subject:(mouse)

1. Lau, Bonnie W. CXCR4/SDF1 in recruitment of stem cells to orthotopic murine malignant mesothelioma spheroids.

Degree: PhD, Division of Biology and Medicine. Pathobiology, 2009, Brown University

URL: https://repository.library.brown.edu/studio/item/bdr:148/

► Malignant mesothelioma is an aggressive cancer of the mesothelial lining causally linked to asbestos exposure and is highly resistant to current therapies. We hypothesize a… (more)

▼ Malignant mesothelioma is an aggressive cancer of the mesothelial lining causally linked to asbestos exposure and is highly resistant to current therapies. We hypothesize a stem/progenitor cell population is recruited to the tumor and contributes to tumor cell growth and progression. Using an orthotopic murine tumor spheroid model shown to recapitulate human malignant mesothelioma, we identified a stem cell antigen-1 (Sca-1) positive cell population recruited to tumor spheroids in vivo. The Sca-1+ cell population was characterized by immunofluorescence staining and flow cytometry. Candidate chemokines involved in recruitment of this stem/progenitor cell population were identified with SuperArrayTM, and confirmed with ELISA and transwell migration assays. To test whether this recruited cell population contributes to tumor cell proliferation, malignant mesothelioma cells were grown in conditioned media from in vitro cultures and tumor cell proliferation was assessed. To test whether this cell population contributes to tumor progression in vivo, tumor cell-injected mice were treated with chemotactic inhibitors and tumor burden was assessed as compared to vehicle-injected control mice. The Sca-1+ cell population co-expresses markers for T lymphocytes, hematopoietic stem cells and mesenchymal stem cells. The tumor microenvironment expresses the chemokine SDF-1/CXCL12 and the cognate receptor CXCR4 that are involved in recruitment of these cell types. Involvement of the CXCR4/SDF1 chemotactic axis was confirmed when transwell migration of mesenchymal stem cells to lavage fluid was abrogated by treatment with small molecule inhibitors of CXCR4. Once recruited, this stem/progenitor cell population secretes factors that increase tumor cell proliferation. In conclusion, a stem/progenitor cell population is recruited to malignant mesothelioma spheroids, secretes factors that promote tumor cell growth and is a potentially novel therapeutic target. Advisors/Committee Members: Kane, Agnes (director), Broaddus, Courtney (reader), Padbury, James (reader), Morgan, Jeffrey (reader), Zhitkovich, Anatoly (reader).

Subjects/Keywords: mouse model

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APA (6^th Edition):

Lau, B. W. (2009). CXCR4/SDF1 in recruitment of stem cells to orthotopic murine malignant mesothelioma spheroids. (Doctoral Dissertation). Brown University. Retrieved from https://repository.library.brown.edu/studio/item/bdr:148/

Chicago Manual of Style (16^th Edition):

Lau, Bonnie W. “CXCR4/SDF1 in recruitment of stem cells to orthotopic murine malignant mesothelioma spheroids.” 2009. Doctoral Dissertation, Brown University. Accessed February 27, 2021. https://repository.library.brown.edu/studio/item/bdr:148/.

MLA Handbook (7^th Edition):

Lau, Bonnie W. “CXCR4/SDF1 in recruitment of stem cells to orthotopic murine malignant mesothelioma spheroids.” 2009. Web. 27 Feb 2021.

Vancouver:

Lau BW. CXCR4/SDF1 in recruitment of stem cells to orthotopic murine malignant mesothelioma spheroids. [Internet] [Doctoral dissertation]. Brown University; 2009. [cited 2021 Feb 27]. Available from: https://repository.library.brown.edu/studio/item/bdr:148/.

Council of Science Editors:

Lau BW. CXCR4/SDF1 in recruitment of stem cells to orthotopic murine malignant mesothelioma spheroids. [Doctoral Dissertation]. Brown University; 2009. Available from: https://repository.library.brown.edu/studio/item/bdr:148/

University of Toronto

2. Kim, Dennis. Molecular Genetic Analysis of the Mouse Anorexia Mutation.

Degree: 2010, University of Toronto

URL: http://hdl.handle.net/1807/32211

►

The serotonergic system regulates numerous behaviours and disruptions in this system have been associated with disorders of mood and mind. Although molecular genetic analysis has… (more)

Subjects/Keywords: serotonin; mouse; 0369

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APA (6^th Edition):

Kim, D. (2010). Molecular Genetic Analysis of the Mouse Anorexia Mutation. (Masters Thesis). University of Toronto. Retrieved from http://hdl.handle.net/1807/32211

Chicago Manual of Style (16^th Edition):

Kim, Dennis. “Molecular Genetic Analysis of the Mouse Anorexia Mutation.” 2010. Masters Thesis, University of Toronto. Accessed February 27, 2021. http://hdl.handle.net/1807/32211.

MLA Handbook (7^th Edition):

Kim, Dennis. “Molecular Genetic Analysis of the Mouse Anorexia Mutation.” 2010. Web. 27 Feb 2021.

Vancouver:

Kim D. Molecular Genetic Analysis of the Mouse Anorexia Mutation. [Internet] [Masters thesis]. University of Toronto; 2010. [cited 2021 Feb 27]. Available from: http://hdl.handle.net/1807/32211.

Council of Science Editors:

Kim D. Molecular Genetic Analysis of the Mouse Anorexia Mutation. [Masters Thesis]. University of Toronto; 2010. Available from: http://hdl.handle.net/1807/32211

Dalhousie University

3. King, Jillian. Visual Adaptation in Mouse Primary Visual Cortex.

Degree: MS, Department of Psychology and Neuroscience, 2014, Dalhousie University

URL: http://hdl.handle.net/10222/55995

► Studying vision in mice is a relatively recent endeavor, with most research dating within the last 10 years. One goal of this research is to… (more)

Subjects/Keywords: mouse; vision; adaptation

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APA (6^th Edition):

King, J. (2014). Visual Adaptation in Mouse Primary Visual Cortex. (Masters Thesis). Dalhousie University. Retrieved from http://hdl.handle.net/10222/55995

Chicago Manual of Style (16^th Edition):

King, Jillian. “Visual Adaptation in Mouse Primary Visual Cortex.” 2014. Masters Thesis, Dalhousie University. Accessed February 27, 2021. http://hdl.handle.net/10222/55995.

MLA Handbook (7^th Edition):

King, Jillian. “Visual Adaptation in Mouse Primary Visual Cortex.” 2014. Web. 27 Feb 2021.

Vancouver:

King J. Visual Adaptation in Mouse Primary Visual Cortex. [Internet] [Masters thesis]. Dalhousie University; 2014. [cited 2021 Feb 27]. Available from: http://hdl.handle.net/10222/55995.

