• Refine Query
  • Source
  • Publication year
  • to
  • Language
  • 178
  • 28
  • 22
  • 18
  • 16
  • 13
  • 9
  • 6
  • 3
  • Tagged with
  • 381
  • 381
  • 55
  • 50
  • 47
  • 41
  • 38
  • 36
  • 36
  • 33
  • 30
  • 29
  • 27
  • 26
  • 24
  • About
  • The Global ETD Search service is a free service for researchers to find electronic theses and dissertations. This service is provided by the Networked Digital Library of Theses and Dissertations.
    Our metadata is collected from universities around the world. If you manage a university/consortium/country archive and want to be added, details can be found on the NDLTD website.
241

In Vivo Characterization of Pathologies Associated with Severe Influenza Virus Infection

Kenney, Adam D. January 2021 (has links)
No description available.
242

Sex-Specific Effects of a Mediterranean-Based Diet on Behavioural and Serotonin-Related Colonic and Hippocampal Changes in a Mouse Model of Prenatal Stress

Lefebvre, Geneviève 28 August 2023 (has links)
Prenatal stress may increase the risk for depression in offspring and it has been suggested that this could be linked to alterations in tryptophan metabolism, leading to serotonergic changes. Dietary patterns based on the Mediterranean (Med) diet, which includes foods rich in nutrients involved in the tryptophan-serotonin pathway, have been linked to depressive symptom improvements when used as an intervention. This thesis examined, in a mouse model, whether a Med-based diet normalized depressive-like behaviour and changes in the serotonin system in the colon and hippocampus resulting from a repeated physical restraint stressor administered during the second trimester in adult C57BL/6N female and male offspring. The Med-based diet modulated behaviour and hippocampal serotonin receptors primarily in females and changed the enzyme involved in the colonic serotonergic pathway in males. These results suggest that a Med-based diet may help improve behavioural disturbances stemming from prenatal stress in a sex-specific way, perhaps through its actions on the gut-brain serotonin system.
243

Characterizing femoral structure of the Ts66Yah mouse model of Down syndrome

Kourtney N Sloan (16642212) 30 August 2023 (has links)
<p>  </p> <p>Down syndrome (DS) is caused by the partial or complete trisomy of human chromosome 21 (Hsa21) and can result in skeletal deficits, including lower bone mineral density (BMD) and increased risk of fracture and osteoporosis or osteopenia earlier than the general population. Mouse models of DS have been developed to understand the genetic mechanisms resulting in these phenotypes, but models differ due to the complex genetic nature of DS and differing genome structures between humans and mice. Ts65Dn mice have been a popular model of DS as they contain ~50% of Hsa21 orthologous genes on a freely segregating minichromosome, but there is speculation that the phenotypes are exaggerated by non-Hsa21 orthologous trisomic genes also present. To address this issue, the Ts66Yah mouse model was developed to remove the non-Hsa21 orthologous trisomic genes. In this study, male and female Ts66Yah mouse femurs were evaluated during bone accrual and peak bone mass to investigate structural differences using micro-computed tomography. Additionally, the role of trisomic <em>Dyrk1a</em>, a Hsa21 gene previously linked to bone deficits in Ts65Dn mice, was evaluated through genetic and pharmacological means in Ts66Yah femurs at postnatal day 36. Ts66Yah mice were found to have little or no trabecular deficits at any age evaluated, but sex-dependent cortical deficits were present at all ages investigated. Reducing <em>Dyrk1a</em> copy number in Ts66Yah mice significantly improved cortical deficits but did not return cortical bone to euploid levels. Pharmacological treatment with DYRK1A inhibitor L21 was confounded by multiple variables, making it difficult to draw conclusions about DYRK1A inhibition in this manner. Overall, these results indicate trabecular deficits associated with Ts65Dn mice may be due to the non-Hsa21 orthologous trisomic genes, and more Hsa21 orthologous trisomic genes are necessary to produce trabecular deficits in DS model mice. As more mouse models of DS are developed, multiple models need to be assessed to accurately define DS-associated phenotypes and test potential treatments.</p>
244

Identification of disease susceptibility regions on chromosome 17 in a spondyloarthritis mouse model

