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1.
Iarocci, Andrew Lee.
ErbB2 Expression Increases in the Spinal Cord of FVB/nJ Mice Following Infection with Theiler's Murine Encephalomyelitis Virus.
Degree: M.S. in Medical Microbiology and Immunology, Medical Microbiology and Immunology (graduate program), 2012, Creighton University
URL: http://hdl.handle.net/10504/31220 
► The neuregulins are a family of epidermal growth factors necessary for nervous system development. Neuregulins signal via the epidermal growth factor family of tyrosine kinase…
(more)
▼ The neuregulins are a family of epidermal growth factors necessary for nervous system development. Neuregulins signal via the epidermal growth factor family of tyrosine kinase receptors (ErbB1, ErbB2, ErbB3, and ErbB4). ErbB3 and ErbB4 bind neuregulins with high affinity, although to transduce an effective signal ErbB3 and ErbB4 must heterodimerize with ErbB1 or ErbB2 after ligand binding. Both ErbB3 and ErbB4 heterodimerize primarily with ErbB2. Using the Theiler’s murine encephalomyelitis virus (TMEV) model of demyelinating
disease, we infected FVB/nJ mice and we assessed the kinetics and expression of ErbB2 in the spinal cord of TMEV-infected mice early and late in the course of the development of demyelinating lesions. The data demonstrate that ErbB2, but not ErbB1, is upregulated in the spinal cord of TMEV-infected FVB/nJ mice in the early phase of demyelinating
disease. Interestingly, cells of the immune system (T cells, B cells, and macrophages) express ErbB2, and immunoreactivity to ErbB2 increases upon stimulation of the cells with Concanavalin A. Together, these data suggest that neuregulins may interact with infiltrating immune cells, which are well-described participants in the pathology observed in TMEV-induced demyelination.
Advisors/Committee Members: Drescher, Kristen M. (advisor), Iarocci, Andrew Lee (cuauthor).
Subjects/Keywords: Neuregulins; Theilovirus; Disease Models, Animal
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APA (6th Edition):
Iarocci, A. L. (2012). ErbB2 Expression Increases in the Spinal Cord of FVB/nJ Mice Following Infection with Theiler's Murine Encephalomyelitis Virus. (Masters Thesis). Creighton University. Retrieved from http://hdl.handle.net/10504/31220
Chicago Manual of Style (16th Edition):
Iarocci, Andrew Lee. “ErbB2 Expression Increases in the Spinal Cord of FVB/nJ Mice Following Infection with Theiler's Murine Encephalomyelitis Virus.” 2012. Masters Thesis, Creighton University. Accessed March 07, 2021.
http://hdl.handle.net/10504/31220.
MLA Handbook (7th Edition):
Iarocci, Andrew Lee. “ErbB2 Expression Increases in the Spinal Cord of FVB/nJ Mice Following Infection with Theiler's Murine Encephalomyelitis Virus.” 2012. Web. 07 Mar 2021.
Vancouver:
Iarocci AL. ErbB2 Expression Increases in the Spinal Cord of FVB/nJ Mice Following Infection with Theiler's Murine Encephalomyelitis Virus. [Internet] [Masters thesis]. Creighton University; 2012. [cited 2021 Mar 07].
Available from: http://hdl.handle.net/10504/31220.
Council of Science Editors:
Iarocci AL. ErbB2 Expression Increases in the Spinal Cord of FVB/nJ Mice Following Infection with Theiler's Murine Encephalomyelitis Virus. [Masters Thesis]. Creighton University; 2012. Available from: http://hdl.handle.net/10504/31220
University of Texas Southwestern Medical Center
2.
Lancaster, Karen.
Mechanisms Controlling Virulence Thresholds of Mixed Viral Populations and Identification of Novel Host Barriers to Poliovirus Neuropathogenesis.
Degree: 2012, University of Texas Southwestern Medical Center
URL: http://hdl.handle.net/2152.5/1030
► Neurotropic viruses comprise some of the worlds most widespread and deadly pathogens, including West Nile virus, rabies virus, and poliovirus. Poliovirus, as a model neurotropic…
(more)
▼ Neurotropic viruses comprise some of the worlds most widespread and deadly pathogens, including West Nile virus, rabies virus, and poliovirus. Poliovirus, as a model neurotropic virus, is also an RNA virus. RNA viruses have high mutation rates and a propensity to revert attenuating mutations, contributing to
disease and complicating treatment and vaccine development. Despite worldwide epidemics in the early nineteenth century, paralysis from poliovirus is a rare event occurring in less than 1% of poliovirus infections. This suggests the presence of viral and host barriers limiting
disease. Here we examined viral barriers by exploring the concept of virulence thresholds using mixtures of virulent and attenuated viruses in a transgenic mouse model of poliovirus infection. We determined that 1000-fold excess of an attenuated strain of poliovirus was protective against
disease induced by the virulent strain. Protection was induced locally, was a poliovirus specific effect, and inactivated virus conferred protection. Treatment with a poliovirus receptor-blocking antibody phenocopied the protective effect of inactivated viruses in vitro and in vivo, suggesting virulence thresholds may be modulated by competition for viral receptor. Furthermore, we found the attenuated virus became virulent in immune-deficient mice due to enhanced replication and reversion of attenuating mutations. We also identified additional host barriers limiting pathogenesis using a novel hybridization-based viral diversity assay to quantify the efficiency of poliovirus transport from the periphery to the central nervous system. We found viral replication in peripheral axons is limited and the type I interferon response limits viral replication in peripheral tissues, protecting against
disease. Significantly, we discovered that retrograde axonal transport of poliovirus in the sciatic nerve was inefficient and only 20% of viral pool members reaching the brain. The efficiency of viral transport increased upon muscle damage, leading to increased viral diversity and pathogenesis. In summary, we identified a viral induced mechanism controlling virulence of mixed viral populations, and characterized three host barriers that restrict poliovirus pathogenesis in the nervous system. The identification of these barriers restricting virulence may help explain the rare incidence of neurological complications following poliovirus infection and aid in our understanding of viral population dynamics and pathogenesis.
Advisors/Committee Members: Pfeiffer, Julie K..
Subjects/Keywords: RNA Viruses; Poliomyelitis; Antibodies; Disease Models, Animal
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APA (6th Edition):
Lancaster, K. (2012). Mechanisms Controlling Virulence Thresholds of Mixed Viral Populations and Identification of Novel Host Barriers to Poliovirus Neuropathogenesis. (Thesis). University of Texas Southwestern Medical Center. Retrieved from http://hdl.handle.net/2152.5/1030
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Lancaster, Karen. “Mechanisms Controlling Virulence Thresholds of Mixed Viral Populations and Identification of Novel Host Barriers to Poliovirus Neuropathogenesis.” 2012. Thesis, University of Texas Southwestern Medical Center. Accessed March 07, 2021.
http://hdl.handle.net/2152.5/1030.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Lancaster, Karen. “Mechanisms Controlling Virulence Thresholds of Mixed Viral Populations and Identification of Novel Host Barriers to Poliovirus Neuropathogenesis.” 2012. Web. 07 Mar 2021.
Vancouver:
Lancaster K. Mechanisms Controlling Virulence Thresholds of Mixed Viral Populations and Identification of Novel Host Barriers to Poliovirus Neuropathogenesis. [Internet] [Thesis]. University of Texas Southwestern Medical Center; 2012. [cited 2021 Mar 07].
Available from: http://hdl.handle.net/2152.5/1030.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Lancaster K. Mechanisms Controlling Virulence Thresholds of Mixed Viral Populations and Identification of Novel Host Barriers to Poliovirus Neuropathogenesis. [Thesis]. University of Texas Southwestern Medical Center; 2012. Available from: http://hdl.handle.net/2152.5/1030
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Texas Southwestern Medical Center
3.
Shi, Xiaolei.
Metabolomic Investigation of Melanoma Metastasis in a Patient-Derived Xenograft Mouse Model.
Degree: 2017, University of Texas Southwestern Medical Center
URL: http://hdl.handle.net/2152.5/7193
► Metabolic reprogramming is considered a major factor in cellular transformation and tumor initiation, but whether or how metabolism supports tumor metastasis remains an open question.…
(more)
▼ Metabolic reprogramming is considered a major factor in cellular transformation and tumor initiation, but whether or how metabolism supports tumor metastasis remains an open question. This study seeks to identify metabolic predictors of metastasis, with the rationale that understanding metabolic changes accompanying metastasis may lead to new therapies to prevent metastatic cancer.
We used a set of patient-derived xenograft mouse
models of melanoma, in which the metastatic potential of individual tumor lines correlated strongly with the history of metastasis in the patient donors. Six tumor lines with low metastatic potential (L-met) and nine with high metastatic potential (H-met) were implanted into several mice individually, then several fragments were isolated from each tumor, yielding a total of 182 individual tumor fragments for metabolomics. A tandem mass spectrometry (MS/MS)-based analytical platform was used to characterize 133 metabolites extracted from each tumor specimen. We then used a suite of statistical tools to identify metabolites differentiating H-met from L-met tumors.
We identified durable metabolomic signatures correlating with molecular and biological features of the tumors. BRAF-mutant tumors had metabolomic and metabolic flux features of enhanced glycolysis compared to BRAF-wild type tumors. Tumors that metastasized efficiently from their primary sites had elevated levels of metabolites related to protein methylation, including trimethyllysine (TML). TML levels correlated with histone H3 trimethylation at lysines 9 and 27, and methylation at these sites was also enhanced in efficiently metastasizing tumors. Erasing either of these marks by genetically or pharmacologically silencing the histone methyltransferases SETDB1 or EZH2 had no effect on primary tumor growth but reduced cellular invasiveness, circulating tumor cell count and metastatic spread. Thus, metabolite profiling can uncover targetable epigenetic requirements for the metastasis of human melanoma cells.
Advisors/Committee Members: Zhu, Hao, DeBerardinis, Ralph J., Wang, Richard, Morrison, Sean J., Davies, Michael.
Subjects/Keywords: Disease Models, Animal; Melanoma; Metabolomics; Neoplasm Metastasis
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APA ·
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CSE |
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APA (6th Edition):
Shi, X. (2017). Metabolomic Investigation of Melanoma Metastasis in a Patient-Derived Xenograft Mouse Model. (Thesis). University of Texas Southwestern Medical Center. Retrieved from http://hdl.handle.net/2152.5/7193
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Shi, Xiaolei. “Metabolomic Investigation of Melanoma Metastasis in a Patient-Derived Xenograft Mouse Model.” 2017. Thesis, University of Texas Southwestern Medical Center. Accessed March 07, 2021.
http://hdl.handle.net/2152.5/7193.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Shi, Xiaolei. “Metabolomic Investigation of Melanoma Metastasis in a Patient-Derived Xenograft Mouse Model.” 2017. Web. 07 Mar 2021.
Vancouver:
Shi X. Metabolomic Investigation of Melanoma Metastasis in a Patient-Derived Xenograft Mouse Model. [Internet] [Thesis]. University of Texas Southwestern Medical Center; 2017. [cited 2021 Mar 07].
Available from: http://hdl.handle.net/2152.5/7193.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Shi X. Metabolomic Investigation of Melanoma Metastasis in a Patient-Derived Xenograft Mouse Model. [Thesis]. University of Texas Southwestern Medical Center; 2017. Available from: http://hdl.handle.net/2152.5/7193
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Texas Southwestern Medical Center
4.
Seamans, Katherine Webster.
Behavioral, Neurochemical, and Histological Characterization of Mice Deficient for Parkin, DJ-1, and Antioxidant Proteins.
Degree: 2011, University of Texas Southwestern Medical Center
URL: http://hdl.handle.net/2152.5/885
► Parkinson’s disease is a progressive neurodegenerative disease characterized by a loss of dopaminergic neurons in the substantia nigra. The cause of Parkinson’s disease remains uncertain,…
(more)
▼ Parkinson’s
disease is a progressive neurodegenerative
disease characterized by a loss of dopaminergic neurons in the substantia nigra. The cause of Parkinson’s
disease remains uncertain, however, evidence implicates mitochondrial dysfunction and oxidative stress with selective vulnerability of dopaminergic neurons. Although most cases of Parkinson’s
disease are sporadic, 5-10% of cases are caused by mutations in a single gene. Loss-of-function mutations in parkin and DJ-1 were the first to be linked to recessively inherited parkinsonism. Surprisingly, mice bearing similar loss-of-function mutations in parkin and DJ-1 do not show age-dependent loss of nigral dopaminergic neurons or depletion of dopamine in the striatum. Although the normal cellular functions of Parkin and DJ-1 remain unclear, we hypothesized that Parkin and DJ-1 protect cells from oxidative stress and that loss-of-function mutations in these genes cause neurodegeneration in Parkinson’s
disease by rendering cells more sensitive to mitochondrial dysfunction and oxidative stress. We crossed mice deficient for Parkin and DJ-1 with mice deficient for the major mitochondrial antioxidant protein Mn-superoxide dismutase or Cu/Zn-superoxide dismutase. Previous studies have shown that mice with reduced levels of Cu/Zn-superoxide dismutase or Mn-superoxide dismutase are more sensitive to dopaminergic neurotoxins whereas mice with increased levels of superoxide dismutase are more resistant to dopaminergic neurotoxins. We predicted that reducing levels of antioxidant proteins in parkin-/-DJ-1-/- mice would result in age-dependent nigral cell loss, striatal dopamine depletion or behavioral abnormalities. Characterization of these mice for behavioral abnormalities, neurotransmitter defects and neuropathology, revealed significant behavioral abnormalities in the mutant mice even in the absence of significant changes to dopamine levels in the striatum, dopamine receptor density, or dopaminergic neuron numbers. Aged parkin-/-DJ-1-/- and Mn-superoxide dismutase triple deficient mice have a surprising enhanced rotorod performance without the presence of an anxiety phenotype or hyperactivity. Cu/Zn-superoxide dismutase and Mn-superoxide dismutase triple deficient mice have elevated levels of dopamine in the striatum, however none of the mice present with nigral cell loss. Levels of D1-like and D2-like dopamine receptors in the striatum were unchanged. It is evident from our studies that on a parkin/DJ-1 null background, additional loss of major antioxidant proteins does not lead to a progressive loss of dopaminergic neurons in mice.
Advisors/Committee Members: Goldberg, Matthew S..