Council of Science Editors:

King J. Visual Adaptation in Mouse Primary Visual Cortex. [Masters Thesis]. Dalhousie University; 2014. Available from: http://hdl.handle.net/10222/55995

University of Adelaide

4. Shahrin, Nur Hezrin. Investigation of KLF5 function in normal haemopoiesis.

Degree: 2015, University of Adelaide

URL: http://hdl.handle.net/2440/92812

► Krüppel-like factor 5 (KLF5) is a zinc-finger transcription factor known to have regulatory roles in the growth and differentiation of many adult tissues. In humans,… (more)

▼ Krüppel-like factor 5 (KLF5) is a zinc-finger transcription factor known to have regulatory roles in the growth and differentiation of many adult tissues. In humans, KLF5 is located at 13q21-22, which is frequently lost in multiple tumour types, including tumours of the breast, endometrium, ovary and prostate where it is associated with loss of KLF5 expression. Little is known about the potential role of KLF5 in the haemopoietic system. Previous work by us and others has shown that KLF5 has a functional role in induction of differentiation of the myeloid compartment. In acute myeloid leukaemia (AML), our group has previously show that KLF5 expression is reduced relatively to normal CD34⁺ cells and that reduction of expression is associated with hypermethylation in intron 1. We also found that hypermethylation of KLF5 was associated with poor outcome, identifying KLF5 as an important target for further investigation in haemopoiesis and particularly the myeloid compartment. To extend the functional analysis of Klf5, an in vivo gene-ablation model was generated. As nonconditional Klf5 knockout mice (KO) die at embryonic day 8.5, pan-haemopoietic Klf5 conditional gene KO mice were generated by crossing Klf5fl/fl [fl/fl superscript] mice with Vav-cre transgenic mice. The Klf5fl/flVav-cre⁺ʹ⁻ [fl/fl superscript] and Klf5fl/fl [fl/fl superscript] mice were analysed at 3, 9 and 12 month of age for defects in steady state haemopoiesis. Peripheral blood (PB) analysis of 9 and 12 month old mice revealed that Klf5fl/flVav-cre⁺ʹ⁻ [fl/fl superscript] animals displayed significantly higher values for total white blood cell (WBC) count. To further characterise the changes in blood cell populations, flow cytometry was used with a range of different lineage antibody markers. The peripheral blood data indicated a decrease in the granulocytes of Klf5fl/flVav-cre⁺ʹ⁻ [fl/fl superscript] mice as well as an increase in the T-cell compartment. Interestingly, we also showed that the Klf5fl/flVav-cre⁺ʹ⁻ [fl/fl superscript] mice have increased numbers of blood and bone marrow eosinophils compared to Klf5fl/f [fl/fl superscript] mice. Consistently, we found significantly increased numbers of eosinophils in the lungs of Klf5fl/flVav-cre⁺ʹ⁻ [fl/fl superscript] mice compared to Klf5fl/fl [fl/fl superscript] mice. The spleen weight of Klf5fl/flVav-cre⁺ʹ⁻ [fl/fl superscript] mice was significantly higher compared to Klf5fl/fl [fl/fl superscript] mice. In addition, clonal assays conducted from the spleen of 9 and 12 month old mice showed a significant increase in colony number in the Klf5fl/flVav-cre⁺ʹ⁻ [fl/fl superscript]mice compared to Klf5fl/fl [fl/fl superscript] mice. This correlated with the flow cytometry data which showed a significant increase in haemopoietic stem cell (HSC) populations; short-term HSC (ST-HSC) and multipotent progenitor (MPP) in the spleen of Klf5fl/flVav-cre⁺ʹ⁻ [fl/fl superscript] mice. In summary, this study revealed multiple functional roles for Klf5 in haemopoiesis. Firstly, these studies demonstrated that as predicted… Advisors/Committee Members: D'Andrea, Richard James (advisor), Brown, Anna Louise (advisor), School of Molecular and Biomedical Science (school).

Subjects/Keywords: KLF5; haemopoiesis; mouse

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APA (6^th Edition):

Shahrin, N. H. (2015). Investigation of KLF5 function in normal haemopoiesis. (Thesis). University of Adelaide. Retrieved from http://hdl.handle.net/2440/92812

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Shahrin, Nur Hezrin. “Investigation of KLF5 function in normal haemopoiesis.” 2015. Thesis, University of Adelaide. Accessed February 27, 2021. http://hdl.handle.net/2440/92812.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Shahrin, Nur Hezrin. “Investigation of KLF5 function in normal haemopoiesis.” 2015. Web. 27 Feb 2021.

Vancouver:

Shahrin NH. Investigation of KLF5 function in normal haemopoiesis. [Internet] [Thesis]. University of Adelaide; 2015. [cited 2021 Feb 27]. Available from: http://hdl.handle.net/2440/92812.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Shahrin NH. Investigation of KLF5 function in normal haemopoiesis. [Thesis]. University of Adelaide; 2015. Available from: http://hdl.handle.net/2440/92812

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Hawaii – Manoa

5. Raman, Arjun Venkat. Utilization of selenium in the mouse brain : implications for neurological disease.

Degree: 2016, University of Hawaii – Manoa

URL: http://hdl.handle.net/10125/101018

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Ph.D. University of Hawaii at Manoa 2012.

Selenium is a chemical element that is an essential micronutrient associated with various aspects of human health. The… (more)

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Ph.D. University of Hawaii at Manoa 2012.

Selenium is a chemical element that is an essential micronutrient associated with various aspects of human health. The biochemical activity of selenium is mediated by proteins, which incorporate it into the amino acid selenocysteine (Sec). There are 25 genes in humans encoding Sec-containing selenoproteins. The functionally characterized selenoproteins are oxidoreductase enzymes involved in cellular oxidation-reduction reactions. Most selenoproteins are expressed in the mammalian brain, and dietary selenium deficiency causes preferential retention in brain relative to other body organs. Further, dietary selenium deficiency and specific selenoproteins are associated with various brain diseases. Mouse models have been extensively used to study the function and handling of selenium in mammals. Genetic deletion of a Sec-rich protein in mice causes brain selenium deficiency, neurodegeneration and neurological impairment, and disruption of a phospholipid hydroperoxidase selenoenzyme causes rapid neurodegeneration. Therefore, selenoprotein expression and function promotes a healthy nervous system. However, selenium metabolism and the function of several selenoproteins in brain are not clearly defined. The overall purpose of this work is to clarify the function and utilization of selenium in the mammalian brain, to reveal implications for developmental and neurological diseases. The goal of these studies is to investigate changes in brain function and selenoprotein expression under conditions of altered selenium metabolism in mice. The research presented in this dissertation covers three major topics that are separated into chapters. To investigate selenium distribution in the brain, the neurological consequences of disrupting selenium transport and recycling in mice are assessed and compared. Disruption of selenium transport caused more profound neurological consequences than disruption of selenium recycling. To investigate potential functions of selenium in the nervous system, select selenoproteins were examined for cellular and subcellular expression in cells and brain tissue from transgenic and control mice. Select selenoproteins and synthesis factors were observed at synapses, suggesting localized expression and physiological relevance. To investigate a potential interaction between selenium and methamphetamine, expression profiling of selenoproteins in mouse brain after exposure to methamphetamine is described. Selenoprotein synthesis was adversely affected by methamphetamine administration in mice. These results confirm the importance of selenium in the mammalian brain.