Irving, Jeofferey-Ann 28 February 2024 (has links)
BACKGROUND: Spondyloarthritis is a subset of inflammatory rheumatic diseases that includes ankylosing spondyloarthritis, psoriatic arthritis, undifferentiated spondyloarthritis, and arthritis related to inflammatory bowel. The IL-23 cytokine has been implicated in the pathogenesis of spondyloarthritis. B10.RIII mice hydrodynamically injected with IL-23 minicircle overexpress the IL-23 cytokine, which leads to the development of spondyloarthritis-like disease. It is important to note that B10.RIII is a major histocompatibility complex (MHC) congenic mouse strain that is susceptible to autoimmune and autoinflammatory diseases where the background strain, C57BL/10 (B10), or the MHC donor strain, RIIIS/J, is resistant. For instance, the B10.RIII strain of mice is susceptible to IL-23-induced arthritis, while the B10 background strain is not. Large contaminating RIII-derived regions outside of the selected congenic interval on chromosome 17 were identified on chromosomes 10, 14, 15, and 17. Genetic variations in these intervals may contribute to the susceptibility of the B10.RIII mice to arthritis induced by IL-23 minicircle. OBJECTIVE: This study aimed to interrogate the arthritis phenotype after IL-23 minicircle injection in Chr17 subcongenic B10.RIII mice. In addition, chromosome 17 RIII-derived Ilrun gene and its role in regulating the Interferon signaling pathway between the B10.RIII and B10 mice were investigated. METHOD: Chromosome 17 subcongenic mice were generated by crossing B10.RIII mice with B10 mice and backcrossing the offspring to the B10.RIII mice. Offspring heterozygous b/r for the Chr17 region were then intercrossed to generate B10.RIII mice that are identical to the B10.RIII mice, except at chromosome 17, where they had the genotypes Chr17b/b, Chr17b/r, or Chr17r/r. These mice were then hydrodynamically injected with IL-23 minicircle DNA, and disease development was monitored every other day for two weeks using two parameters: clinical arthritis score and paw swelling. Bone marrow-derived macrophages were differentiated in vitro from B10.RIII and B10 mice. Cells were stimulated with TLR agonists (Pam3CSK4, Poly (I:C), LPS) that induce either the Ilrun-regulated Interferon signaling pathway or the NF-kB signaling pathway. Gene expression changes of NF-kB and Interferon-induced genes were measured using real-time quantitative PCR. TNF protein concentration in the supernatant was measured by ELISA. RESULTS: Upon IL-23 minicircle injection, Chr17r/r and Chr17b/r B10.RIII mice developed arthritis while Chr17b/b B10.RIII mice did not. In addition, the disease severity increased with the number of r alleles as the Chr17r/r B10.RIII mice had a higher clinical score and paw swelling when compared to the heterozygote Chr17b/r mice. Gene expression analysis of NF-kB and Interferon response genes revealed that there was no difference in the induction of NF-kB and Interferon response genes in bone marrow-derived macrophages from B10.RIII and B10 mice. In addition, there was also no difference in the induction of the Ilrun gene in bone marrow-derived macrophages from B10.RIII and B10 mice. CONCLUSION: The B10.RIII(71NS)/Sn strain contains three major RIII/WySn-derived regions outside of the congenic MHC region. The chromosome 17 cluster appears to play a role in susceptibility to IL-23 minicircle-induced arthritis. In vitro studies with bone marrow-derived macrophages failed to show functional differences in Ilrun between the B10.RIII and B10 mice. Future studies will interrogate chromosome 17 RIII-derived regions in arthritis development in more detail and investigate the role of Ilrun in immune responses using Ilrun knock-out mice. / 2025-02-28T00:00:00Z
245

ANTERIOR SEGMENT DYSGENESIS AND GLAUCOMATOUS FEATURES OBSERVED FOLLOWING CONDITIONAL DELETION OF AP-2β IN THE NEURAL CREST CELL POPULATION / AP-2β IN THE DEVELOPMENT OF THE ANTERIOR SEGMENT OF THE EYE