Subjects/Keywords: Receptors, Dopamine; Parkinson Disease; Models, Animal
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APA (6th Edition):
Seamans, K. W. (2011). Behavioral, Neurochemical, and Histological Characterization of Mice Deficient for Parkin, DJ-1, and Antioxidant Proteins. (Thesis). University of Texas Southwestern Medical Center. Retrieved from http://hdl.handle.net/2152.5/885
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Seamans, Katherine Webster. “Behavioral, Neurochemical, and Histological Characterization of Mice Deficient for Parkin, DJ-1, and Antioxidant Proteins.” 2011. Thesis, University of Texas Southwestern Medical Center. Accessed March 07, 2021.
http://hdl.handle.net/2152.5/885.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Seamans, Katherine Webster. “Behavioral, Neurochemical, and Histological Characterization of Mice Deficient for Parkin, DJ-1, and Antioxidant Proteins.” 2011. Web. 07 Mar 2021.
Vancouver:
Seamans KW. Behavioral, Neurochemical, and Histological Characterization of Mice Deficient for Parkin, DJ-1, and Antioxidant Proteins. [Internet] [Thesis]. University of Texas Southwestern Medical Center; 2011. [cited 2021 Mar 07].
Available from: http://hdl.handle.net/2152.5/885.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Seamans KW. Behavioral, Neurochemical, and Histological Characterization of Mice Deficient for Parkin, DJ-1, and Antioxidant Proteins. [Thesis]. University of Texas Southwestern Medical Center; 2011. Available from: http://hdl.handle.net/2152.5/885
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Guelph
5.
Enns, Lea R.
Individual Level Models of Infectious Disease Transmission For Animal Experiments.
Degree: MS, Department of Mathematics and Statistics, 2015, University of Guelph
URL: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/9398
► The control of infectious disease transmission among animals is crucial in minimizing risk to public health. Typically, such diseases are controlled with the help of…
(more)
▼ The control of infectious
disease transmission among animals is crucial in minimizing risk to public health. Typically, such diseases are controlled with the help of treatments, or vaccines. Through mathematical and statistical modelling, we can develop
models that simulate the effects of treatment designs, and other variables, on
disease spread, to gain perspective on their underlying characteristics. We present a series of four individual-level
models (ILMs) to explore
disease spread in
animal experiments that are arranged in multiple sub-populations, such as pens or cages. Model parameters are then estimated within a Bayesian framework, using Markov chain Monte Carlo (MCMC) techniques. Average posterior means and MSEs are used to compare and analyze the accuracy of parameter estimates and the trend in bias among varying sizes of the sub-populations.
Advisors/Committee Members: Deardon, R. (advisor), Feng, Z. (advisor).
Subjects/Keywords: individual level models; infectious disease; animal experiments
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APA (6th Edition):
Enns, L. R. (2015). Individual Level Models of Infectious Disease Transmission For Animal Experiments. (Masters Thesis). University of Guelph. Retrieved from https://atrium.lib.uoguelph.ca/xmlui/handle/10214/9398
Chicago Manual of Style (16th Edition):
Enns, Lea R. “Individual Level Models of Infectious Disease Transmission For Animal Experiments.” 2015. Masters Thesis, University of Guelph. Accessed March 07, 2021.
https://atrium.lib.uoguelph.ca/xmlui/handle/10214/9398.
MLA Handbook (7th Edition):
Enns, Lea R. “Individual Level Models of Infectious Disease Transmission For Animal Experiments.” 2015. Web. 07 Mar 2021.
Vancouver:
Enns LR. Individual Level Models of Infectious Disease Transmission For Animal Experiments. [Internet] [Masters thesis]. University of Guelph; 2015. [cited 2021 Mar 07].
Available from: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/9398.
Council of Science Editors:
Enns LR. Individual Level Models of Infectious Disease Transmission For Animal Experiments. [Masters Thesis]. University of Guelph; 2015. Available from: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/9398
Massey University
6.
Russ, Anna-Lynne Elizabeth.
Effects of dietary sheep, cow and goat milk solids on colitis in the interleukin-10 gene deficient mouse model of inflammatory bowel disease.
Degree: PhD, Physiology, 2013, Massey University
URL: http://hdl.handle.net/10179/4326
► Inflammatory Bowel Disease (IBD) is a group of chronic, immunologically-mediated gastrointestinal disorders resulting from interactions between environmental influences, host genetic susceptibility, and the intestinal microbiota.…
(more)
▼ Inflammatory Bowel Disease (IBD) is a group of chronic, immunologically-mediated gastrointestinal disorders resulting from interactions between environmental influences, host genetic susceptibility, and the intestinal microbiota. Dietary factors can ameliorate symptoms, providing a rationale for using targeted nutrition to alleviate symptoms. Food components, including milk-derived oligosaccharides and conjugated linoleic acid, have shown anti-inflammatory effects in IBD patients or animal models of IBD. Additionally, some ruminant milks are perceived by some IBD patients to have more beneficial effects on their symptoms (goat, sheep) than others (cow). Soy-based milk substitutes are perceived to be more beneficial than milk. No reports describe the effects of milk solids from different species on molecular pathways in the intestine that might explain differential effects in IBD. This thesis aimed to investigate the effects of dietary intervention with milk solids on the severity of colitis (histology) and molecular pathways (microarrays and qPCR) in the interleukin-10 gene deficient (Il10-/-) mouse model of IBD.
First, laser microdissection (LMD) combined with microarrays was used to analyse colon epithelium gene expression in 6 and 12 week old Il10-/- mice fed a control diet. This indicated that intact colon was an appropriate tissue in which to study global changes in gene expression when colitis is established. It also showed that studying colon epithelium during the early stages of inflammation (6 weeks old) may identify molecular changes not seen in intact colon. Secondly, analysis of DNA methylation changes (both globally, and in specific inflammation-associated genes (Ppara, Stat1 and Tap2)) in Il10-/- mouse colon showed that changes in total DNA methylation were correlated with changes in global gene expression, and changes in Stat1 methylation during inflammation correlated with Stat1 gene expression. However, these techniques had limitations for obtaining a global overview of molecular changes (DNA methylation) in response to dietary intervention in established inflammation (LMD) and therefore were not applied in the dietary intervention study. Finally, diets containing goat and cow whole milk solids (40% w/w) fed for 6 weeks had anti-inflammatory effects in the colon of 11-12 week old Il10-/- mice, shown by a reduction in colitis severity and immune-related gene expression. Further research is required to elucidate the physiological and molecular mechanisms of these anti-inflammatory effects.
Subjects/Keywords: Inflammatory bowel disease (IBD);
Animal models
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APA (6th Edition):
Russ, A. E. (2013). Effects of dietary sheep, cow and goat milk solids on colitis in the interleukin-10 gene deficient mouse model of inflammatory bowel disease. (Doctoral Dissertation). Massey University. Retrieved from http://hdl.handle.net/10179/4326
Chicago Manual of Style (16th Edition):
Russ, Anna-Lynne Elizabeth. “Effects of dietary sheep, cow and goat milk solids on colitis in the interleukin-10 gene deficient mouse model of inflammatory bowel disease.” 2013. Doctoral Dissertation, Massey University. Accessed March 07, 2021.
http://hdl.handle.net/10179/4326.
MLA Handbook (7th Edition):
Russ, Anna-Lynne Elizabeth. “Effects of dietary sheep, cow and goat milk solids on colitis in the interleukin-10 gene deficient mouse model of inflammatory bowel disease.” 2013. Web. 07 Mar 2021.
Vancouver:
Russ AE. Effects of dietary sheep, cow and goat milk solids on colitis in the interleukin-10 gene deficient mouse model of inflammatory bowel disease. [Internet] [Doctoral dissertation]. Massey University; 2013. [cited 2021 Mar 07].
Available from: http://hdl.handle.net/10179/4326.
Council of Science Editors:
Russ AE. Effects of dietary sheep, cow and goat milk solids on colitis in the interleukin-10 gene deficient mouse model of inflammatory bowel disease. [Doctoral Dissertation]. Massey University; 2013. Available from: http://hdl.handle.net/10179/4326
University of Sydney
7.
El Massri, Nabil.
The impact of photobiomodulation in animal models of Parkinson's disease and ageing
.
Degree: 2018, University of Sydney
URL: http://hdl.handle.net/2123/19702
► The aim of this thesis was to explore whether photobiomodulation improved behaviour and offered neuroprotection in animal models of Parkinson's disease and in ageing. The…
(more)
▼ The aim of this thesis was to explore whether photobiomodulation improved behaviour and offered neuroprotection in animal models of Parkinson's disease and in ageing. The results are presented as publications following a literature review and ending with a general discussion. For Parkinson's disease, a mouse and monkey MPTP model were used, while for ageing, the twelve month mouse model was used. Photobiomodulation was applied either extracranially in mice or intracranially in monkeys. These applications were used as to ensure that photobiomodulation reached the distressed cells directly, offering the best chance of survival. There were five major sets of results. First, photobiomodulation led to improvements in locomotive behaviour in the mouse and monkey model of Parkinson’s disease, together with a reduction of the "human-like" signs in the monkey model. Second, photobiomodulation was an effective neuroprotective agent for the dopaminergic system in these models. Third, photobiomodulation was associated with clear reductions in gliosis, decreasing both the number and size of the glial cells in the ageing and Parkinson's disease models. Fourth, photobiomodulation prompted the expression of glial derived neurotrophic factor, together with the dopaminergic phenotype, in the striatum of the monkey model of Parkinson's disease. Fifth, there was an extensive encephalopsin network evident across the mouse and monkey striatum. This system was unaffected by either ageing, MPTP insult nor photobiomodulation. In summary, the results have provided evidence that photobiomodulation improved behaviour, was neuroprotective and reduced gliosis in a mouse and monkey model of Parkinson's disease, and reduced gliosis in an ageing mouse model. The results also revealed an extensive light-sensitive opsin network within the striatum, that can potentially impact on aspects of striatal function. Overall, the findings should hopefully serve as a template for translation to the clinic.
Subjects/Keywords: photobiomodulation;
animal models;
Parkinson's disease;
ageing
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APA ·
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to Zotero / EndNote / Reference
Manager
APA (6th Edition):
El Massri, N. (2018). The impact of photobiomodulation in animal models of Parkinson's disease and ageing
. (Thesis). University of Sydney. Retrieved from http://hdl.handle.net/2123/19702
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
El Massri, Nabil. “The impact of photobiomodulation in animal models of Parkinson's disease and ageing
.” 2018. Thesis, University of Sydney. Accessed March 07, 2021.
http://hdl.handle.net/2123/19702.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
El Massri, Nabil. “The impact of photobiomodulation in animal models of Parkinson's disease and ageing
.” 2018. Web. 07 Mar 2021.
Vancouver:
El Massri N. The impact of photobiomodulation in animal models of Parkinson's disease and ageing
. [Internet] [Thesis]. University of Sydney; 2018. [cited 2021 Mar 07].
Available from: http://hdl.handle.net/2123/19702.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
El Massri N. The impact of photobiomodulation in animal models of Parkinson's disease and ageing
. [Thesis]. University of Sydney; 2018. Available from: http://hdl.handle.net/2123/19702
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Michigan State University
8.
Matin, Nusrat.
Soluble epoxide hydrolase inhibition improves dilation in parenchymal arterioles and prevents memory impairment inhypertensive rats with chronic cerebral hypoperfusion.
Degree: 2016, Michigan State University
URL: http://etd.lib.msu.edu/islandora/object/etd:4208
► Thesis Ph. D. Michigan State University. Pharmacology and Toxicology 2016
Parenchymal arterioles (PAs) control blood flow to the neurovascular unit that consists of the neurons,…
(more)
▼ Thesis Ph. D. Michigan State University. Pharmacology and Toxicology 2016
Parenchymal arterioles (PAs) control blood flow to the neurovascular unit that consists of the neurons, glia and capillaries. Epidemiological studies highlight the involvement of PA dysfunction as being a key driver of cerebral small vessel disease, a leading cause of vascular cognitive impairment (VCI). Despite this the structural and functional features of PAs in physiological and pathological models have been largely unexplored. There are no therapeutic interventions to halt the progression of VCI, a spectrum of cognitive disorders with a cerebrovascular origin. Chronic cerebral hypoperfusion (CCH) and hypertension are major risk factors of VCI. Understanding the combined effects of these morbidities on PA structure and function could provide mechanistic insights into VCI and assist in designing therapies for the condition. In cerebral arteries epoxyeicosatrienoic acids (EETs) are potent dilators that modulate neurovascular coupling. Soluble epoxide hydrolase (sEH) rapidly metabolizes EETs to less active metabolites, thus inhibition of sEH is pharmacologically feasible means of enhancing the pleiotropic effects of EETs by increasing their half-life. The present dissertation describes studies to validate and study a clinically relevant model of VCI induced by bilateral common carotid artery stenosis (BCAS) in adult normotensive Wistar Kyoto (WKY) rats and in spontaneously hypertensive stroke prone rats (SHRSP). The working hypothesis was that impaired endothelium dependent dilation and remodeling in PAs after BCAS would accompany cognitive dysfunction in WKY rats (Chapter 2) and SHRSP (Chapter 3). Data are shown as mean ± SEM, Sham vs BCAS. Impaired memory and spatial learning abilities were observed in WKY rats with BCAS. BCAS impaired endothelial function in PAs from WKY rats, as evidenced by reduced carbachol mediated dilation (% dilation at 10-5M: 29.6 ± 8.1 vs -10.2 ± 7.4, p<0.05). In SHRSP with BCAS memory was impaired, however there was no difference in spatial learning abilities. BCAS also impaired endothelial function in PAs from SHRSP (% dilation at 10-5M: 17.5 ±5.3 vs -0.2 ± 2.9, p<0.05). I hypothesized that effects of CCH on cognitive function and PA dilation would be exacerbated in SHRSP. However, Sham SHRSP had impaired spatial learning abilities and PA dilation compared to Sham WKY rats and BCAS did not worsen these impairments. Furthermore, I hypothesized that chronic administration of a sEH inhibitor in SHRSP with BCAS would prevent CCH induced cognitive impairment by preventing endothelium dysfunction, and arteriole remodeling in the PAs (Chapter 4). Inhibition of sEH improved memory function, increased mRNA markers of neuroprotection and improved PA dilatory function (% dilation at 10-5M, BCAS + vehicle vs BCAS + sEH inhibitor: 3.6 ± 2.4 vs 14.9 ± 3.0, p<0.05). These studies suggest that chronic inhibition of sEH prevents CCH induced memory impairment via neuronal and vascular effects.