Subjects/Keywords: selenium; mouse; brain

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APA (6^th Edition):

Raman, A. V. (2016). Utilization of selenium in the mouse brain : implications for neurological disease. (Thesis). University of Hawaii – Manoa. Retrieved from http://hdl.handle.net/10125/101018

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Raman, Arjun Venkat. “Utilization of selenium in the mouse brain : implications for neurological disease.” 2016. Thesis, University of Hawaii – Manoa. Accessed February 27, 2021. http://hdl.handle.net/10125/101018.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Raman, Arjun Venkat. “Utilization of selenium in the mouse brain : implications for neurological disease.” 2016. Web. 27 Feb 2021.

Vancouver:

Raman AV. Utilization of selenium in the mouse brain : implications for neurological disease. [Internet] [Thesis]. University of Hawaii – Manoa; 2016. [cited 2021 Feb 27]. Available from: http://hdl.handle.net/10125/101018.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Raman AV. Utilization of selenium in the mouse brain : implications for neurological disease. [Thesis]. University of Hawaii – Manoa; 2016. Available from: http://hdl.handle.net/10125/101018

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Texas – Austin

6. -7420-459X. Computations in the early visual system in the mouse.

Degree: PhD, Neuroscience, 2019, University of Texas – Austin

URL: http://dx.doi.org/10.26153/tsw/5681

► In this dissertation, I have explored the mechanisms underlying the selectivity of different visual features in the mouse. I have compared these mechanisms to the… (more)

▼ In this dissertation, I have explored the mechanisms underlying the selectivity of different visual features in the mouse. I have compared these mechanisms to the canonical mechanisms for extracting these features. In chapter 2, I have demonstrated existence of nonclassical receptive fields in which the orientation preference can depend on the spatial frequency, in the mouse visual cortex. I have compared the experimental data with a model based on random connectivity between cells which predicts existence of such receptive fields. In chapter 3, I have studied the input differences between V1 neurons with varying degrees of linearity in spatial summation. I have demonstrated evidence of connectivity which deviates from the standard hierarchical connectivity model. I show that nonlinear cells in the mouse V1 can receive thalamic input which can itself be nonlinear and also orientation selective. In chapter 4, I have studied the development of binocular disparity tuning and using monocular deprivation. I show that disparity selectivity in the mouse is reduced following contralateral eye deprivation during critical period. This effect is due to a disruption of existing disparity selectivity in the circuit following deprivation, as we observe no difference in degree of selectivity between adult animals and young mice before critical period. This disruption may be due to formation of new inputs which disrupt the matching between left and right eye existing inputs. We provide evidence for this by demonstrating a reduction in spatial acuity for the open eye inputs following deprivation. Across all of these studies, I demonstrate multiple instances in which the mouse pathways differ from the classical early visual pathways. But I also find evidence for a distinctive connectivity, similar to the classical models. My thesis highlights the diversity in circuit computations which leads to the processing outcomes that are shared across the mammalian species Advisors/Committee Members: Priebe, Nicholas (advisor), Aldrich, Richard W (committee member), Fiete, Ila (committee member), Huk, Alexander C (committee member), Movshon, J Anthony (committee member).

Subjects/Keywords: Mouse; Vision; Neurons; Mouse visual system; Mouse visual features; Mouse visual cortex

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APA (6^th Edition):

-7420-459X. (2019). Computations in the early visual system in the mouse. (Doctoral Dissertation). University of Texas – Austin. Retrieved from http://dx.doi.org/10.26153/tsw/5681

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete

Chicago Manual of Style (16^th Edition):

-7420-459X. “Computations in the early visual system in the mouse.” 2019. Doctoral Dissertation, University of Texas – Austin. Accessed February 27, 2021. http://dx.doi.org/10.26153/tsw/5681.

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete

MLA Handbook (7^th Edition):

-7420-459X. “Computations in the early visual system in the mouse.” 2019. Web. 27 Feb 2021.

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete

Vancouver:

-7420-459X. Computations in the early visual system in the mouse. [Internet] [Doctoral dissertation]. University of Texas – Austin; 2019. [cited 2021 Feb 27]. Available from: http://dx.doi.org/10.26153/tsw/5681.

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete

Council of Science Editors:

-7420-459X. Computations in the early visual system in the mouse. [Doctoral Dissertation]. University of Texas – Austin; 2019. Available from: http://dx.doi.org/10.26153/tsw/5681

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete

University of Cambridge

7. Orietti, Lorenzo. Mechanisms and dynamics of size regulation and lumen formation in mouse double embryos.

Degree: PhD, 2019, University of Cambridge

URL: https://www.repository.cam.ac.uk/handle/1810/307794

► Mouse embryogenesis is a paradigmatic example of regulative development, as embryos are able to compensate for alterations in the number of cells and to generate… (more)

Subjects/Keywords: Mouse Embryos; Mouse stem cell; Size regulation; Mouse Morphogenesis

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APA (6^th Edition):

Orietti, L. (2019). Mechanisms and dynamics of size regulation and lumen formation in mouse double embryos. (Doctoral Dissertation). University of Cambridge. Retrieved from https://www.repository.cam.ac.uk/handle/1810/307794

Chicago Manual of Style (16^th Edition):

Orietti, Lorenzo. “Mechanisms and dynamics of size regulation and lumen formation in mouse double embryos.” 2019. Doctoral Dissertation, University of Cambridge. Accessed February 27, 2021. https://www.repository.cam.ac.uk/handle/1810/307794.

MLA Handbook (7^th Edition):

Orietti, Lorenzo. “Mechanisms and dynamics of size regulation and lumen formation in mouse double embryos.” 2019. Web. 27 Feb 2021.

Vancouver:

Orietti L. Mechanisms and dynamics of size regulation and lumen formation in mouse double embryos. [Internet] [Doctoral dissertation]. University of Cambridge; 2019. [cited 2021 Feb 27]. Available from: https://www.repository.cam.ac.uk/handle/1810/307794.