Martino, Vanessa 20 November 2015 (has links)
Glaucoma is a heterogeneous group of diseases that is currently considered to be the leading cause of irreversible blindness worldwide. Of the identified risk factors, elevated intraocular pressure remains the only modifiable risk factor that can be targeted clinically. Ocular hypertension is often a result of dysregulation of aqueous humour fluid dynamics in the anterior eye segment. Aqueous humour drainage is regulated by structures located in the anterior chamber of the eye. In some circumstances dysregulation occurs due to developmental abnormalities of these structures. The malformation of structures in the anterior segment is thought to be due to a defect in the differentiation and/or migration of the periocular mesenchyme during development. Unique to vertebrates, the neural crest cell (NCC) population contributes to the periocular mesenchyme and is instrumental to the proper development of structures in the anterior segment. For many years our laboratory has examined the role of the Activating Protein-2 (AP-2) transcription factors that are expressed in the neural crest and vital during the development of the eye. The purpose of this research project is to investigate the role of AP-2β in the NCC population during the development of the anterior segment of the eye. Conditional deletion of AP-2β expression in the NCC population demonstrated that mutants have dysgenesis of structures in the anterior segment including defects of the corneal endothelium, corneal stroma, ciliary body and a closed iridocorneal angle. Loss of retinal ganglion cells and their axons was also observed, likely due to the disruption of aqueous outflow, suggesting the development of glaucoma. The data generated from this research project will be critical in elucidating the role of AP-2β in the genetic cascade dictating the development of the anterior eye segment in addition to providing scientific research with a novel model of glaucomatous optic neuropathy. / Thesis / Master of Science (MSc)
246

Characterization of Snyder-Robinson Syndrome (SRS) in Mutant Mice and Treatment with a Novel Spermine Prodrug to Rebalance Intracellular Polyamine Levels

Mitra, Deepshikha 01 January 2023 (has links) (PDF)
Snyder-Robinson syndrome (SRS) is an X-linked neurodegenerative disorder affecting males. The disease appears early in childhood with symptoms like bone abnormalities, reduced muscle mass, and mobility issues. It results from disrupted polyamine biosynthesis, which is due to a mutation in spermine synthase (Sms). This causes an abnormally elevated Spermidine: Spermine ratios. There is no approved SRS treatment, rather only management of symptoms. A genetic mouse model for the SmsG56S mutation found in some SRS patients was characterized, and a novel spermine Prodrug treatment was tested. The hypothesis is that male SmsG56S mutant mice exhibit polyamine dysregulation and SRS traits, while Prodrug intervention may rebalance abnormal ratios and facilitate a normalized phenotype. Mice were phenotyped in pure C57BL/6J, mixed C3H, and backcrossed C57BL/6J x C3H backgrounds. Lethality of the mutation, especially in C57BL/6J mice, was an obstacle. Viable mutant mice exhibited reduced body weight, typically smaller size, and lower bone densities compared to age-matched wild-type mice. Prodrug treatment was performed using different dosing strategies and in all backgrounds. Upon histological examination, testes and bone exhibited subtle defects in affected mutant male mice, while no detectable differences were found in skeletal muscle, liver, or kidney compared to wild-type mice. Acute prodrug treatment using oral gavage 5 times per week over 2 weeks was found to rebalance the Spermidine: Spermine ratio. Repeated efforts to dose Prodrug over a longer 6-8 week duration in mice required lower intraperitoneal doses but outcomes may have been moderated by the mice background. Overall, the SmsG56S phenotype in the testes and bone are consistent with other mutant Sms models, although C57BL/6J mice seemed to be more sensitive to the SmsG56S mutation. Further testing of Prodrug is needed, including in younger mice and for a longer duration of treatment, to evaluate Prodrug effectiveness in improving traits in SmsG56S mice.
247

In situ tissue engineering using angiogenic peptide nanofibers to enhance diabetic wound healing

Balaji, Swathi January 2010 (has links)
No description available.
248

Quantitative analysis of glycinergic neurons including Ia inhibitory interneurons in the ventral spinal cord using a BAC-GlyT2-eGFP transgenic mouse model

Painter, Palak Rajeshkumar 28 September 2012 (has links)
No description available.
249

Investigations into the role of proinflammatory cytokines in the pathogenesis of gastric epithelial proliferation in chronic helicobacter pylori gastritis

Peterson, Richard A., II January 2003 (has links)
No description available.
250

Mammalian Atypical E2Fs Link Endocycle Control to Cancer

Chen, Hui-Zi 21 October 2011 (has links)
No description available.

Page generated in 0.08 seconds