Description based on online…
Advisors/Committee Members: Dorrance, Anne M, Jackson, William F, Galligan, James J, Robison, Michelle M.
Subjects/Keywords: Vascular dementia – Animal models; Cerebrovascular disease – Animal models; Hydrolases; Cerebrovascular disease – Treatment; Pharmacology
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APA (6th Edition):
Matin, N. (2016). Soluble epoxide hydrolase inhibition improves dilation in parenchymal arterioles and prevents memory impairment inhypertensive rats with chronic cerebral hypoperfusion. (Thesis). Michigan State University. Retrieved from http://etd.lib.msu.edu/islandora/object/etd:4208
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Matin, Nusrat. “Soluble epoxide hydrolase inhibition improves dilation in parenchymal arterioles and prevents memory impairment inhypertensive rats with chronic cerebral hypoperfusion.” 2016. Thesis, Michigan State University. Accessed March 07, 2021.
http://etd.lib.msu.edu/islandora/object/etd:4208.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Matin, Nusrat. “Soluble epoxide hydrolase inhibition improves dilation in parenchymal arterioles and prevents memory impairment inhypertensive rats with chronic cerebral hypoperfusion.” 2016. Web. 07 Mar 2021.
Vancouver:
Matin N. Soluble epoxide hydrolase inhibition improves dilation in parenchymal arterioles and prevents memory impairment inhypertensive rats with chronic cerebral hypoperfusion. [Internet] [Thesis]. Michigan State University; 2016. [cited 2021 Mar 07].
Available from: http://etd.lib.msu.edu/islandora/object/etd:4208.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Matin N. Soluble epoxide hydrolase inhibition improves dilation in parenchymal arterioles and prevents memory impairment inhypertensive rats with chronic cerebral hypoperfusion. [Thesis]. Michigan State University; 2016. Available from: http://etd.lib.msu.edu/islandora/object/etd:4208
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Drexel University
9.
Marshall, Courtney Anne.
D3 Receptor Agonism Attenuates Deficits Observed in Rodents with 6-OHDA-Induced Medial Forebrain Bundle Lesions.
Degree: 2018, Drexel University
URL: https://idea.library.drexel.edu/islandora/object/idea%3A8257
► Parkinson’s Disease (PD) is a neurodegenerative disorder associated with the progressive loss of dopaminergic neurons in the substantia nigra. This pathology impairs the dopaminergic nigrostriatal…
(more)
▼ Parkinson’s Disease (PD) is a neurodegenerative disorder associated with the progressive loss of dopaminergic neurons in the substantia nigra. This pathology impairs the dopaminergic nigrostriatal pathway, thereby reducing dopamine (DA) input to the striatum and eliciting motor deficits. In addition to these motor deficits, PD patients are often afflicted by non-motor symptoms such as mild cognitive impairment (PD-MCI). PD-MCI patients display deficits in executive function and pathological alterations within the prefrontal cortex (PFC). Specifically, decreases in DA D3 receptor (D3R) expression in the PFC correlate with decreases in cognitive performance. The role of D3Rs in PD are well-established in motor impairments, but their effect on cognitive tasks is yet to be investigated. Additionally, pharmacological agents that target the D3R concurrently demonstrate affinity for other DA receptors. Our lab has developed a selective D3R agonist called SK609 to specifically examine D3R agonism in a hemiparkinson rodent model. We utilized behavioral assays that assess sustained attention and cognitive flexibility, two PFC-mediated tasks compromised in PD-MCI. We found that SK609 dose dependently ameliorated cognitive deficits in lesioned rodents. Taken together, we demonstrated that the prefrontal loss of D3Rs observed in patients may contribute to cognitive impairment by promoting adverse effects in DA signaling. Therefore, D3R agonism, and the consequential normalizing of prefrontal function, may be a therapeutic target for PD-MCI patients.
Ph.D., Neuroscience – Drexel University, 2018
Advisors/Committee Members: Kortagere, Sandhya, College of Medicine.
Subjects/Keywords: Neurosciences; Dopamine – Receptors; Dopamine – Agonists; Parkinson's disease; Parkinson's disease – Animal models
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APA (6th Edition):
Marshall, C. A. (2018). D3 Receptor Agonism Attenuates Deficits Observed in Rodents with 6-OHDA-Induced Medial Forebrain Bundle Lesions. (Thesis). Drexel University. Retrieved from https://idea.library.drexel.edu/islandora/object/idea%3A8257
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Marshall, Courtney Anne. “D3 Receptor Agonism Attenuates Deficits Observed in Rodents with 6-OHDA-Induced Medial Forebrain Bundle Lesions.” 2018. Thesis, Drexel University. Accessed March 07, 2021.
https://idea.library.drexel.edu/islandora/object/idea%3A8257.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Marshall, Courtney Anne. “D3 Receptor Agonism Attenuates Deficits Observed in Rodents with 6-OHDA-Induced Medial Forebrain Bundle Lesions.” 2018. Web. 07 Mar 2021.
Vancouver:
Marshall CA. D3 Receptor Agonism Attenuates Deficits Observed in Rodents with 6-OHDA-Induced Medial Forebrain Bundle Lesions. [Internet] [Thesis]. Drexel University; 2018. [cited 2021 Mar 07].
Available from: https://idea.library.drexel.edu/islandora/object/idea%3A8257.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Marshall CA. D3 Receptor Agonism Attenuates Deficits Observed in Rodents with 6-OHDA-Induced Medial Forebrain Bundle Lesions. [Thesis]. Drexel University; 2018. Available from: https://idea.library.drexel.edu/islandora/object/idea%3A8257
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Macquarie University
10.
Hunt, Louise Ruby.
The effect of complex environmental enrichment on locomotor, memory and affective function following dopamine receptor antagonism in adult rats with an investigation into a model of early-stage Parkinson's disease in aged rats.
Degree: 2012, Macquarie University
URL: http://hdl.handle.net/1959.14/264953
► 1. Introduction – 2. The effect of complex environmental enrichment on locomotor, memory and affective function following dopamine receptor antagonism in rats – 3. Motor…
(more)
▼ 1. Introduction – 2. The effect of complex environmental enrichment on locomotor, memory and affective function following dopamine receptor antagonism in rats – 3. Motor and non-motor functioning following modest nigral dopamine depletion: a model of early stage PD in aged rats – 4. Discussion.
Parkinson's disease (PD) is a neurodegenerative disease that impairs motor movement and is associated with cognitive and affective disturbances. Rodent models of PD demonstrate that complex environmental enrichment (CEE) can protect against motor dysfunction and improve neural survival in these dopaminergic-lesioned rodents. A few studies show that cognitive deficits can be observed in early-stage PD rats, but to date, no intervention has attempted to treat these induced deficits. Aim: In preparation for developing an early-stage PD rat model, this paper explored whether CEE could alleviate induced motor, cognitive or mood dysfunction as induced by the transient effects of dopamine antagonism on Sprague Dawley rats. Specifically, Study 1 (Chapter 2) explored whether brief CEE was effective in protecting against locomotor, memory or depressive symptoms in rats administered dopamine antagonists (either SCH23390 or pimozide). Results demonstrated that CEE differentially protected against attenuation of spontaneous locomotor activity and improved motivated exploratory behaviour, of enriched rats challenged with the D₁ receptor antagonist SCH23390, but did not prevent attenuation of sucrose consumption induced by the D₂ receptor antagonist pimozide. Study 2 (Chapter 3) explored whether memory or affective disturbances could be produced in an early-stage PD rat model, using 6-OHDA to induce dopaminergic cell loss within the substantia nigra of the brain in aged rats. Neither memory nor anhedonic disturbances were evident in the early-stage PD rats. Subsequently, a CEE intervention was not introduced to these animals. Methodological alterations are discussed to improve both cognitive and affective testing of early-stage PD rats.
1 online resource (xii, 125 pages) illustrations
Advisors/Committee Members: Macquarie University. Dept. of Psychology.
Subjects/Keywords: Parkinson's disease; Parkinson's disease – Research; Parkinson's disease – Animal models; Cognition disorders; Movement disorders; environmental enrichment; cognition; rats; dopamine; Parkinson's disease
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APA ·
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CSE |
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to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Hunt, L. R. (2012). The effect of complex environmental enrichment on locomotor, memory and affective function following dopamine receptor antagonism in adult rats with an investigation into a model of early-stage Parkinson's disease in aged rats. (Thesis). Macquarie University. Retrieved from http://hdl.handle.net/1959.14/264953
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Hunt, Louise Ruby. “The effect of complex environmental enrichment on locomotor, memory and affective function following dopamine receptor antagonism in adult rats with an investigation into a model of early-stage Parkinson's disease in aged rats.” 2012. Thesis, Macquarie University. Accessed March 07, 2021.
http://hdl.handle.net/1959.14/264953.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Hunt, Louise Ruby. “The effect of complex environmental enrichment on locomotor, memory and affective function following dopamine receptor antagonism in adult rats with an investigation into a model of early-stage Parkinson's disease in aged rats.” 2012. Web. 07 Mar 2021.
Vancouver:
Hunt LR. The effect of complex environmental enrichment on locomotor, memory and affective function following dopamine receptor antagonism in adult rats with an investigation into a model of early-stage Parkinson's disease in aged rats. [Internet] [Thesis]. Macquarie University; 2012. [cited 2021 Mar 07].
Available from: http://hdl.handle.net/1959.14/264953.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Hunt LR. The effect of complex environmental enrichment on locomotor, memory and affective function following dopamine receptor antagonism in adult rats with an investigation into a model of early-stage Parkinson's disease in aged rats. [Thesis]. Macquarie University; 2012. Available from: http://hdl.handle.net/1959.14/264953
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Texas Southwestern Medical Center
11.
Luitel, Krishna.
Investigating the Effects of Particle Radiation Exposure on Lung Carcinogenesis.
Degree: 2019, University of Texas Southwestern Medical Center
URL: http://hdl.handle.net/2152.5/6625
► Lung cancer accounts for more cancer-related deaths than any other cancer type among both men and women. The overall increase in radiation risk for human…
(more)
▼ Lung cancer accounts for more cancer-related deaths than any other cancer type among both men and women. The overall increase in radiation risk for human cancer types has been substantiated by the epidemiological data obtained from atomic bomb survivors and uranium mine workers. The lung has a large surface area which makes it a prominent target for radiation exposure making it susceptible to radiation-induced cancer. Recently particle radiation therapy such as the use of protons and carbon has increased in the treatment of cancer. The long-term biological effects of proton radiation remain less well characterized in terms of radiotherapy and well as for astronauts during deep space explorations.
We compared the long-term side effects of proton radiation to equivalent doses of X-rays in the initiation and progression of premalignant lesions in a transgenic mouse lung cancer model (K-rasLA1). We show proton irradiation causes more complex DNA damage that is not completely repaired resulting in increased oxidative stress in the lungs both acutely and persistently. Proton irradiated mice had lower median survival and increased carcinoma incidence as compared to un-irradiated controls or X-ray exposed mice.
Additionally, the space radiation environment consists of a wide variety of ion species with a various range of energies. To understand the effects of mixed ion beam radiation, we exposed K-rasLA-1 mice with three ion beams: Proton (H), Helium (He), and Silicon (Si) at a low dose rate of 0.5cGy/min. Using the three ion beams, we performed whole body irradiation in two different orders: 3B-1 (H-He-Si) and 3B-2 (Si-He-H) and used only H as a reference. We found that whole-body irradiation with 3B-1 increases the incidence of cancer initiation and systemic oxidative stress in mice 100 days post-irradiation compared to 3B-2 and H irradiation. Additionally, we saw an increase in adenomas with atypia and adenocarcinomas in 3B-1 irradiated mice but not in 3B-2 and H irradiated mice. We also found that a non-toxic anti-inflammatory, anti-oxidative radioprotector (CDDO-EA) reduced 3B-1 induced oxidative stress and cancer initiation almost back to baseline. Thus, exposure to 3B-1 elicits significant changes in lung cancer initiation that can be mitigated using CDDO-EA.
Advisors/Committee Members: Shay, Jerry W., Chen, Benjamin P., Aroumougame, Asaithamby, Akbay, Esra A..
Subjects/Keywords: Disease Models, Animal; Inflammation; Lung Neoplasms; Neoplasms, Radiation-Induced; Protons
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APA ·
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APA (6th Edition):
Luitel, K. (2019). Investigating the Effects of Particle Radiation Exposure on Lung Carcinogenesis. (Thesis). University of Texas Southwestern Medical Center. Retrieved from http://hdl.handle.net/2152.5/6625
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Luitel, Krishna. “Investigating the Effects of Particle Radiation Exposure on Lung Carcinogenesis.” 2019. Thesis, University of Texas Southwestern Medical Center. Accessed March 07, 2021.
http://hdl.handle.net/2152.5/6625.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Luitel, Krishna. “Investigating the Effects of Particle Radiation Exposure on Lung Carcinogenesis.” 2019. Web. 07 Mar 2021.
Vancouver:
Luitel K. Investigating the Effects of Particle Radiation Exposure on Lung Carcinogenesis. [Internet] [Thesis]. University of Texas Southwestern Medical Center; 2019. [cited 2021 Mar 07].
Available from: http://hdl.handle.net/2152.5/6625.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Luitel K. Investigating the Effects of Particle Radiation Exposure on Lung Carcinogenesis. [Thesis]. University of Texas Southwestern Medical Center; 2019. Available from: http://hdl.handle.net/2152.5/6625
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Texas Southwestern Medical Center
12.
Krishnan, Vaishnav.
Vulnerability and Resilience to Social Defeat: The Role of Neuroplasticity Within the Mesolimbic Dopamine Circuit.
Degree: 2010, University of Texas Southwestern Medical Center
URL: http://hdl.handle.net/2152.5/708
► The pathophysiology of major depression and post-traumatic stress disorder are poorly understood. In particular, while stressful life events are an important cause of psychopathology, most…
(more)
▼ The pathophysiology of major depression and post-traumatic stress disorder are poorly understood. In particular, while stressful life events are an important cause of psychopathology, most individuals exposed to adversity maintain normal psychological functioning. The molecular mechanisms underlying this “resilience” are poorly understood. Here, we demonstrate that an inbred population of mice subjected to social defeat can be separated into susceptible and unsusceptible subpopulations which differ along several behavioral and physiological domains. Through a series of molecular and electrophysiological techniques, we identify signature adaptations within the mesolimbic dopamine circuit that are uniquely associated with vulnerability and, by a combination of viral-mediated gene transfer and genetic mouse
models, we demonstrate how these adaptations are causally linked to a vulnerable phenotype. We also show that molecular recapitulations of adaptations associated with the unsusceptible phenotype are sufficient to promote resilient behavior. Our results validate a multidisciplinary approach to examine the neurobiological mechanisms of variations in stress resistance, and illustrate the importance of plasticity within the brain’s reward circuits in actively maintaining an emotional homeostasis.