Council of Science Editors:

Orietti L. Mechanisms and dynamics of size regulation and lumen formation in mouse double embryos. [Doctoral Dissertation]. University of Cambridge; 2019. Available from: https://www.repository.cam.ac.uk/handle/1810/307794

University of Cambridge

8. Singla, Shruti. Mechanisms behind the fate of early chromosomal and transcriptional heterogeneities in the mouse embryo.

Degree: PhD, 2020, University of Cambridge

URL: https://www.repository.cam.ac.uk/handle/1810/305192

► A series of events during the first four days of mouse embryo development leads to the formation of a blastocyst. The blastocyst consists of neatly… (more)

▼ A series of events during the first four days of mouse embryo development leads to the formation of a blastocyst. The blastocyst consists of neatly segregated three lineages: the epiblast (EPI), which will form the fetus, the extra-embryonic primitive endoderm and the outer layer of the extra-embryonic trophectoderm (TE). This organization prepares the embryo for implantation and subsequent development. This study aims to explore two broad questions: 1) what mechanisms dictate the fate of the progenies of the chromosomally abnormal cells generated during the 4-8 cell stage division; 2) how the transcriptional heterogeneities between the blastomeres of the 4-cell stage embryo affect subsequent lineage segregation. A high incidence of aneuploidy in the early cleavage divisions is considered the principal cause for low human fecundity and developmental defects. However, there is a dramatic decline in the prevalence of aneuploidy as gestation progresses. To understand the fate of aneuploid cells, a mouse model of chromosome mosaicism was used. In vitro culture system and live imaging demonstrated that aneuploid cells were eliminated from the EPI by apoptosis both during pre- and peri-implantation development. Also, aneuploid cells displayed chronic proteotoxic stress. Subsequently, p53-mediated autophagy eliminated aneuploid cells from the EPI. Unlike aneuploid embryos, 1:1 diploid-aneuploid mosaic embryos show developmental potential equivalent to diploids. Their peri-implantation development was followed, and it was found that while aneuploid cells in the EPI underwent apoptosis, the diploid cells over-proliferated to regulate the overall EPI size. These results elucidate the cellular and molecular mechanisms used by mouse embryo to refine the EPI cell population and ensure only the chromosomally fit cells proceed through the development of the fetus. The second part of the study investigates into the early molecular players that bias cell fate decisions. Sox21 was earlier identified as the most heterogeneous gene at the 4-cell stage that can influence cell fate decision. The deep sequencing of Sox21 knockout and wild-type embryos was carried out at the 4-cell stage and compared. Klf2 and Tdgf1 were found to be important downstream targets of Sox21 that influence lineage segregation. Depletion of both these genes predisposed cells to the TE lineage. Co-overexpression of both these genes rescued the effect of Sox21 knockdown on cell fate. These results demonstrate the mechanism by which Sox21 heterogeneity, from as early as the 4-cell stage, biases cell fate. Together, these findings indicate the fundamental mechanisms used by mouse embryo to ensure developmental plasticity.

Subjects/Keywords: embryology; mouse preimplantation; mouse postimplantation; mouse periimplantation; autophagy; aneuploidy; apoptosis; heterogeneity; plasticity

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APA (6^th Edition):

Singla, S. (2020). Mechanisms behind the fate of early chromosomal and transcriptional heterogeneities in the mouse embryo. (Doctoral Dissertation). University of Cambridge. Retrieved from https://www.repository.cam.ac.uk/handle/1810/305192

Chicago Manual of Style (16^th Edition):

Singla, Shruti. “Mechanisms behind the fate of early chromosomal and transcriptional heterogeneities in the mouse embryo.” 2020. Doctoral Dissertation, University of Cambridge. Accessed February 27, 2021. https://www.repository.cam.ac.uk/handle/1810/305192.

MLA Handbook (7^th Edition):

Singla, Shruti. “Mechanisms behind the fate of early chromosomal and transcriptional heterogeneities in the mouse embryo.” 2020. Web. 27 Feb 2021.

Vancouver:

Singla S. Mechanisms behind the fate of early chromosomal and transcriptional heterogeneities in the mouse embryo. [Internet] [Doctoral dissertation]. University of Cambridge; 2020. [cited 2021 Feb 27]. Available from: https://www.repository.cam.ac.uk/handle/1810/305192.

Council of Science Editors:

Singla S. Mechanisms behind the fate of early chromosomal and transcriptional heterogeneities in the mouse embryo. [Doctoral Dissertation]. University of Cambridge; 2020. Available from: https://www.repository.cam.ac.uk/handle/1810/305192

Universiteit Utrecht

9. Lange, T.A.D. The role of Cdx in embryonic and adult mammalian hematopoiesis.

Degree: 2011, Universiteit Utrecht

URL: http://dspace.library.uu.nl:8080/handle/1874/209132

► All blood cells orginate from a common stem cell in the bone marrow: the hematopoietic stem cell (HSC), which is characterized by two main properties:… (more)

▼ All blood cells orginate from a common stem cell in the bone marrow: the hematopoietic stem cell (HSC), which is characterized by two main properties: self-renewal and multipotency. Hematopoiesis is a hierarchical system with the HSC at the top. During embryogenesis, hematopoietic cells and progenitors with broader potentials are progressively generated. Mammalian hematopoietic development begins in extra-embryonic structures and continues within the embryo proper. In the conceptus, the mesoderm is patterned along the anterior-posterior (A-P) axis. The positional identity of the mesoderm on the A-P axis is regulated by Hox genes. Cdx genes, another homeobox gene family, are required for the posterior growth of axial tissues during development. Cdx genes are known to act upstream of Hox. The first evidence for a role for Cdx in hematopoiesis was established in zebrafish. Using embryoid bodies, it was shown that the Cdx genes promote embryonic hematopoiesis in the mouse by upregulating target Hox genes. Induction of Cdx4 promotes proliferation of hematopoietic progenitors. HSCs were more successfully derived from ESCs upon Cdx4 and Hoxb4 induction. Cdx gene deficiency jeopardizes embryonic hematopoiesis, with severe consequences for blood development upon Cdx2 mutations. As adult Cdx4 knockout mice only displayed minimal hematopoietic abnormalities, Cdx4 is dispensable for adult hematopoiesis. Previous studies on Cdx1 and Cdx2 mutants did not report any hematopoietic malformations either. However, it was demonstrated that overexpression of Cdx4 promotes leukemia in adult mice and that ectopic expression of Cdx2 is a key event in myeloid leukemia. The Cdx genes thus act as stimulators of hematopoietic progenitor maintenance and proliferation. Loss of function of Cdx impairs embryonic hematopoiesis, whereas gain of function in the adult bone marrow results in overproliferation of hematopoietic progenitors, which can instigate leukemia. Advisors/Committee Members: Deschamps, J..

