die wydverspreide voorkoms van hierdie organisme in klipdassie bevolkings is gevolglik verkry en verskaf momentum om die aard van verskil in virulensie tussen dié patogene te bestudeer. vii Voorts is M. tuberculosis infeksie bestudeer in honde wat in kontak is met menslike TB pasiënte en word die eerste geval van honde TB dus in Suid-Afrika beskryf. In hierdie groep diere, is 'n hoë vlak van M. tuberculosis infeksie geïdentifiseer deur gebruik te maak van 'n nuut ontwikkelde IGVT vir die diagnose van honde TB. Gevolglik ondersteun dié studie bevindinge van menslike studies wat toon dat besondere hoë vlakke van M. tuberculosis oordrag voorkom gedurende die verloop van die siekte. Verder toon die studie dat geïnfekteerde troeteldiere 'n bron van menslike infeksie kan wees. 'n Poging om 'n vloeisitometriese toets te ontwikkel om die aard van selgefundeerde immuunreaksies te bestudeer in honde met TB toon die beperkings van dergelike studies in spesies waarin die immuunsisteem gebrekkig gekarakteriseer is. Die gebruik van IGVT'e in die diagnose van TB is verder ondersoek deur 'n menslike toets (QuantiFERON-TB Gold, In-Tube Method) aan te pas vir die gebruik van nie-menslike primaat gevalle. Hierdie studies toon gevolglik dat so 'n aanpassing toepaslik is vir hoogs sensitiewe deteksie van TB in chacma bobbejane (Papio ursinus) en rhesus ape (Macaca mulatta), en mag ook aangepas word vir gebruik in ander spesies. Tog word die beperkings van hierdie toets om infeksie wat spesifiek deur M. tuberculosis veroorsaak uitgelig. Ter afsluiting word hierdie studie in konteks geplaas deur 'n oorsig te gee van bogenoemde- en soortgelyke gevalle van dierlike infeksie deur mikobakterieë in Suid-Afrika. Hierdie studies bevestig dat dieremodelle steeds belangrike toevoegings maak tydens die bestudering van TB en lig veral die moontlikhede uit dat bestudering van natuulike TB in diere kan lei tot die ontdekking van nuwe insigte ten opsigte van die siekte self.

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48

Hejmanowski, Ashley Q. "Allelic and genetic heterogeneity of two common genetic diseases." The Ohio State University, 2004. http://rave.ohiolink.edu/etdc/view?acc_num=osu1095309751.

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49

Buonincontri, Guido. "Advanced MRI for cardiac assessment in mice." Thesis, University of Cambridge, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.648679.

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Briggs, Whitney. "Evaluation and optimization of quantitative analysis methods for Clostridium perfringens detection in broiler intestinal samples to use with necrotic enteritis challenge models." The Ohio State University, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=osu1587491319889086.

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