Advisors/Committee Members: Nestler, Eric J..
Subjects/Keywords: Psychiatry; Disease Models, Animal; Research
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APA (6th Edition):
Krishnan, V. (2010). Vulnerability and Resilience to Social Defeat: The Role of Neuroplasticity Within the Mesolimbic Dopamine Circuit. (Thesis). University of Texas Southwestern Medical Center. Retrieved from http://hdl.handle.net/2152.5/708
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Krishnan, Vaishnav. “Vulnerability and Resilience to Social Defeat: The Role of Neuroplasticity Within the Mesolimbic Dopamine Circuit.” 2010. Thesis, University of Texas Southwestern Medical Center. Accessed March 07, 2021.
http://hdl.handle.net/2152.5/708.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Krishnan, Vaishnav. “Vulnerability and Resilience to Social Defeat: The Role of Neuroplasticity Within the Mesolimbic Dopamine Circuit.” 2010. Web. 07 Mar 2021.
Vancouver:
Krishnan V. Vulnerability and Resilience to Social Defeat: The Role of Neuroplasticity Within the Mesolimbic Dopamine Circuit. [Internet] [Thesis]. University of Texas Southwestern Medical Center; 2010. [cited 2021 Mar 07].
Available from: http://hdl.handle.net/2152.5/708.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Krishnan V. Vulnerability and Resilience to Social Defeat: The Role of Neuroplasticity Within the Mesolimbic Dopamine Circuit. [Thesis]. University of Texas Southwestern Medical Center; 2010. Available from: http://hdl.handle.net/2152.5/708
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Universidade Nova
13.
Afonso, Ricardo Alexandre da Silva Santos.
Sensibilidade à insulina pós-prandial: mecanismos fisiológicos e de activação e fisiopatologia na obesidade.
Degree: 2008, Universidade Nova
URL: http://www.rcaap.pt/detail.jsp?id=oai:run.unl.pt:10362/5102
► RESUMO A acção hipoglicemiante da insulina é máxima no estado pós-prandial e depende da substância hepática sensibilizadora da insulina (HISS). Esta dissertação visa o estudo…
(more)
▼ RESUMO
A acção hipoglicemiante da insulina é máxima no estado pós-prandial e depende
da substância hepática sensibilizadora da insulina (HISS). Esta dissertação visa o estudo
do mecanismo de acção da insulina no estado pós-prandial e em particular da via
dependente da HISS, em modelos animais fisiológicos e patológicos (obesidade e
diabetes mellitus tipo 2).
Avaliaram-se diferentes tipos de refeição quanto ao seu efeito potenciador da
acção da insulina, em ratos Sprague-Dawley (modelo fisiológico). A administração
intragástrica de glícidos não afecta a acção da insulina, mas a refeição mista (lípidos,
glícidos e proteínas), promove a sensibilização para a acção da insulina, através de um
processo que parece ser iniciado no intestino e envolve a activação da via da HISS.
Nos estudos de obesidade, o primeiro modelo utilizado foi o rato alimentado com
dieta hiperlipídica (HFD), no qual se observou uma insulinorresistência pós-prandial
devida quase exclusivamente à perda de acção da HISS, que se correlaciona com a
adiposidade (corporal e abdominal) e parece ser devida à diminuição da sua síntese.
O segundo modelo de obesidade usado foi o rato Zucker obeso (OZR), modelo
genético que apresenta uma diminuição idêntica de ambas as componentes de acção da
insulina (dependente e independente da HISS). A alteração na via da HISS parece
localizar-se a jusante da sua síntese, sugerindo que um ou vários pontos comuns entre
as vias de sinalização intracelular da HISS e da insulina per se estão alterados,
resultando num diminuto aporte de glucose. No OZR, a acção da HISS não se altera com
a idade, apresentando-se baixa também às 52 semanas de idade. Em ratos não obesos
(LZR), a acção da HISS diminui entre as 9 e 52 semanas, sendo acompanhada por um
decréscimo menos acentuado, embora significativo, da acção da insulina per se. A
diminuição da acção da HISS com a idade parece ser a principal causa de
insulinorresistência pós-prandial em LZR velhos, não se agravando no OZR.
No modelo de diabetes tipo 2 estudado, o rato Zucker diabético (ZDF), também
ambas as componentes de acção da insulina estavam diminuídas. No entanto, a
alimentação com ração Purina, ligeiramente mais energética e lipídica do que a ração
standard, agrava a disfunção da via da HISS nestes animais, sugerindo que a
sensibilidade à insulina em ratos ZDF é muito susceptível a factores nutricionais.
A via da HISS é essencial para potenciar a acção da insulina do estado de jejum
para o pós-prandial e a sua disfunção é em grande medida responsável pela
insulinorresistência observada nos modelos animais de obesidade e diabetes estudados.
xix
SUMMARY
Hypoglycemic insulin action is maximal in the postprandial state and depends on
the hepatic insulin sensitizing substance (HISS). The present thesis focus on the
postprandial insulin action and, in particular, on the HISS-dependent pathway, both in physiological and pathological (obesity and type 2 diabetes mellitus)
animal models.
Different meals were tested in Sprague-Dawley rats (physiological model) for
their capacity to…
Advisors/Committee Members: Macedo, Maria Paula.
Subjects/Keywords: Diabetes Mellitus - physiophatology; Obesity-complications ; Disease Models, Animal ; Insulin Resistance; Fisiologia
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APA ·
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MLA ·
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Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Afonso, R. A. d. S. S. (2008). Sensibilidade à insulina pós-prandial: mecanismos fisiológicos e de activação e fisiopatologia na obesidade. (Thesis). Universidade Nova. Retrieved from http://www.rcaap.pt/detail.jsp?id=oai:run.unl.pt:10362/5102
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Afonso, Ricardo Alexandre da Silva Santos. “Sensibilidade à insulina pós-prandial: mecanismos fisiológicos e de activação e fisiopatologia na obesidade.” 2008. Thesis, Universidade Nova. Accessed March 07, 2021.
http://www.rcaap.pt/detail.jsp?id=oai:run.unl.pt:10362/5102.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Afonso, Ricardo Alexandre da Silva Santos. “Sensibilidade à insulina pós-prandial: mecanismos fisiológicos e de activação e fisiopatologia na obesidade.” 2008. Web. 07 Mar 2021.
Vancouver:
Afonso RAdSS. Sensibilidade à insulina pós-prandial: mecanismos fisiológicos e de activação e fisiopatologia na obesidade. [Internet] [Thesis]. Universidade Nova; 2008. [cited 2021 Mar 07].
Available from: http://www.rcaap.pt/detail.jsp?id=oai:run.unl.pt:10362/5102.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Afonso RAdSS. Sensibilidade à insulina pós-prandial: mecanismos fisiológicos e de activação e fisiopatologia na obesidade. [Thesis]. Universidade Nova; 2008. Available from: http://www.rcaap.pt/detail.jsp?id=oai:run.unl.pt:10362/5102
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of California – San Francisco
14.
Bien-Ly, Nga.
INVESTIGATING THE EFFECT OF C-TERMINAL TRUNCATED APOLIPOPROTEIN E4 ON AMYLOID-BETA-INDUCED NEURONAL AND BEHAVIORAL DEFICITS IN MICE.
Degree: Biomedical Sciences, 2011, University of California – San Francisco
URL: http://www.escholarship.org/uc/item/5nn9k8p1
► Among the common apolipoprotein (apo) E isoforms (apoE2, apoE3, and apoE4), apoE4 is the major known genetic risk factor for Alzheimer's disease (AD). Previous in…
(more)
▼ Among the common apolipoprotein (apo) E isoforms (apoE2, apoE3, and apoE4), apoE4 is the major known genetic risk factor for Alzheimer's disease (AD). Previous in vitro and in vivo experiments showed that apoE4 preferentially undergoes aberrant cleavage in neurons, yielding neurotoxic C-terminal-truncated fragments. To study the effect of these fragments on amyloid-beta (Abeta) clearance/deposition and their potential synergy with Abeta in eliciting neuronal and behavioral deficits, transgenic mice expressing human apoE3, apoE4, or apoE4(delta272-299) were cross-bred with mice expressing human amyloid precursor protein harboring familial AD mutations (hAPPFAD). At 6-8 months of age, hAPPFAD mice expressing human apoE3 or apoE4 had 94% and 89% less hippocampal Abeta(1-x), respectively, than hAPPFAD mice lacking apoE, while hAPPFAD mice expressing mouse apoE had the highest Abeta levels. Abeta deposition in hAPPFAD mice expressing human apoE3 or apoE4 was 89% and 87% less than hAPPFAD mice without apoE, respectively. Thus, human apoE stimulates Abeta clearance, but mouse apoE does not. Expression of apoE4(delta272-299) reduced total Abeta levels by only 63% and Abeta deposition by 46%, compared to hAPPFAD mice without apoE. Unlike apoE3 and apoE4, the C-terminal-truncated apoE4 bound Abeta peptides poorly, leading to decreased Abeta clearance and increased Abeta deposition. Despite their lower levels of Abeta and Abeta deposition, hAPPFAD/apoE4(delta272-299) mice accumulated potential pathogenic Abeta oligomers and displayed neuronal and behavioral deficits similar to or more severe than those in hAPPFAD mice lacking apoE. Thus, the C-terminal-truncated apoE4 fragment inefficiently clears Abeta peptides and has enhanced toxicity in the presence of low levels of Abeta to elicit neuronal and behavioral deficits in mice.
Subjects/Keywords: Neurosciences; Morphology; Behavioral Sciences; Alzheimer's disease; animal models; apoE; neurodegeneration
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APA (6th Edition):
Bien-Ly, N. (2011). INVESTIGATING THE EFFECT OF C-TERMINAL TRUNCATED APOLIPOPROTEIN E4 ON AMYLOID-BETA-INDUCED NEURONAL AND BEHAVIORAL DEFICITS IN MICE. (Thesis). University of California – San Francisco. Retrieved from http://www.escholarship.org/uc/item/5nn9k8p1
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Bien-Ly, Nga. “INVESTIGATING THE EFFECT OF C-TERMINAL TRUNCATED APOLIPOPROTEIN E4 ON AMYLOID-BETA-INDUCED NEURONAL AND BEHAVIORAL DEFICITS IN MICE.” 2011. Thesis, University of California – San Francisco. Accessed March 07, 2021.
http://www.escholarship.org/uc/item/5nn9k8p1.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Bien-Ly, Nga. “INVESTIGATING THE EFFECT OF C-TERMINAL TRUNCATED APOLIPOPROTEIN E4 ON AMYLOID-BETA-INDUCED NEURONAL AND BEHAVIORAL DEFICITS IN MICE.” 2011. Web. 07 Mar 2021.
Vancouver:
Bien-Ly N. INVESTIGATING THE EFFECT OF C-TERMINAL TRUNCATED APOLIPOPROTEIN E4 ON AMYLOID-BETA-INDUCED NEURONAL AND BEHAVIORAL DEFICITS IN MICE. [Internet] [Thesis]. University of California – San Francisco; 2011. [cited 2021 Mar 07].
Available from: http://www.escholarship.org/uc/item/5nn9k8p1.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Bien-Ly N. INVESTIGATING THE EFFECT OF C-TERMINAL TRUNCATED APOLIPOPROTEIN E4 ON AMYLOID-BETA-INDUCED NEURONAL AND BEHAVIORAL DEFICITS IN MICE. [Thesis]. University of California – San Francisco; 2011. Available from: http://www.escholarship.org/uc/item/5nn9k8p1
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
National University of Ireland – Galway
15.
Naughton, Carol.
Development and characterisation of novel gene-environment interaction rat models of Parkinson's disease
.
Degree: 2016, National University of Ireland – Galway
URL: http://hdl.handle.net/10379/5984
► Despite its discovery almost 60 years ago, levodopa remains the most effective therapy for the treatment of the motor symptoms associated with Parkinson’s disease. However,…
(more)
▼ Despite its discovery almost 60 years ago, levodopa remains the most effective therapy for the treatment of the motor symptoms associated with Parkinson’s
disease. However, chronic use of levodopa is associated with serious side effects such as the emergence of dyskinesias, on-off effects and is also limited by the fact that it is purely symptomatic and does not slow progression of the
disease. One of the reasons suggested for the paucity of
disease-modifying therapies for Parkinson’s
disease is the lack of relevant
animal models which reliably recapitulate the features of the human
disease. To date, Parkinson’s
disease has been modelled extensively in preclinical animals using selective catecholaminergic neurotoxins such as 6-hydroxydopamine and MPTP, and is typically induced using a single insult. Unfortunately, these
models bear little etiological resemblance to the human condition as Parkinson’s
disease is thought to arise as a result of complex interactions between underlying genetics and exposure to environmental factors. Therefore, the overarching aim of this project was to develop a novel model of Parkinson’s
disease incorporating both genetic and environmental exposures. Not only would this shed further light on relevant gene-environments interactions in the context of the etiology of Parkinson’s
disease, but would also provide a novel gene-environment model for testing potential neuroprotective and
disease-modifying therapies for this condition.
In order to facilitate development of a novel gene-environment model, we first characterised the motor and neuropathological impairments induced by the Parkinson’s
disease-associated pesticide, rotenone, and the bacterial inflammagen,
Lipopolysaccharide (LPS) and compared them directly to those induced by the ‘gold standard’ catecholamine neurotoxin, 6-OHDA. We then went on to assess the impact of dual exposure of rats to overexpression of the Parkinson’s
disease-associated protein, -synuclein, and bacterial-like neuroinflammation and neurodegeneration driven by LPS. Finally, we investigated the impact of -synuclein overexpression in combination with the agritoxin-driven Parkinsonism induced by rotenone. With the single lesion
models induced by 6-OHDA, rotenone and LPS, we found that despite similar levels of neurodegeneration, the neurotoxic, environmental and bacterial triggers induced distinctly different patterns of motor dysfunction. With the dual exposure gene-environment studies, we found that exposing rats to both AAV--synuclein and LPS did not exacerbate the Parkinsonism caused by either toxin alone. In contrast, dual exposure to AAV--synuclein and rotenone significantly exacerbated the level of motor dysfunction and neurodegeneration caused by the genetic or environmental factor alone.