Subjects/Keywords: hematopoiesis; mouse; Cdx; leukemia

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APA (6^th Edition):

Lange, T. A. D. (2011). The role of Cdx in embryonic and adult mammalian hematopoiesis. (Masters Thesis). Universiteit Utrecht. Retrieved from http://dspace.library.uu.nl:8080/handle/1874/209132

Chicago Manual of Style (16^th Edition):

Lange, T A D. “The role of Cdx in embryonic and adult mammalian hematopoiesis.” 2011. Masters Thesis, Universiteit Utrecht. Accessed February 27, 2021. http://dspace.library.uu.nl:8080/handle/1874/209132.

MLA Handbook (7^th Edition):

Lange, T A D. “The role of Cdx in embryonic and adult mammalian hematopoiesis.” 2011. Web. 27 Feb 2021.

Vancouver:

Lange TAD. The role of Cdx in embryonic and adult mammalian hematopoiesis. [Internet] [Masters thesis]. Universiteit Utrecht; 2011. [cited 2021 Feb 27]. Available from: http://dspace.library.uu.nl:8080/handle/1874/209132.

Council of Science Editors:

Lange TAD. The role of Cdx in embryonic and adult mammalian hematopoiesis. [Masters Thesis]. Universiteit Utrecht; 2011. Available from: http://dspace.library.uu.nl:8080/handle/1874/209132

Cape Peninsula University of Technology

10. Petrova, Antoinette. Modulation of ultrviolet light induced skin carcinogenesis by extracts of Rooibos and Honeybush using a mouse model:elucidating possible protective mechanisms .

Degree: 2009, Cape Peninsula University of Technology

URL: http://etd.cput.ac.za/handle/20.500.11838/1487

► This thesis provides the first scientific evidence of the photoprotective properties of rooibos and honeybush herbal tea extracts and to some extent, two major honeybush… (more)

▼ This thesis provides the first scientific evidence of the photoprotective properties of rooibos and honeybush herbal tea extracts and to some extent, two major honeybush polyphenols, hesperidin and mangiferin. These properties were demonstrated using in vivo models by: Providing evidence for the inhibition of tumour promotion by ultraviolet B (UVB) radiation in a two-stage skin carcinogenesis mouse model. Topical application of polyphenol-rich extracts of rooibos and honeybush prior to UVB tumour promotion of 7,12-dimethylbenz[a]anthracene (DMBA)-initiated mouse skin, inhibited the formation of tumours. The rooibos and honeybush extracts decreased the incidence and volume of the tumours. Topical application of hesperidin and mangiferin were less effective than the honeybush extracts as only the tumour volume was decreased, but not the incidence. Providing evidence for the inhibition of photodamage of the skin by UVB exposure in a mouse model. Topical application of polyphenolic rich extracts of honeybush prior to UVB irradiation of mouse skin reduced erythema, peeling, oedema and hyperplasia. The depletion of antioxidant enzymes catalase and superoxide dismutase (SOD) was prevented. The extracts protected the skin from oxidative and direct DNA damage, and reduced lipid peroxidation. The induction of cyclooxygenase-2 (COX-2) and ornithine decarboxylase (ODC) was also reduced. Topical application of the polyphenols hesperidin and mangiferin showed reduced protective effects compared to the extracts. Suggesting the possible mechanisms by which honeybush and the polyphenols protect against photocarcinogenesis such as reducing tumour promotion, inflammation and oxidative stress. Suggesting the benefits of including honeybush and rooibos as cosmeceuticals in skin care products and sunscreens as part of the strategy for preventing skin cancer. Discussing the recommendations for further study such as investigating more specific chemopreventive activities of these two South African herbal teas and their polyphenols, dose response studies and clinical evaluations.

Subjects/Keywords: rooibos; honeybush; carcinogenesis; mouse model

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APA (6^th Edition):

Petrova, A. (2009). Modulation of ultrviolet light induced skin carcinogenesis by extracts of Rooibos and Honeybush using a mouse model:elucidating possible protective mechanisms . (Thesis). Cape Peninsula University of Technology. Retrieved from http://etd.cput.ac.za/handle/20.500.11838/1487

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Petrova, Antoinette. “Modulation of ultrviolet light induced skin carcinogenesis by extracts of Rooibos and Honeybush using a mouse model:elucidating possible protective mechanisms .” 2009. Thesis, Cape Peninsula University of Technology. Accessed February 27, 2021. http://etd.cput.ac.za/handle/20.500.11838/1487.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Petrova, Antoinette. “Modulation of ultrviolet light induced skin carcinogenesis by extracts of Rooibos and Honeybush using a mouse model:elucidating possible protective mechanisms .” 2009. Web. 27 Feb 2021.

Vancouver:

Petrova A. Modulation of ultrviolet light induced skin carcinogenesis by extracts of Rooibos and Honeybush using a mouse model:elucidating possible protective mechanisms . [Internet] [Thesis]. Cape Peninsula University of Technology; 2009. [cited 2021 Feb 27]. Available from: http://etd.cput.ac.za/handle/20.500.11838/1487.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Petrova A. Modulation of ultrviolet light induced skin carcinogenesis by extracts of Rooibos and Honeybush using a mouse model:elucidating possible protective mechanisms . [Thesis]. Cape Peninsula University of Technology; 2009. Available from: http://etd.cput.ac.za/handle/20.500.11838/1487

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Utah

11. Arch, Dorinda Deana. Altered liver parameters in a genetic mouse model of porphyria cutanea tarda and possible involvement of ABC transporters in the disease.

Degree: PhD, Pharmacology & Toxicology;, 2010, University of Utah

URL: http://content.lib.utah.edu/cdm/singleitem/collection/etd2/id/62/rec/68

► The project sought to examine the changes in the liver associated with porphyria and whether ATP binding cassette (ABC) transporters in the hepatocyte might in… (more)

Subjects/Keywords: Liver parameters; Mouse model

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APA (6^th Edition):

Arch, D. D. (2010). Altered liver parameters in a genetic mouse model of porphyria cutanea tarda and possible involvement of ABC transporters in the disease. (Doctoral Dissertation). University of Utah. Retrieved from http://content.lib.utah.edu/cdm/singleitem/collection/etd2/id/62/rec/68

Chicago Manual of Style (16^th Edition):

Arch, Dorinda Deana. “Altered liver parameters in a genetic mouse model of porphyria cutanea tarda and possible involvement of ABC transporters in the disease.” 2010. Doctoral Dissertation, University of Utah. Accessed February 27, 2021. http://content.lib.utah.edu/cdm/singleitem/collection/etd2/id/62/rec/68.

MLA Handbook (7^th Edition):

Arch, Dorinda Deana. “Altered liver parameters in a genetic mouse model of porphyria cutanea tarda and possible involvement of ABC transporters in the disease.” 2010. Web. 27 Feb 2021.

Vancouver:

Arch DD. Altered liver parameters in a genetic mouse model of porphyria cutanea tarda and possible involvement of ABC transporters in the disease. [Internet] [Doctoral dissertation]. University of Utah; 2010. [cited 2021 Feb 27]. Available from: http://content.lib.utah.edu/cdm/singleitem/collection/etd2/id/62/rec/68.

Council of Science Editors:

Arch DD. Altered liver parameters in a genetic mouse model of porphyria cutanea tarda and possible involvement of ABC transporters in the disease. [Doctoral Dissertation]. University of Utah; 2010. Available from: http://content.lib.utah.edu/cdm/singleitem/collection/etd2/id/62/rec/68

UCLA

12. Berquist, Sean. Sound Production in the Isolated Mouse Larynx.

Degree: Physiological Science, 2013, UCLA

URL: http://www.escholarship.org/uc/item/0hr2b5x5

► Recent evidence indicates that laboratory mice use elaborate ultrasonic songs, and this behavior possibly may be learned. In the present study, air pressure was manipulated… (more)

Subjects/Keywords: Physiology; larynx; mouse; phonation

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APA (6^th Edition):

Berquist, S. (2013). Sound Production in the Isolated Mouse Larynx. (Thesis). UCLA. Retrieved from http://www.escholarship.org/uc/item/0hr2b5x5

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Berquist, Sean. “Sound Production in the Isolated Mouse Larynx.” 2013. Thesis, UCLA. Accessed February 27, 2021. http://www.escholarship.org/uc/item/0hr2b5x5.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Berquist, Sean. “Sound Production in the Isolated Mouse Larynx.” 2013. Web. 27 Feb 2021.

Vancouver:

Berquist S. Sound Production in the Isolated Mouse Larynx. [Internet] [Thesis]. UCLA; 2013. [cited 2021 Feb 27]. Available from: http://www.escholarship.org/uc/item/0hr2b5x5.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Berquist S. Sound Production in the Isolated Mouse Larynx. [Thesis]. UCLA; 2013. Available from: http://www.escholarship.org/uc/item/0hr2b5x5

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Alberta

13. Yang, Fang. Characterizing the role of CECR1 in cat eye syndrome by using mouse models.

Degree: MS, Department of Biological Sciences, 2010, University of Alberta

URL: https://era.library.ualberta.ca/files/w0892c29j

► CECR1 (cat eye syndrome chromosome region, candidate 1) is located on chromosome 22q11.2. Duplication of this region results in the human disorder cat eye syndrome… (more)

Subjects/Keywords: CECR1; mouse; cat eye syndrome

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APA (6^th Edition):

Yang, F. (2010). Characterizing the role of CECR1 in cat eye syndrome by using mouse models. (Masters Thesis). University of Alberta. Retrieved from https://era.library.ualberta.ca/files/w0892c29j

Chicago Manual of Style (16^th Edition):

Yang, Fang. “Characterizing the role of CECR1 in cat eye syndrome by using mouse models.” 2010. Masters Thesis, University of Alberta. Accessed February 27, 2021. https://era.library.ualberta.ca/files/w0892c29j.

MLA Handbook (7^th Edition):

Yang, Fang. “Characterizing the role of CECR1 in cat eye syndrome by using mouse models.” 2010. Web. 27 Feb 2021.

Vancouver:

Yang F. Characterizing the role of CECR1 in cat eye syndrome by using mouse models. [Internet] [Masters thesis]. University of Alberta; 2010. [cited 2021 Feb 27]. Available from: https://era.library.ualberta.ca/files/w0892c29j.

Council of Science Editors:

Yang F. Characterizing the role of CECR1 in cat eye syndrome by using mouse models. [Masters Thesis]. University of Alberta; 2010. Available from: https://era.library.ualberta.ca/files/w0892c29j

Cornell University

14. Ko, Frank. In Vivo Noninvasive Mouse Model Of Load Induced Osteoarthritis.

Degree: PhD, Mechanical Engineering, 2014, Cornell University

URL: http://hdl.handle.net/1813/37056

► Osteoarthritis (OA) is the leading cause of disability among the elderly population, affecting approximately 27 millions Americans and costing $60 billion in related-health care costs.… (more)

▼ Osteoarthritis (OA) is the leading cause of disability among the elderly population, affecting approximately 27 millions Americans and costing $60 billion in related-health care costs. Mouse models of OA have been developed to study the mechanisms of OA and therapeutic interventions. However, traditional animal models induce OA pathology through traumatic surgeries, which only represent 10% of human OA patients. Thus, in this thesis, a novel noninvasive OA mouse model was developed, characterized, and applied to transgenic mice. The changes in articular cartilage and subchondral bone were analyzed by histology, immunohistochemistry, and microcomputed tomography. To develop a noninvasive OA mouse model, an in vivo tibial loading model was used to investigate the adaptive responses of cartilage and bone to mechanical loading and to assess the influence of load level and duration. Peak cyclic compression of 4.5 and 9.0N was applied to the left tibia via the knee joint of adult (26-week-old) male mice for 1, 2, and 6 weeks at 1200 cycles/day. In addition, 9.0N loading was utilized in young (10-week-old) mice. Loading promoted cartilage damage, cartilage thinning, and subchondral cortical bone thickening in both age groups. Both age groups developed periarticular osteophytes at the tibial plateau in response to the 9.0N load, but no osteophyte formation occurred in adult mice subjected to 4.5N load. Development of a novel noninvasive loading model was followed by investigating the traumatic vs. nontraumatic nature of cyclic loading of the mouse knee joint. To differentiate traumatic tissue damage versus cell-mediated processes in the development of OA pathology, a single nondestructive 5-minute loading session was applied to the left tibia of adult (26-weekold) mice at a peak load of 9.0N. Knee joints were subsequently analyzed at 0, 1 and 2 weeks after loading. At T = 0, no change was evident in cartilage or subchondral bone. However, cartilage pathology demonstrated by localized thinning, proteoglycan loss, and inhibition of chondrocyte autophagy occurred at 1 and 2 weeks after the single session of loading. Transient cancellous bone loss was evident at 1 week, associated with increased osteoclast number, reversed at 2 weeks. Finally, the in vivo tibial loading model was implemented to study the role of Dickkopf1, an inhibitor of the Wnt pathway, in the development of load-induced OA. To identify the role of Dickkopf-1 protein in OA, novel viable mice with Dickkopf-1 knockout and Wnt3 knockdown (Dkk1-/-;Wnt3+/-) were used. The left tibia of 10-week-old Dkk1-/-;Wnt3+/- and respective control groups, littermate control (Dkk1+/+;Wnt3+/+) and Wnt3 knockdown (Dkk1+/+;Wnt3+/-) mice, underwent cyclic compression at a peak load of 9.0N for 2 weeks. As a result of loading, both Dkk1-/-;Wnt3+/- and Dkk1+/+;Wnt3+/+ mice demonstrated cartilage erosion, subchondral cancellous bone loss, and osteophyte formation. However, Dkk1+/+;Wnt3+/- mice did not undergo cartilage degeneration and showed limited osteophyte formation, indicating… Advisors/Committee Members: van der Meulen, Marjolein (chair), Hernandez, Christopher J. (committee member), Farnum, Cornelia E (committee member), Wright, Timothy M. (committee member).