Overall, this research has shown that different Parkinson’s
disease-related neurotoxins can induce different patterns of motor dysfunction indicating the importance of the choice of lesioning agent in preclinical Parkinson’s
disease studies. We have also shown…
Advisors/Committee Members: Dowd, Eilís (advisor).
Subjects/Keywords: Parkinson's Disease;
Gene-environment interactions;
Animal models;
Pharmacology and Therapeutics
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APA ·
Chicago ·
MLA ·
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CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Naughton, C. (2016). Development and characterisation of novel gene-environment interaction rat models of Parkinson's disease
. (Thesis). National University of Ireland – Galway. Retrieved from http://hdl.handle.net/10379/5984
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Naughton, Carol. “Development and characterisation of novel gene-environment interaction rat models of Parkinson's disease
.” 2016. Thesis, National University of Ireland – Galway. Accessed March 07, 2021.
http://hdl.handle.net/10379/5984.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Naughton, Carol. “Development and characterisation of novel gene-environment interaction rat models of Parkinson's disease
.” 2016. Web. 07 Mar 2021.
Vancouver:
Naughton C. Development and characterisation of novel gene-environment interaction rat models of Parkinson's disease
. [Internet] [Thesis]. National University of Ireland – Galway; 2016. [cited 2021 Mar 07].
Available from: http://hdl.handle.net/10379/5984.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Naughton C. Development and characterisation of novel gene-environment interaction rat models of Parkinson's disease
. [Thesis]. National University of Ireland – Galway; 2016. Available from: http://hdl.handle.net/10379/5984
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
16.
Staunton, Lisa.
Proteomic Profiling of Animal Models of Myotonia and Motor Neuron Disease.
Degree: 2011, RIAN
URL: http://eprints.maynoothuniversity.ie/2862/
► Skeletal muscle provides an organism with a means of reacting to its environments. It is a complex and versatile tissue that is capable of change…
(more)
▼ Skeletal muscle provides an organism with a means of reacting to its environments. It is a complex and versatile tissue that is capable of change under a variety of conditions. For example extensive literature has shown muscle transformation from slow-to-fast by decreased motor nerve activity, hypogravity, physical inactivity and in diseased states. Similarly muscle transformation from fast-to-slow can be evoked by increased muscle nerve activity or exercise. The multitude of protein changes that has been identified by muscle transformation indicates it is a complex process that can change a wide variety of the muscle tissues architecture, metabolism and function.
Proteomic profiling of two very different diseased states has allowed the identification of muscle transformation occurring in opposite directions. Myotonia a common feature found in myotonic dystrophies is characterized by skeletal muscle membrane hyperexcitability. Proteomic profiling was carried out on three independent spontaneous mutant mice and allowed us to compare secondary effects of hyperexcitabilty on skeletal muscle. Severly myotonic mice MTO and ADR displayed a muscle transformation from fast-to-slow. The more mildly affected MTO*5J mutant showed slight changes in proteins associated with fast and slow muscle.
In comparison to the myotonic diseased state we carried out proteomic profiling of skeletal muscle tissue from the Wobbler mouse; an animal model of motor neuron degeneration. In contrast to myotonia the WR protein profile displayed a slow-to-fast muscle transformation.
The detailed MS-based analysis of diseased skeletal muscle has shown that proteomics is highly suitable to determine change in the isoform expression pattern of muscle proteins. Identified proteins can be used as potential factors for the establishment of comprehensive biomarker signature of myotonic and motor neuron diseases.
Subjects/Keywords: Biology; Proteomic Profiling; Animal Models; Myotonia; Motor Neuron Disease
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Staunton, L. (2011). Proteomic Profiling of Animal Models of Myotonia and Motor Neuron Disease. (Thesis). RIAN. Retrieved from http://eprints.maynoothuniversity.ie/2862/
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Staunton, Lisa. “Proteomic Profiling of Animal Models of Myotonia and Motor Neuron Disease.” 2011. Thesis, RIAN. Accessed March 07, 2021.
http://eprints.maynoothuniversity.ie/2862/.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Staunton, Lisa. “Proteomic Profiling of Animal Models of Myotonia and Motor Neuron Disease.” 2011. Web. 07 Mar 2021.
Vancouver:
Staunton L. Proteomic Profiling of Animal Models of Myotonia and Motor Neuron Disease. [Internet] [Thesis]. RIAN; 2011. [cited 2021 Mar 07].
Available from: http://eprints.maynoothuniversity.ie/2862/.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Staunton L. Proteomic Profiling of Animal Models of Myotonia and Motor Neuron Disease. [Thesis]. RIAN; 2011. Available from: http://eprints.maynoothuniversity.ie/2862/
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Washington
17.
Aloi, Macarena Sofia.
miR-155 expression modulates microglia functions in vitro and in the APP/PS1 mouse model of Alzheimer’s disease.
Degree: PhD, 2019, University of Washington
URL: http://hdl.handle.net/1773/44877
► Alzheimer’s Disease (AD) is characterized by the accumulation of extracellular Amyloid-β (Aβ) as well as both CNS and systemic inflammation. Microglia, myeloid cells resident to…
(more)
▼ Alzheimer’s
Disease (AD) is characterized by the accumulation of extracellular Amyloid-β (Aβ) as well as both CNS and systemic inflammation. Microglia, myeloid cells resident to the CNS, use microRNAs to rapidly respond to inflammatory signals. MicroRNA (miRNA) profiles are altered in the tissue, circulating monocytes, and serum of AD patients. MiR-155 is a specific miRNA that modulates the phasic inflammatory responses of innate immune cells, however its precise role in AD pathogenesis remains unknown. We hypothesized that miR-155 participates in AD pathophysiology by regulating microglia responses to Aβ in vitro and in vivo. In cultured neonatal microglia, we observed that modulation of miR-155 expression impacts the internalization of fibrillar Aβ at the plasma membrane and to low-pH compartments. In mouse
models of AD, microglia specific knock-out of miR-155 decreased accumulation of Aβ. In addition, we also observed that microglia specific deletion of miR-155 acutely increased seizures and seizure-related mortality in two mouse
models of AD. Reduced Aβ plaques after miR-155 deletion in microglia suggests increased clearance and the hypothesis that in AD
models, microglia facilitate epileptogenesis by increased internalization of synaptic material along with removal of Aβ. Together, these findings identify miR-155 expression in microglia as a potential regulator of synaptic homeostasis and microglia responses to Aβ in mouse
models of AD.
Advisors/Committee Members: Garden, Gwenn A (advisor).
Subjects/Keywords: Alzheimer's Disease; Animal models; Microglia; microRNA; Seizures; Neurosciences; Pathology; Pathology
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Aloi, M. S. (2019). miR-155 expression modulates microglia functions in vitro and in the APP/PS1 mouse model of Alzheimer’s disease. (Doctoral Dissertation). University of Washington. Retrieved from http://hdl.handle.net/1773/44877
Chicago Manual of Style (16th Edition):
Aloi, Macarena Sofia. “miR-155 expression modulates microglia functions in vitro and in the APP/PS1 mouse model of Alzheimer’s disease.” 2019. Doctoral Dissertation, University of Washington. Accessed March 07, 2021.
http://hdl.handle.net/1773/44877.
MLA Handbook (7th Edition):
Aloi, Macarena Sofia. “miR-155 expression modulates microglia functions in vitro and in the APP/PS1 mouse model of Alzheimer’s disease.” 2019. Web. 07 Mar 2021.
Vancouver:
Aloi MS. miR-155 expression modulates microglia functions in vitro and in the APP/PS1 mouse model of Alzheimer’s disease. [Internet] [Doctoral dissertation]. University of Washington; 2019. [cited 2021 Mar 07].
Available from: http://hdl.handle.net/1773/44877.
Council of Science Editors:
Aloi MS. miR-155 expression modulates microglia functions in vitro and in the APP/PS1 mouse model of Alzheimer’s disease. [Doctoral Dissertation]. University of Washington; 2019. Available from: http://hdl.handle.net/1773/44877
University of Washington
18.
Cao, Jessica.
Therapeutic potential of the endocannabinoid system in a novel mouse model of Huntington’s Disease.
Degree: PhD, 2018, University of Washington
URL: http://hdl.handle.net/1773/41839
► Huntington’s Disease is a fatal, inherited neurodegenerative disease characterized by profound disturbances of the basal ganglia and gradual deterioration of motor and cognitive functions with…
(more)
▼ Huntington’s
Disease is a fatal, inherited neurodegenerative
disease characterized by profound disturbances of the basal ganglia and gradual deterioration of motor and cognitive functions with development of psychiatric deficits. Early impairment of the endogenous cannabinoid signaling system is thought to be one of many hallmarks of this neurodegenerative
disease and a possible molecular event that drives
disease pathogenesis. Reduction of this system suggests absence of its many neuroprotective qualities and that this may contribute to the neuropathology in Huntington’s
Disease. The purpose of this thesis is to characterize novel lines of the HdhQ mouse model that accurately recapitulate Huntington’s
Disease and to use that model to explore the therapeutic potential of the endogenous cannabinoid signaling system in delaying or preventing
disease development. In this thesis, I report that the HdhQ350/+ model, the HdhQ line expressing 350 polyglutamines, exhibits both sex-dependent behavioral impairments and neuropathology despite males and females expressing equal mutant huntingtin protein levels, suggesting a sex-dependent effect of expanded polyglutamines in mouse
models. Additionally, I report that the HdhQ200/200 mouse, the line homozygous for 200 polyglutamines, more accurately replicates Huntington’s
Disease, both behaviorally and pathologically. Short-term pharmacological enhancement of endogenous cannabinoids in this mouse model through ABHD6 inhibition shows potential in rescuing select behavioral impairments. Together, this doctoral thesis puts forth efforts to understand the impact of polyglutamine expansions in mouse
models and to uncover a novel therapeutic in the treatment of Huntington’s
Disease by exploring the promising domain of the endocannabinoid signaling system.
Advisors/Committee Members: Stella, Nephi (advisor).
Subjects/Keywords: ABHD6; animal models; endocannbinoids; Huntington's Disease; polyglutamine; Pharmacology; Neurosciences; Pharmacology
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Record Details
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Cao, J. (2018). Therapeutic potential of the endocannabinoid system in a novel mouse model of Huntington’s Disease. (Doctoral Dissertation). University of Washington. Retrieved from http://hdl.handle.net/1773/41839
Chicago Manual of Style (16th Edition):
Cao, Jessica. “Therapeutic potential of the endocannabinoid system in a novel mouse model of Huntington’s Disease.” 2018. Doctoral Dissertation, University of Washington. Accessed March 07, 2021.
http://hdl.handle.net/1773/41839.
MLA Handbook (7th Edition):
Cao, Jessica. “Therapeutic potential of the endocannabinoid system in a novel mouse model of Huntington’s Disease.” 2018. Web. 07 Mar 2021.
Vancouver:
Cao J. Therapeutic potential of the endocannabinoid system in a novel mouse model of Huntington’s Disease. [Internet] [Doctoral dissertation]. University of Washington; 2018. [cited 2021 Mar 07].
Available from: http://hdl.handle.net/1773/41839.
Council of Science Editors:
Cao J. Therapeutic potential of the endocannabinoid system in a novel mouse model of Huntington’s Disease. [Doctoral Dissertation]. University of Washington; 2018. Available from: http://hdl.handle.net/1773/41839
19.
Staunton, Lisa.
Proteomic Profiling of Animal Models of Myotonia and Motor Neuron Disease.
Degree: 2011, RIAN
URL: http://mural.maynoothuniversity.ie/2862/
► Skeletal muscle provides an organism with a means of reacting to its environments. It is a complex and versatile tissue that is capable of change…
(more)
▼ Skeletal muscle provides an organism with a means of reacting to its environments. It is a complex and versatile tissue that is capable of change under a variety of conditions. For example extensive literature has shown muscle transformation from slow-to-fast by decreased motor nerve activity, hypogravity, physical inactivity and in diseased states. Similarly muscle transformation from fast-to-slow can be evoked by increased muscle nerve activity or exercise. The multitude of protein changes that has been identified by muscle transformation indicates it is a complex process that can change a wide variety of the muscle tissues architecture, metabolism and function.
Proteomic profiling of two very different diseased states has allowed the identification of muscle transformation occurring in opposite directions. Myotonia a common feature found in myotonic dystrophies is characterized by skeletal muscle membrane hyperexcitability. Proteomic profiling was carried out on three independent spontaneous mutant mice and allowed us to compare secondary effects of hyperexcitabilty on skeletal muscle. Severly myotonic mice MTO and ADR displayed a muscle transformation from fast-to-slow. The more mildly affected MTO*5J mutant showed slight changes in proteins associated with fast and slow muscle.
In comparison to the myotonic diseased state we carried out proteomic profiling of skeletal muscle tissue from the Wobbler mouse; an animal model of motor neuron degeneration. In contrast to myotonia the WR protein profile displayed a slow-to-fast muscle transformation.
The detailed MS-based analysis of diseased skeletal muscle has shown that proteomics is highly suitable to determine change in the isoform expression pattern of muscle proteins. Identified proteins can be used as potential factors for the establishment of comprehensive biomarker signature of myotonic and motor neuron diseases.
Subjects/Keywords: Biology; Proteomic Profiling; Animal Models; Myotonia; Motor Neuron Disease
Record Details
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Share »
Record Details
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Cite
« Share
❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Staunton, L. (2011). Proteomic Profiling of Animal Models of Myotonia and Motor Neuron Disease. (Thesis). RIAN. Retrieved from http://mural.maynoothuniversity.ie/2862/
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Staunton, Lisa. “Proteomic Profiling of Animal Models of Myotonia and Motor Neuron Disease.” 2011. Thesis, RIAN. Accessed March 07, 2021.
http://mural.maynoothuniversity.ie/2862/.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Staunton, Lisa. “Proteomic Profiling of Animal Models of Myotonia and Motor Neuron Disease.” 2011. Web. 07 Mar 2021.
Vancouver:
Staunton L. Proteomic Profiling of Animal Models of Myotonia and Motor Neuron Disease. [Internet] [Thesis]. RIAN; 2011. [cited 2021 Mar 07].
Available from: http://mural.maynoothuniversity.ie/2862/.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Staunton L. Proteomic Profiling of Animal Models of Myotonia and Motor Neuron Disease. [Thesis]. RIAN; 2011. Available from: http://mural.maynoothuniversity.ie/2862/
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
20.
Holland, Ashling.
Proteomic Profiling of Animal Models of Motor Neuron Disease
and Muscular Dystrophy.
Degree: 2015, RIAN
URL: http://mural.maynoothuniversity.ie/6767/
► Proteomic profiling plays a decisive role in the identification of novel biomarkers of neuromuscular disorders and the elucidation of new pathobiochemical mechanisms that underlie these…
(more)
▼ Proteomic profiling plays a decisive role in the identification of novel biomarkers
of neuromuscular disorders and the elucidation of new pathobiochemical
mechanisms that underlie these diseases. Detailed mass spectrometryQbased
analysis of various diseased muscle groups from animal models of motor neuron
disease and XQlinked muscular dystrophy is presented, in addition to motor
neuron disease associated globozoospermia. This research has shown that both
gel electrophoresis based and/or liquid chromatography for largeQscale protein
separation, and labelQfree mass spectrometry basedQproteomics are highly
suitable to determine changes in the isoform expression pattern of muscle and
testis proteins. The work presented outlines major categories of protein families
that have been identified by proteomicsQbased screening approaches in
conjunction with biochemical verification analyses. This research has
successfully established comprehensive biomarker signatures that have the
potential to be used for the evaluation of new treatments and therapeutics,
improve the understanding of pathobiochemical processes of the different
diseases under investigation and diagnostics and prognostics of motor neuron
disease, impaired spermiogenesis and XQlinked muscular dystrophy.
Subjects/Keywords: Proteomic Profiling; Animal Models; Motor Neuron Disease; Muscular Dystrophy
Record Details
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Record Details
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Holland, A. (2015). Proteomic Profiling of Animal Models of Motor Neuron Disease
and Muscular Dystrophy. (Thesis). RIAN. Retrieved from http://mural.maynoothuniversity.ie/6767/
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Holland, Ashling. “Proteomic Profiling of Animal Models of Motor Neuron Disease
and Muscular Dystrophy.” 2015. Thesis, RIAN. Accessed March 07, 2021.
http://mural.maynoothuniversity.ie/6767/.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Holland, Ashling. “Proteomic Profiling of Animal Models of Motor Neuron Disease
and Muscular Dystrophy.” 2015. Web. 07 Mar 2021.
Vancouver:
Holland A. Proteomic Profiling of Animal Models of Motor Neuron Disease
and Muscular Dystrophy. [Internet] [Thesis]. RIAN; 2015. [cited 2021 Mar 07].
Available from: http://mural.maynoothuniversity.ie/6767/.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Holland A. Proteomic Profiling of Animal Models of Motor Neuron Disease
and Muscular Dystrophy. [Thesis]. RIAN; 2015. Available from: http://mural.maynoothuniversity.ie/6767/
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
21.
Maranis, Sotirios.
Μελέτη της ανάπτυξης φαρμακοεπαγώμενων υπερκινησιών σε πειραματικά μοντέλα νόσου Πάρκισον.
Degree: 2017, University of Ioannina; Πανεπιστήμιο Ιωαννίνων
URL: http://hdl.handle.net/10442/hedi/45014
► Long-term levodopa replacement therapy in Parkinson’s disease is confounded by abnormal involuntary movements, known as Levodopa Induced Dyskinesia (LID). Dysfunctional glutamatergic neurotransmission has been implicated…
(more)
▼ Long-term levodopa replacement therapy in Parkinson’s disease is confounded by abnormal involuntary movements, known as Levodopa Induced Dyskinesia (LID). Dysfunctional glutamatergic neurotransmission has been implicated in the pathogenesis of LID making metabotropic and ionotropic glutamate receptors attractive novel therapeutic targets. The objective was to investigate the antidyskinetic site of action of different glutamate receptor antagonists in the brain. For that purpose, receptor antagonists were administered by intracerebral infusion in the caudate-putamen (CPu), the substantia nigra zona reticulata (SNr) or the subthalamic nucleus (STN) of 6-OHDA-lesioned rats exhibiting LID. Τhe striatum proved important in the antidyskinetic action of NMDA and AMPA receptor antagonists. The metabotropic receptor antagonist demonstrated ani-dykinetic action after administration in subthalamic nucleus. This fact highlights the importance of the metabotropic glutamate receptors that reside in the STN as future therapeutic targets in the treatment of LID.
Η μακρόχρονη θεραπεία με λεβοντόπα επηρεάζεται από την εμφάνιση μη φυσιολογικών ακούσιων κινήσεων, γνωστή ως «επαγόμενη από λεβοντόπα δυσκινησία». Οι δομικές μεταβολές των υποδοχέων του γλουταμικου συμβάλουν στην παθοφυσιολογία της δυσκινησίας. Σε μια προσπάθεια κατανόησης του μηχανισμού καθώς και εντοπισμού της αντι-δυσκινητικής δράσης των ειδικών ανταγωνιστών των γλουταμινικών υποδοχέων πραγματοποιήθηκε ενδοεγκεφαλική έγχυση διαφόρων ανταγωνιστών σε συγκεκριμένους πυρήνες σε επίμυες με δυσκινησία. Η χορήγηση των ανταγωνιστών των NMDA και AMPA υποδοχέων του γλουταμικού μείωσε τη δυσκινησία όταν η έγχυση έγινε στον κερκοφόρο πυρήνα. Από την άλλη μεριά, ο ανταγωνιστής των μεταβοτροπικών υποδοχέων υποτύπου 5 του γλουταμικου παρουσίασε αντιδυσκινητική δράση μόνο μετά από έγχυση του στον υποθαλαμικό πυρήνα καθιστώντας τον σημαντικό μελλοντικό θεραπευτικό στόχο για την αντιμετώπιση της δυσκινησίας.
Subjects/Keywords: Νόσος Πάρκινσον; Υπερκινησία; Πειραματικά μοντέλα; Parkinson's disease; Dyskinesia; Animal models
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APA (6th Edition):
Maranis, S. (2017). Μελέτη της ανάπτυξης φαρμακοεπαγώμενων υπερκινησιών σε πειραματικά μοντέλα νόσου Πάρκισον. (Thesis). University of Ioannina; Πανεπιστήμιο Ιωαννίνων. Retrieved from http://hdl.handle.net/10442/hedi/45014
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Maranis, Sotirios. “Μελέτη της ανάπτυξης φαρμακοεπαγώμενων υπερκινησιών σε πειραματικά μοντέλα νόσου Πάρκισον.” 2017. Thesis, University of Ioannina; Πανεπιστήμιο Ιωαννίνων. Accessed March 07, 2021.
http://hdl.handle.net/10442/hedi/45014.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Maranis, Sotirios. “Μελέτη της ανάπτυξης φαρμακοεπαγώμενων υπερκινησιών σε πειραματικά μοντέλα νόσου Πάρκισον.” 2017. Web. 07 Mar 2021.
Vancouver:
Maranis S. Μελέτη της ανάπτυξης φαρμακοεπαγώμενων υπερκινησιών σε πειραματικά μοντέλα νόσου Πάρκισον. [Internet] [Thesis]. University of Ioannina; Πανεπιστήμιο Ιωαννίνων; 2017. [cited 2021 Mar 07].
Available from: http://hdl.handle.net/10442/hedi/45014.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Maranis S. Μελέτη της ανάπτυξης φαρμακοεπαγώμενων υπερκινησιών σε πειραματικά μοντέλα νόσου Πάρκισον. [Thesis]. University of Ioannina; Πανεπιστήμιο Ιωαννίνων; 2017. Available from: http://hdl.handle.net/10442/hedi/45014
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Missouri – Columbia
22.
Villalón Landeros, Eric, 1986-.
Peripheral nervous system alterations in disease and injury.
Degree: 2016, University of Missouri – Columbia
URL: http://hdl.handle.net/10355/59789
► Charcot-Marie-Tooth (CMT) is the most common inherited neuropathy of the PNS affecting approximately 2.8 million people. CMT type 2E, an axonal form of CMT, has…
(more)
▼ Charcot-Marie-Tooth (CMT) is the most common inherited neuropathy of the PNS affecting approximately 2.8 million people. CMT type 2E, an axonal form of CMT, has been linked to mutations in the neurofilament light gene (nefl) and leads to distal neuropathy characterized by reduced nerve conduction velocity, muscle atrophy and sensory loss. However, the mechanisms of
disease pathogenesis are not well understood. My work characterizes a CMT2E mouse model and reveals new insights into
disease pathogenesis. Moreover, patients suffering with CMT are susceptible to develop exacerbation of neuropathy following a traumatic event. My work also provides insights into exacerbation of neuropathy in our CMT mouse model. Lastly, following remyelination of peripheral nerves after injury, internode lengths are significantly reduced. My work provides the first molecular basis for the reduction in internode length after remyelination and identifies a potential target for therapeutic intervention aimed at enhancing recovery from demyelinating diseases or nerve injuries.
Advisors/Committee Members: Garcia, Michael L., 1968- (advisor).
Subjects/Keywords: Charcot-Marie-Tooth disease; Diseases – Animal models; Nerves, Peripheral; Neuropathy
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APA ·
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Export
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APA (6th Edition):
Villalón Landeros, Eric, 1. (2016). Peripheral nervous system alterations in disease and injury. (Thesis). University of Missouri – Columbia. Retrieved from http://hdl.handle.net/10355/59789
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Villalón Landeros, Eric, 1986-. “Peripheral nervous system alterations in disease and injury.” 2016. Thesis, University of Missouri – Columbia. Accessed March 07, 2021.
http://hdl.handle.net/10355/59789.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Villalón Landeros, Eric, 1986-. “Peripheral nervous system alterations in disease and injury.” 2016. Web. 07 Mar 2021.
Vancouver:
Villalón Landeros, Eric 1. Peripheral nervous system alterations in disease and injury. [Internet] [Thesis]. University of Missouri – Columbia; 2016. [cited 2021 Mar 07].
Available from: http://hdl.handle.net/10355/59789.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Villalón Landeros, Eric 1. Peripheral nervous system alterations in disease and injury. [Thesis]. University of Missouri – Columbia; 2016. Available from: http://hdl.handle.net/10355/59789
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Western Washington University
23.
Minnig, Shawn.
Behavioral Characterization of a Knock-in Mouse Model of Huntington's Disease.
Degree: MS, Psychology, 2016, Western Washington University
URL: https://doi.org/10.25710/f5yg-9v24
;
https://cedar.wwu.edu/wwuet/479
► Huntington’s disease (HD) is a progressive, fatal neurodegenerative disease caused by an inherited CAG expansion on the Huntingtin (HTT) gene resulting in cognitive, affective,…
(more)
▼ Huntington’s
disease (HD) is a progressive, fatal neurodegenerative
disease caused by an inherited CAG expansion on the Huntingtin (
HTT) gene resulting in cognitive, affective, and motor related symptoms. Although clinical diagnosis depends on the presence of Huntington’s chorea, a movement disorder consisting of irregular movements, cognitive symptoms appear 10-15 years prior during the pre-manifest stage of the
disease and are more debilitating to patients. One of the most important advances in HD research has been the generation of mouse
models that recapitulate the features of human HD, allowing researchers to identify the pathogenic mechanisms associated with the
disease and test the potential therapeutic treatments. Unfortunately, many treatments that have been successful in mouse
models have failed to translate to humans when tested in pre-clinical trials. This is partly because experimenters have largely focused on improving late-stage features of HD such as cell death and motor dysfunction, and utilized transgenic mouse that are severely impaired but poorly reproduce the pathogenic processes that underlie the
disease. In contrast, knock-in (KI) mouse
models are genetically faithful to the human condition but remain underutilized in pre-clinical research due to their slower progression and subtle overt phenotype. This thesis characterized the behavioral deficits associated with the <em>Htt
Q111/+ </em>KI mouse model of HD and discovered novel cognitive phenotypes that are characteristic of the pre-manifest stage of the
disease. At nine months of age, <em>Htt
Q111/+ </em>mice display improved procedural memory on the two-cue MWM, hypoactivity, reduced velocity, and increased anxiety during open field exploration, and intact spatial LTM with a reduction in the total number of investigations toward both objects during an object location task. Together, these tasks provide a number of robust behavioral phenotypes for use in pre-clinical research conducted in the <em>Htt
Q111/+ </em>mouse model of HD in the future.
Advisors/Committee Members: Carroll, Jeffrey B. (Jeffrey Bryan), 1977-, Grimm, Jeffrey W., Symons, Larry.
Subjects/Keywords: Psychology; Huntington's disease – Animal models; Huntington's disease – Research; Mice as laboratory animals – Behavior; masters theses
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APA (6th Edition):
Minnig, S. (2016). Behavioral Characterization of a Knock-in Mouse Model of Huntington's Disease. (Masters Thesis). Western Washington University. Retrieved from https://doi.org/10.25710/f5yg-9v24 ; https://cedar.wwu.edu/wwuet/479
Chicago Manual of Style (16th Edition):
Minnig, Shawn. “Behavioral Characterization of a Knock-in Mouse Model of Huntington's Disease.” 2016. Masters Thesis, Western Washington University. Accessed March 07, 2021.
https://doi.org/10.25710/f5yg-9v24 ; https://cedar.wwu.edu/wwuet/479.
MLA Handbook (7th Edition):
Minnig, Shawn. “Behavioral Characterization of a Knock-in Mouse Model of Huntington's Disease.” 2016. Web. 07 Mar 2021.
Vancouver:
Minnig S. Behavioral Characterization of a Knock-in Mouse Model of Huntington's Disease. [Internet] [Masters thesis]. Western Washington University; 2016. [cited 2021 Mar 07].
Available from: https://doi.org/10.25710/f5yg-9v24 ; https://cedar.wwu.edu/wwuet/479.
Council of Science Editors:
Minnig S. Behavioral Characterization of a Knock-in Mouse Model of Huntington's Disease. [Masters Thesis]. Western Washington University; 2016. Available from: https://doi.org/10.25710/f5yg-9v24 ; https://cedar.wwu.edu/wwuet/479
24.
Francisco Edson Ximenes Gomes Pereira.
Development and a form of endometriose validation subcutaneous under study for possible mechanisms of rats phatophysiological and drug effect.