Subjects/Keywords: Osteoarthritis; Mouse model; Mechanical loading

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APA (6^th Edition):

Ko, F. (2014). In Vivo Noninvasive Mouse Model Of Load Induced Osteoarthritis. (Doctoral Dissertation). Cornell University. Retrieved from http://hdl.handle.net/1813/37056

Chicago Manual of Style (16^th Edition):

Ko, Frank. “In Vivo Noninvasive Mouse Model Of Load Induced Osteoarthritis.” 2014. Doctoral Dissertation, Cornell University. Accessed February 27, 2021. http://hdl.handle.net/1813/37056.

MLA Handbook (7^th Edition):

Ko, Frank. “In Vivo Noninvasive Mouse Model Of Load Induced Osteoarthritis.” 2014. Web. 27 Feb 2021.

Vancouver:

Ko F. In Vivo Noninvasive Mouse Model Of Load Induced Osteoarthritis. [Internet] [Doctoral dissertation]. Cornell University; 2014. [cited 2021 Feb 27]. Available from: http://hdl.handle.net/1813/37056.

Council of Science Editors:

Ko F. In Vivo Noninvasive Mouse Model Of Load Induced Osteoarthritis. [Doctoral Dissertation]. Cornell University; 2014. Available from: http://hdl.handle.net/1813/37056

Cornell University

15. Pattabiraman, Shrivatsav. Brwd1, A Ubiquitously Expressed Gene, Has Non Redundant Sexually Dimorphic Functions In The Mammalian Germlinepage.

Degree: PhD, Molecular and Cell Biology, 2014, Cornell University

URL: http://hdl.handle.net/1813/36178

► Normal spermiogenesis requires the transcription of many genes that occurs exclusively after meiosis. This wave of transcriptional changes in haploid spermatids is well-documented, but the… (more)

Subjects/Keywords: brwd1; fertility; mouse; transcription; spermiogenesis

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APA (6^th Edition):

Pattabiraman, S. (2014). Brwd1, A Ubiquitously Expressed Gene, Has Non Redundant Sexually Dimorphic Functions In The Mammalian Germlinepage. (Doctoral Dissertation). Cornell University. Retrieved from http://hdl.handle.net/1813/36178

Chicago Manual of Style (16^th Edition):

Pattabiraman, Shrivatsav. “Brwd1, A Ubiquitously Expressed Gene, Has Non Redundant Sexually Dimorphic Functions In The Mammalian Germlinepage.” 2014. Doctoral Dissertation, Cornell University. Accessed February 27, 2021. http://hdl.handle.net/1813/36178.

MLA Handbook (7^th Edition):

Pattabiraman, Shrivatsav. “Brwd1, A Ubiquitously Expressed Gene, Has Non Redundant Sexually Dimorphic Functions In The Mammalian Germlinepage.” 2014. Web. 27 Feb 2021.

Vancouver:

Pattabiraman S. Brwd1, A Ubiquitously Expressed Gene, Has Non Redundant Sexually Dimorphic Functions In The Mammalian Germlinepage. [Internet] [Doctoral dissertation]. Cornell University; 2014. [cited 2021 Feb 27]. Available from: http://hdl.handle.net/1813/36178.

Council of Science Editors:

Pattabiraman S. Brwd1, A Ubiquitously Expressed Gene, Has Non Redundant Sexually Dimorphic Functions In The Mammalian Germlinepage. [Doctoral Dissertation]. Cornell University; 2014. Available from: http://hdl.handle.net/1813/36178

Vanderbilt University

16. Guney, Michelle Aylin. The Role of Connective Tissue Growth Factor in Islet Morphogenesis and Beta Cell Proliferation.

Degree: PhD, Molecular Physiology and Biophysics, 2011, Vanderbilt University

URL: http://hdl.handle.net/1803/11291

► Pancreatic beta cells are the only cell type in the body that can produce insulin, a hormone required for maintaining glucose homeostasis. Type 1 and… (more)

▼ Pancreatic beta cells are the only cell type in the body that can produce insulin, a hormone required for maintaining glucose homeostasis. Type 1 and type 2 diabetes result from an absolute or relative reduction in functional beta cell mass, respectively. One approach to replacing lost beta cell mass is transplantation of islets from cadaveric donors; however, this approach is limited by lack of adequate amounts of donor tissue. Therefore, there has been much interest in identifying factors that enhance beta cell differentiation and proliferation in vivo or in vitro. Connective tissue growth factor (CTGF) is a secreted molecule expressed in pancreatic endothelial cells, beta cells, and ducts during pancreas development. CTGF is required for proper lineage allocation and islet morphogenesis during development and for beta cell proliferation at late gestation. The current study investigated the tissue interactions by which CTGF promotes normal pancreatic islet development. These results show that CTGF produced by both endothelial cells and beta cells is required for embryonic beta cell proliferation, making CTGF the first identified secreted endothelial-derived or beta cell-derived factor which regulates embryonic beta cell proliferation. Removing CTGF from any one source in the pancreas impairs embryonic beta cell proliferation, indicating that beta cell proliferation is particularly sensitive to the level of CTGF. In contrast, inactivating CTGF from one source in the pancreas does not affect lineage allocation or islet morphogenesis, indicating that these sources of CTGF act redundantly to promote these processes. This dissertation also demonstrated that over-expression of CTGF in beta cells during embryogenesis using an inducible transgenic system increases islet mass by promoting endocrine cell proliferation. Together, these findings demonstrate that CTGF acts in both an autocrine and paracrine manner during pancreas development and suggest that CTGF has the potential to enhance beta cell proliferation or differentiation in diabetic models. Advisors/Committee Members: Douglas Mortlock (committee member), Anna Means (committee member), Roland Stein (committee member), Ambra Pozzi (committee member), Richard O'Brien (Committee Chair).