Degree: Master, 2013, Universidade Federal do Ceará
URL: http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=14411
;
► Endometriosis is defined as the presence of endometrial tissue (gland and stroma) outside the uterus. The objective of this study was to design a model…
(more)
▼ Endometriosis is defined as the presence of endometrial tissue (gland and stroma) outside the uterus. The objective of this study was to design a model of subcutaneous endometriosis in rats for the evaluation of the effect of drugs and the pathophysiology of endometriosis. Initially, female Wistar rats (Rattus norvergicus) were implanted subcutaneously with 4x4 mm uterine fragments to evaluate endometrioma growth after 1, 7, 14 and 21 days. Endometrial tissue implants were confirmed by histological analysis. The greatest relative weight gain was observed on the 14th day (wet weight 29.17 Â 6.79 mg%; dry weight 5.36 Â 0.97 mg%). Subsequently, animals were assigned to treatment groups and given either estradiol (2.5 mg/kg, 5 mg/kg, 10 mg/kg sc), medroxyprogesterone acetate (0.5 mg/kg, 2 mg/kg, 5 mg/kg sc), triptorelin pamoate (0.18 mg/kg, 0.56 mg/kg sc) and acetylsalicylic acid (3 mg/kg gavage) on the fifth day following implantation. Wet and dry relative weight of the endometrioma were used as a indicator of growth for model of endometriosis. In the group treated with estradiol, the average wet weight and dry weight on the 14 th day following implantation was 36.62 Â 4.97 mg% and 3.97 Â 1 mg% (2.5 mg), 56.37 Â 20.19 mg% and 9.11 Â 3.85 mg% (5 mg), and 173.89 Â 69.53 mg% and 27.67 Â 10.27 mg% (10 mg), respectively. In the group treated with medroxyprogesterone acetate, the corresponding figures were 13.58 Â 2.53 mg% and 2.67 Â 0.5 mg% (0.5 mg), 14.29 Â 2.07 mg% and 3.71 Â 1.31 mg% (2 mg), and 15.33 Â 7.08 mg% and 2.68 Â 1.44 mg% (5 mg). In the group treated with triptorelin pamoate, the corresponding figures were 20.04 Â 4.02 mg% and 5.21 Â 1.54 mg% (0.18 mg), and 10.86 Â 1.88 mg% and 1.89 Â 0.29 mg% (0.56 mg). In the group treated with 3 mg acetylsalicylic acid, the corresponding figures were 12.81 Â 2.04 mg% and 2.09 Â 0.4 mg%. In the estradiol group, growth gain was dose-dependent: animals receiving 10 mg differed significantly from animals receiving lower doses and from untreated animals (p<0.0001). In conclusion, the model was found to be reproducible and easy to use.
A endometriose à definida como a presenÃa de tecido endometrial (glÃndula e estroma) fora do Ãtero (mais precisamente revestimento endometrial). O objetivo foi desenvolver e validar um modelo de endometriose subcutÃnea em ratas para estudo de provÃveis mecanismos fisiopatolÃgicos e do efeito de drogas. Inicialmente, as ratas (Rattus norvergicus, linhagem Wistar) foram implantadas subcutaneamente com fragmentos uterinos 4x4 mm para avaliar o crescimento de endometrioma apÃs 1, 7, 14 e 21dias. Implantes de tecido endometrial foram confirmados por anÃlise histolÃgica. O maior ganho de peso relativo do endometrioma foi observado no dia 14 (peso Ãmido relativo 29,1  6,79 mg%, peso seco relativo 5,36  0,97 mg%). Posteriormente, os animais foram divididos em grupos e receberam estradiol (2,5 mg/kg, 5 mg/kg, 10 mg/kg sc), acetato de medroxiprogesterona (0,5 mg/kg, 2 mg/kg, 5 mg/kg sc), pamoato de triptorrelina (0,18 mg/kg, 0,56 mg/kg sc) e Ãcido…
Advisors/Committee Members: Francisco das Chagas Medeiros, Maria Angelina da Silva Medeiros, Luciano Silveira Pinheiro.
Subjects/Keywords: CIRURGIA; Endometriose; Modelos Animais; Modelos Animais de DoenÃas; Ratos; Endometriosis; Models, Animal; Disease Models, Animal; Rats
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APA (6th Edition):
Pereira, F. E. X. G. (2013). Development and a form of endometriose validation subcutaneous under study for possible mechanisms of rats phatophysiological and drug effect. (Masters Thesis). Universidade Federal do Ceará. Retrieved from http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=14411 ;
Chicago Manual of Style (16th Edition):
Pereira, Francisco Edson Ximenes Gomes. “Development and a form of endometriose validation subcutaneous under study for possible mechanisms of rats phatophysiological and drug effect.” 2013. Masters Thesis, Universidade Federal do Ceará. Accessed March 07, 2021.
http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=14411 ;.
MLA Handbook (7th Edition):
Pereira, Francisco Edson Ximenes Gomes. “Development and a form of endometriose validation subcutaneous under study for possible mechanisms of rats phatophysiological and drug effect.” 2013. Web. 07 Mar 2021.
Vancouver:
Pereira FEXG. Development and a form of endometriose validation subcutaneous under study for possible mechanisms of rats phatophysiological and drug effect. [Internet] [Masters thesis]. Universidade Federal do Ceará 2013. [cited 2021 Mar 07].
Available from: http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=14411 ;.
Council of Science Editors:
Pereira FEXG. Development and a form of endometriose validation subcutaneous under study for possible mechanisms of rats phatophysiological and drug effect. [Masters Thesis]. Universidade Federal do Ceará 2013. Available from: http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=14411 ;
Northeastern University
25.
Barchet, Thomas Matthew.
Novel MRI approaches to the detection and evaluation of neurodegenerative disease.
Degree: PhD, School of Pharmacy, 2015, Northeastern University
URL: http://hdl.handle.net/2047/D20196171
► This dissertation describes a novel approach to noninvasively evaluating animal models of neurodegeneration using magnetic resonance imaging. This work includes studies of three separate models…
(more)
▼ This dissertation describes a novel approach to noninvasively evaluating animal models of neurodegeneration using magnetic resonance imaging. This work includes studies of three separate models of central nervous system disease in which MRI diffusion measurements revealed tissue alterations consistent with the tissue damage known to occur in each model.; The first part presents a fluid-percussion model of traumatic brain injury (TBI). The results of this study demonstrate that percussive injury on two different cortical sites share diffusionally affected subcortical regions. The gray matter regions identified in this study are consistent with the reported damage that occurs after TBI occurs in patients, suggesting that this animal model is highly relevant in the study of TBI, and DTI methods may improve the differential diagnosis of TBI subtypes.; The later part of this dissertation includes work with two models of Parkinson's disease (PD). In a neurotoxin model of PD using systemic exposure to a slow-release formulation of rotenone, the animal develops many pathologies associated with clinical PD. In the PINK1 knockout rat model of PD, the results showed that the model develops a mild PD phenotype with decreased motor activity and altered olfactory response. In both models, there were many extranigral regions identified as having diffusional changes, many of which have been reported to be affected in clinical PD.; This is a novel means of noninvasively identifying CNS changes in neurodegeneration. Without limiting analysis to a priori brain region selection, many affected parts of the brain can be discovered in a single imaging study. These region-wise, whole-brain results can be further investigated to characterize neuropathologies occurring outside the principle injury (distal neurodegeneration in the TBI model) or classically defined disease progression (extranigral changes in PD models). Finding noninvasive imaging biomarkers for CNS disease, as performed in this preclinical work, is paramount to clinical study of disease, where quantitative disease staging based on neuropathology could replace subjective evaluations. This may enable more meaningful recruitment for clinical trials and objective measurement of therapeutic interventions.
Subjects/Keywords: biomarkers; MRI; neurodegeneration; Nervous system; Degeneration; Animal models; Brain; Magnetic resonance imaging; Brain; Wounds and injuries; Animal models; Alzheimer's disease; Animal models; Biochemical markers; Diffusion tensor imaging
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APA (6th Edition):
Barchet, T. M. (2015). Novel MRI approaches to the detection and evaluation of neurodegenerative disease. (Doctoral Dissertation). Northeastern University. Retrieved from http://hdl.handle.net/2047/D20196171
Chicago Manual of Style (16th Edition):
Barchet, Thomas Matthew. “Novel MRI approaches to the detection and evaluation of neurodegenerative disease.” 2015. Doctoral Dissertation, Northeastern University. Accessed March 07, 2021.
http://hdl.handle.net/2047/D20196171.
MLA Handbook (7th Edition):
Barchet, Thomas Matthew. “Novel MRI approaches to the detection and evaluation of neurodegenerative disease.” 2015. Web. 07 Mar 2021.
Vancouver:
Barchet TM. Novel MRI approaches to the detection and evaluation of neurodegenerative disease. [Internet] [Doctoral dissertation]. Northeastern University; 2015. [cited 2021 Mar 07].
Available from: http://hdl.handle.net/2047/D20196171.
Council of Science Editors:
Barchet TM. Novel MRI approaches to the detection and evaluation of neurodegenerative disease. [Doctoral Dissertation]. Northeastern University; 2015. Available from: http://hdl.handle.net/2047/D20196171
University of Zambia
26.
Muyenga, Tumelo.
The effect of Kigelia Africana fruit extract on blood glucose in diabetes induced mice
.
Degree: 2015, University of Zambia
URL: http://dspace.unza.zm:8080/xmlui/handle/123456789/4401
► Objective: To determine the effect Kigelia africana fruit extract has on blood glucose levels of diabetes mice and its phytochemical profile Specific objectives: 1. To…
(more)
▼ Objective: To determine the effect Kigelia africana fruit extract has on blood glucose levels of diabetes mice and its phytochemical profile
Specific objectives:
1. To determine Kigelia africana fruit extracts’ effect on blood glucose levels when used alone and concomitantly with Glibenclamide on mice.
2. To identify the basic phytochemical composition of the fruit extract.
Design: An analytical study involving aqueous and organic extraction of the fruit, conducting phytochemical analysis of the extract and treating diabetes induced mice bred in Physiological Sciences Department of University of Zambia with the extract.
Setting: Departments of Chemistry and Physiological Sciences of the University of Zambia
Method: 35 albino mice (18-30g) allocated in 5 groups of 7 according to treatment. Group 1- Kigelia fruit extract 1000mg/kg, Group 2- Kigelia fruit extract 500mg/kg, Group 3- Glibenclamide 0.25 mg/kg, Group 4- Kigelia fruit extract 500mg/kg and Glibenclamide 0.25mg/kg and Group 5- Normal Saline.
Aqueous and organic extracts were collected from fruit sample by boiling and maceration respectively and tested for tannins, saponins, flavonoids, alkaloids, glycosides and steroids.
Main outcome measures: RBS sugar of below 8mmol/l.
Results: The results showed a greater reduction in blood glucose of mice after treatment with Kigelia extract 1000mg/kg compared to Kigelia 500mg/kg [(5.3 +/- 0.5mmol/l) vs (6.3+/- 0.6mmol/l), (p= 0.005)]. Further, Glibenclamide 0.25mg/kg showed less reduction in blood glucose than Kigelia 1000mg/kg [(7.4+/-0.9mmol/l) vs (5.3 +/- 0.5), (p= 0.00)]. The mean blood glucose levels were lower in mice that received Kigelia extract than those that received both Kigelia extract and Glibenclamide [(5.3 +/- 0.5mmol/l) vs (7.8 +/- 0.6 mmol/l), (p=0.00)]
The fruit extract tested positive for Tannins, Saponins, Flavanoids, Alkaloids, Glycosides and Steroids.
Conclusion: Findings of this study indicate that Kigelia africana fruit extract causes reduction in blood glucose of diabetes induced mice and gives better results when used alone than in concomitant use with Glibenclamide. The study also indicates that the fruit extract has alkaloids, saponins, steroids, glycosides, tannins and flavonoids.
Subjects/Keywords: Diabetes Mellitus;
Diabetes-Animal Model;
Mice-Effect of drugs on;
Disease models, Animals;
Mice
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APA ·
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APA (6th Edition):
Muyenga, T. (2015). The effect of Kigelia Africana fruit extract on blood glucose in diabetes induced mice
. (Thesis). University of Zambia. Retrieved from http://dspace.unza.zm:8080/xmlui/handle/123456789/4401
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Muyenga, Tumelo. “The effect of Kigelia Africana fruit extract on blood glucose in diabetes induced mice
.” 2015. Thesis, University of Zambia. Accessed March 07, 2021.
http://dspace.unza.zm:8080/xmlui/handle/123456789/4401.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Muyenga, Tumelo. “The effect of Kigelia Africana fruit extract on blood glucose in diabetes induced mice
.” 2015. Web. 07 Mar 2021.
Vancouver:
Muyenga T. The effect of Kigelia Africana fruit extract on blood glucose in diabetes induced mice
. [Internet] [Thesis]. University of Zambia; 2015. [cited 2021 Mar 07].
Available from: http://dspace.unza.zm:8080/xmlui/handle/123456789/4401.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Muyenga T. The effect of Kigelia Africana fruit extract on blood glucose in diabetes induced mice
. [Thesis]. University of Zambia; 2015. Available from: http://dspace.unza.zm:8080/xmlui/handle/123456789/4401
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
27.
Ioshimoto, Gabriela Lourençon.
Estudo da eletrorretinografia do camundongo modelo de alzheimer (3xTg-AD).
Degree: Mestrado, Neurociências e Comportamento, 2011, University of São Paulo
URL: http://www.teses.usp.br/teses/disponiveis/47/47135/tde-28042011-155725/
;
► Objetivo: Avaliar eletrofisiologicamente a função da retina do camundongo modelo de Alzheimer (3xTg-AD) comparando com seu controle (b6;129-PS1) em um estudo longitudinal com seis idades…
(more)
▼ Objetivo: Avaliar eletrofisiologicamente a função da retina do camundongo modelo de Alzheimer (3xTg-AD) comparando com seu controle (b6;129-PS1) em um estudo longitudinal com seis idades (2, 4, 6, 8, 10 e 12 meses). Métodos: Eletrorretinogramas (ERGs) foram registrados em 44 camundongos 3xTg-AD e em 23 controles, após administrada anestesia. Para o registro foi colocado um eletrodo de lente de contato sobre a córnea, um eletrodo de referência na cabeça e um terra na cauda. Em sessão de 30-40min de duração foram expostos ao seguinte protocolo de estimulação: 1) Adaptação ao escuro seguida de flashes nas intensidades: 0,003; 0,03; 0,3; 3 e 30 cd.s/m2; 2) Estimulação periódica (30 cd.s/m2) nas freqüências de 12, 18, e 30 Hz, sob luz de fundo (30 cd/m2). Resultados: Os ERGs mostraram dois tipos de respostas escotópicas tanto no grupo dos camundongos controles (b6;129- PS1) quanto nos modelos de Alzheimer. 13% dos camundongos controles e 72% dos modelos de AD apresentaram ERGs com potenciais oscilatórios presentes e tempo implícito da onda-b dentro da faixa esperada (45,31 ± 6,74 ms), enquanto no restante dos grupos, o ERG apresentou latência da onda-b muito aumentada (111,73 ± 22,56 ms) e potenciais oscilatórios ausentes. Devido a estes resultados, os grupos controle e experimental foram subdivididos em: b6;129 com OP, b6;129 sem OP; 3xTg-AD com OP e 3xTg-AD sem OP. Também foi incluído um grupo controle adicional constituído por 9 camundongos C57/B6. Comparando os cinco grupos, nenhuma diferença foi encontrada em relação à amplitude e à latência da onda-a. A amplitude da onda-b também foi semelhante para todos, ao contrário da latência para atingir o pico da onda-b dos grupos b6;129 sem OP e 3xTg-AD sem OP, que se apresentou duas vezes maior do que nos grupos com OP. As amplitudes dos cinco potenciais oscilatórios foram medidas individualmente e não mostraram diferenças entre os controles e os 3xTg-AD. Para o estímulo periódico, a amplitude do 1º harmônico dos grupos com OP mostrou clara diferença entre os grupos controle e o 3xTg-AD, tanto em 12 Hz como em 18 Hz. Os resultados dos dois grupos controle b6;129 e C57/B6 mantiveram-se muito próximos. Os grupos sem OP mantiveram-se sempre próximos a 10 V para as três freqüências de estimulação e mostraram atraso na diferença de fase média do 1º harmônico em 18 e 30 Hz, indicando maior lentidão de resposta, quando comparados aos primeiros. Conclusão: O camundongo 3xTg-AD e seu controle (b6;129) apresentam uma variante lenta e sem OPs do ERG escotópico em parte da população. Células bipolares, amácrinas e ganglionares podem estar alteradas nesses subgrupos (b6;129 sem OP e 3xTg-AD sem OP). Os grupos controle e 3xTg-AD com OPs diferiram quanto à amplitude de resposta à estimulação intermitente, diferença essa que implica em menor capacidade de processamento temporal para o modelo de AD. Sugerimos que as células bipolares de cones podem estar alteradas nos modelos de AD devido às amplitudes mais baixas dos 1os harmônicos desse grupo
Objective: To evaluate…
Advisors/Committee Members: Ventura, Dora Selma Fix.
Subjects/Keywords: Alzheimer disease; Animal models; Camundongos; Doença de Alzheimer; Electroretinography; Eletrorretinografia; Mice; Modelos animais
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APA (6th Edition):
Ioshimoto, G. L. (2011). Estudo da eletrorretinografia do camundongo modelo de alzheimer (3xTg-AD). (Masters Thesis). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/47/47135/tde-28042011-155725/ ;
Chicago Manual of Style (16th Edition):
Ioshimoto, Gabriela Lourençon. “Estudo da eletrorretinografia do camundongo modelo de alzheimer (3xTg-AD).” 2011. Masters Thesis, University of São Paulo. Accessed March 07, 2021.
http://www.teses.usp.br/teses/disponiveis/47/47135/tde-28042011-155725/ ;.
MLA Handbook (7th Edition):
Ioshimoto, Gabriela Lourençon. “Estudo da eletrorretinografia do camundongo modelo de alzheimer (3xTg-AD).” 2011. Web. 07 Mar 2021.
Vancouver:
Ioshimoto GL. Estudo da eletrorretinografia do camundongo modelo de alzheimer (3xTg-AD). [Internet] [Masters thesis]. University of São Paulo; 2011. [cited 2021 Mar 07].
Available from: http://www.teses.usp.br/teses/disponiveis/47/47135/tde-28042011-155725/ ;.
Council of Science Editors:
Ioshimoto GL. Estudo da eletrorretinografia do camundongo modelo de alzheimer (3xTg-AD). [Masters Thesis]. University of São Paulo; 2011. Available from: http://www.teses.usp.br/teses/disponiveis/47/47135/tde-28042011-155725/ ;
Edith Cowan University
28.
Avdesh, Avdesh.
Pharmacological modulation of learning and memory in mice and zebrafish: Implications for Alzheimer’s disease animal models.
Degree: 2013, Edith Cowan University
URL: https://ro.ecu.edu.au/theses/570
► Learning and memory impairments are the clinical manifestations of several neurodegenerative disorders including Alzheimer’s disease (AD), the most common form of dementia affecting millions of…
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▼ Learning and memory impairments are the clinical manifestations of several neurodegenerative disorders including Alzheimer’s disease (AD), the most common form of dementia affecting millions of people worldwide. Current AD treatments target cognitive decline or failure and provide only minor benefits across the array of clinical symptoms. The development of numerous treatment strategies have been trailed in pre-clinical, or human clinical trials. One of the potential candidates to be used for cognitive enhancement is CB1 cannabinoid receptor antagonist. CB1 cannabinoid receptor antagonists have been shown to improve learning and memory in rodents, whereas CB1 cannabinoid receptor agonists have been shown to impair memory. The project has overall aims of (1) investigating the role of CB1 receptors in learning and memory, and assessing the potential of a CB1 receptor antagonist (SR141716A) as a novel cognitive enhancer in mice models; (2) Assessing the potential of zebrafish as an alternative in vivo model for the high-through put assessment of learning and memory. The involvement of cannabinoid CB1 (CB1) receptors in associative learning in two strains of mice (i.e., C57BL/6J and C3H/HeJ) were first investigated. Here, the effects of the cannabinoid CB1 receptor agonist (i.e., CP55940) and antagonist (i.e., SR141716A) on associative learning were assessed in mice using eight-arm radial maze. The results showed that the CB1 receptor agonist impaired reference memory in C57BL/6J but not in C3H/HeJ strains, and the former effect was probably mediated by CB1 receptors since the selective antagonist, SR141716A, reversed these effects. The CP55940 agonist also impaired working memory selectively in the C57BL/6J mice, which was not affected by SR141716A. This study provided evidence for a strain- specific effect of CP55940 on working memory that is likely to be independent of the CB1 receptors. Cannabinoid receptor effects were also evaluated on non-associative learning in mice by measuring habituation of acoustic startle reflex (ASR). CB1 receptor agonist and antagonist's effects were assessed in two different strains of mice (i.e., C57BL/6J and C3H/HeJ). The findings further supported the strain-specific effects of CP55940. This agonist decreased habituation of the ASR in C57BL/6J, but increased habituation in C3H/HeJ. Both of these measures were reversed by SR141716A. This indicates that the cannabinoid agonist exerts its effects on non-associative learning and memory in both strains of mice via CB1 receptors. The advantages of zebrafish in comparison to other common vertebrate models including high fecundity, low maintenance cost, transparent embryos, and rapid development are some reasons for its popularity in genetics, pharmacological and behavioural research. As vertebrates, zebrafish share considerable sequence similarity with humans and are being used as an animal model for various human disease conditions. Here a video and written protocol is presented for the regular care and maintenance of a zebrafish laboratory…
Subjects/Keywords: Learning and memory; mice; zebrafish; Alzheimer's disease; animal models; pharmacological modulation; Medical Sciences
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APA ·
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APA (6th Edition):
Avdesh, A. (2013). Pharmacological modulation of learning and memory in mice and zebrafish: Implications for Alzheimer’s disease animal models. (Thesis). Edith Cowan University. Retrieved from https://ro.ecu.edu.au/theses/570
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Avdesh, Avdesh. “Pharmacological modulation of learning and memory in mice and zebrafish: Implications for Alzheimer’s disease animal models.” 2013. Thesis, Edith Cowan University. Accessed March 07, 2021.
https://ro.ecu.edu.au/theses/570.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Avdesh, Avdesh. “Pharmacological modulation of learning and memory in mice and zebrafish: Implications for Alzheimer’s disease animal models.” 2013. Web. 07 Mar 2021.
Vancouver:
Avdesh A. Pharmacological modulation of learning and memory in mice and zebrafish: Implications for Alzheimer’s disease animal models. [Internet] [Thesis]. Edith Cowan University; 2013. [cited 2021 Mar 07].
Available from: https://ro.ecu.edu.au/theses/570.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Avdesh A. Pharmacological modulation of learning and memory in mice and zebrafish: Implications for Alzheimer’s disease animal models. [Thesis]. Edith Cowan University; 2013. Available from: https://ro.ecu.edu.au/theses/570
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Western Ontario
29.
Lai-Zhao, Yue.
The Role of Synovium and Synovial Macrophages in Experimental Post-Traumatic Knee Osteoarthritis.
Degree: 2020, University of Western Ontario
URL: https://ir.lib.uwo.ca/etd/7075
► In osteoarthritis (OA), synovitis is associated with symptom severity. As synovium secretes both catabolic and anabolic factors into the joint, the impact of synovitis in…
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▼ In osteoarthritis (OA), synovitis is associated with symptom severity. As synovium secretes both catabolic and anabolic factors into the joint, the impact of synovitis in OA remains unclear. We developed a novel co-culture system using tissues from an established rat model of post-traumatic knee OA (PTOA) to study signaling between synovium and chondrocytes. We found that synovium from early stage but not later stage PTOA joints caused an overall protective effect in chondrocytes. We then selectively treated synovial macrophages with liposomal drugs causing depletion, STAT1 inhibition, or STAT6 inhibition in early PTOA joints. We found cartilage damage in vivo was not affected, but chondrocyte responses to treated synovium in vitro indicate that STAT1 inhibition could be protective, while STAT6 inhibition is potentially pro-inflammatory. Thus, we demonstrate that synovial signals affect chondrocyte physiology in the OA knee joint and that targeting synovial macrophages as a potential therapeutic strategy warrants further investigation.
Subjects/Keywords: Animal models of disease; chondrocyte; inflammation; liposomal drug delivery; STAT inhibitors; tissue culture.; Musculoskeletal Diseases
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APA ·
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APA (6th Edition):
Lai-Zhao, Y. (2020). The Role of Synovium and Synovial Macrophages in Experimental Post-Traumatic Knee Osteoarthritis. (Thesis). University of Western Ontario. Retrieved from https://ir.lib.uwo.ca/etd/7075
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Lai-Zhao, Yue. “The Role of Synovium and Synovial Macrophages in Experimental Post-Traumatic Knee Osteoarthritis.” 2020. Thesis, University of Western Ontario. Accessed March 07, 2021.
https://ir.lib.uwo.ca/etd/7075.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Lai-Zhao, Yue. “The Role of Synovium and Synovial Macrophages in Experimental Post-Traumatic Knee Osteoarthritis.” 2020. Web. 07 Mar 2021.
Vancouver:
Lai-Zhao Y. The Role of Synovium and Synovial Macrophages in Experimental Post-Traumatic Knee Osteoarthritis. [Internet] [Thesis]. University of Western Ontario; 2020. [cited 2021 Mar 07].
Available from: https://ir.lib.uwo.ca/etd/7075.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Lai-Zhao Y. The Role of Synovium and Synovial Macrophages in Experimental Post-Traumatic Knee Osteoarthritis. [Thesis]. University of Western Ontario; 2020. Available from: https://ir.lib.uwo.ca/etd/7075
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Toronto
30.
McPhail, Mike Grant.
Histopathology in Skeletal Muscle of Transgenic Mice Suggests Dual-Locus of Onset (DLO) in Kennedy's Disease.
Degree: 2014, University of Toronto
URL: http://hdl.handle.net/1807/68596
► Kennedy's Disease or Spinal-Bulbar Muscular Atrophy (KD/SBMA) is a neuromuscular disease associated with a CAG tri-nucleotide repeat expansion within the androgen receptor (AR) gene. Mouse…
(more)
▼ Kennedy's Disease or Spinal-Bulbar Muscular Atrophy (KD/SBMA) is a neuromuscular disease associated with a CAG tri-nucleotide repeat expansion within the androgen receptor (AR) gene. Mouse models of KD used in this investigation expressed mutant AR either in motor neurons (HB9/AR113 mice) or skeletal muscle (HSA/AR113 mice), revealing abnormalities within the extensor digitorum longus (EDL) and soleus (SOL) muscles. Reduced oxidative metabolism was observed in both HB9/AR113 and HSA/AR113 mice, while a fiber-type switch and a reduction in cell size were only observed in HSA/AR113 mice. Deficits in fiber number and endurance strength were found in HB9/AR113 mice only. These findings support the DLO hypothesis, suggesting that onset of KD involves pathology in motor neurons, and perhaps skeletal muscle. Notably, in vivo evidence of pathology in HB9/AR113 mice is an original finding of this investigation.
M.Sc.
Advisors/Committee Members: Monks, A Douglas, Medical Science.
Subjects/Keywords: Animal Models; Histopathology; Kennedy's Disease; Neuromuscular; polyQ Disorders; Spinal-Bulbar Muscular Atrophy; 0306
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APA ·
Chicago ·
MLA ·
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Export
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APA (6th Edition):
McPhail, M. G. (2014). Histopathology in Skeletal Muscle of Transgenic Mice Suggests Dual-Locus of Onset (DLO) in Kennedy's Disease. (Masters Thesis). University of Toronto. Retrieved from http://hdl.handle.net/1807/68596
Chicago Manual of Style (16th Edition):
McPhail, Mike Grant. “Histopathology in Skeletal Muscle of Transgenic Mice Suggests Dual-Locus of Onset (DLO) in Kennedy's Disease.” 2014. Masters Thesis, University of Toronto. Accessed March 07, 2021.
http://hdl.handle.net/1807/68596.
MLA Handbook (7th Edition):
McPhail, Mike Grant. “Histopathology in Skeletal Muscle of Transgenic Mice Suggests Dual-Locus of Onset (DLO) in Kennedy's Disease.” 2014. Web. 07 Mar 2021.
Vancouver:
McPhail MG. Histopathology in Skeletal Muscle of Transgenic Mice Suggests Dual-Locus of Onset (DLO) in Kennedy's Disease. [Internet] [Masters thesis]. University of Toronto; 2014. [cited 2021 Mar 07].
Available from: http://hdl.handle.net/1807/68596.
Council of Science Editors:
McPhail MG. Histopathology in Skeletal Muscle of Transgenic Mice Suggests Dual-Locus of Onset (DLO) in Kennedy's Disease. [Masters Thesis]. University of Toronto; 2014. Available from: http://hdl.handle.net/1807/68596
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Open Access Theses and Dissertations