Subjects/Keywords: CCN2; pancreas development; knockout mouse

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APA (6^th Edition):

Guney, M. A. (2011). The Role of Connective Tissue Growth Factor in Islet Morphogenesis and Beta Cell Proliferation. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/11291

Chicago Manual of Style (16^th Edition):

Guney, Michelle Aylin. “The Role of Connective Tissue Growth Factor in Islet Morphogenesis and Beta Cell Proliferation.” 2011. Doctoral Dissertation, Vanderbilt University. Accessed February 27, 2021. http://hdl.handle.net/1803/11291.

MLA Handbook (7^th Edition):

Guney, Michelle Aylin. “The Role of Connective Tissue Growth Factor in Islet Morphogenesis and Beta Cell Proliferation.” 2011. Web. 27 Feb 2021.

Vancouver:

Guney MA. The Role of Connective Tissue Growth Factor in Islet Morphogenesis and Beta Cell Proliferation. [Internet] [Doctoral dissertation]. Vanderbilt University; 2011. [cited 2021 Feb 27]. Available from: http://hdl.handle.net/1803/11291.

Council of Science Editors:

Guney MA. The Role of Connective Tissue Growth Factor in Islet Morphogenesis and Beta Cell Proliferation. [Doctoral Dissertation]. Vanderbilt University; 2011. Available from: http://hdl.handle.net/1803/11291

Vanderbilt University

17. Nandana, Srinivas Rao. Mouse Models of Prostate Cancer Progression and Bone Metastasis.

Degree: PhD, Cancer Biology, 2010, Vanderbilt University

URL: http://hdl.handle.net/1803/12940

► CANCER BIOLOGY MOUSE MODELS OF PROSTATE CANCER PROGRESSION AND BONE METASTASIS Srinivas Rao Nandana Dissertation under the direction of Robert J. Matusik, PhD Prostate cancer… (more)

▼ CANCER BIOLOGY MOUSE MODELS OF PROSTATE CANCER PROGRESSION AND BONE METASTASIS Srinivas Rao Nandana Dissertation under the direction of Robert J. Matusik, PhD Prostate cancer is the second leading cause of deaths due to cancer in men in the United States. The American Cancer Society has projected that 192,280 new cases and 27,360 deaths will occur in the year 2009. Mostly, men over the age of 50 are afflicted by the disease and more than 70% of the men diagnosed with prostate cancer are over the age of 65. Most of the patients who suffer from prostate cancer do not die due to the tumor at the primary site but rather due to complications when the tumor has spread to the bone. It is estimated that each year, about 350,000 people die of bone metastasis in the United States. The causative tumor becomes incurable once the bone has been invaded and only 25% of prostate cancer patients are able to live 5 years subsequent to their diagnosis of bone metastasis. The interaction between prostate cancer cells and the bone creates a vicious cycle of bone formation and bone destruction thereby destabilizing the inherently delicate homeostasis within the bone. In prostate cancer, this process leads to metastatic lesions that are predominantly osteoblastic. However within the background of bone formation, several groups have reported that bone resorption is an integral part of prostate cancer bone lesions. Therefore, early detection and treatment before the tumor metastasizes is critical for the survival of the patient. Creating and characterizing mouse models that better mimic the progression in human prostate cancer is a powerful tool to study and delineate the various steps in tumor progression. Most of the currently available mouse models of prostate cancer successfully recapitulate the early steps of tumor progression in the primary site but fail to metastasize to other organs especially to the bone. Amongst the existing ones, transgenic models that are created by dysregulating a gene that is widely known to be altered in human prostate cancer are considered to be more reflective of the human disease. This is in contrast to transgenic mouse models that overexpress the small t and large T antigens that despite the phenotype they produce, are considered to have little physiological significance. This first part of the thesis describes the creation and characterization of the hepsin/myc bigenic model that develops adenocarcinoma in the primary site. The second part of the thesis describes a model that delineates the interactions between prostate cancer cells and the bone microenvironment. This is approached by dysregulating the T-box transcription factor Tbx2 in PC3 human prostate cancer cells and looking at the effect of this dysregulation on the interaction of the cells with the bone microenvironment. Approved______________________________________Date_________ Advisors/Committee Members: Dr.'s Robert Matusik, Vito Quaranta, Neil Bhowmick (committee member).

Subjects/Keywords: Metastasis; Mouse

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APA (6^th Edition):

Nandana, S. R. (2010). Mouse Models of Prostate Cancer Progression and Bone Metastasis. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/12940

Chicago Manual of Style (16^th Edition):

Nandana, Srinivas Rao. “Mouse Models of Prostate Cancer Progression and Bone Metastasis.” 2010. Doctoral Dissertation, Vanderbilt University. Accessed February 27, 2021. http://hdl.handle.net/1803/12940.

MLA Handbook (7^th Edition):

Nandana, Srinivas Rao. “Mouse Models of Prostate Cancer Progression and Bone Metastasis.” 2010. Web. 27 Feb 2021.

Vancouver:

Nandana SR. Mouse Models of Prostate Cancer Progression and Bone Metastasis. [Internet] [Doctoral dissertation]. Vanderbilt University; 2010. [cited 2021 Feb 27]. Available from: http://hdl.handle.net/1803/12940.

Council of Science Editors:

Nandana SR. Mouse Models of Prostate Cancer Progression and Bone Metastasis. [Doctoral Dissertation]. Vanderbilt University; 2010. Available from: http://hdl.handle.net/1803/12940

Texas A&M University

18. Villarreal, Dorissa. Neurotropism of Theiler's murine encephalomyelitis virus.

Degree: MS, Veterinary Microbiology, 2005, Texas A&M University

URL: http://hdl.handle.net/1969.1/2647

► Theiler??s murine encephalomyelitis virus (TMEV) can infect the central nervous system (CNS) and cause neurological damage. The exact route by which TMEV enters the CNS… (more)

Subjects/Keywords: Mouse; Virus

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APA (6^th Edition):

Villarreal, D. (2005). Neurotropism of Theiler's murine encephalomyelitis virus. (Masters Thesis). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/2647

Chicago Manual of Style (16^th Edition):

Villarreal, Dorissa. “Neurotropism of Theiler's murine encephalomyelitis virus.” 2005. Masters Thesis, Texas A&M University. Accessed February 27, 2021. http://hdl.handle.net/1969.1/2647.

MLA Handbook (7^th Edition):

Villarreal, Dorissa. “Neurotropism of Theiler's murine encephalomyelitis virus.” 2005. Web. 27 Feb 2021.

Vancouver:

Villarreal D. Neurotropism of Theiler's murine encephalomyelitis virus. [Internet] [Masters thesis]. Texas A&M University; 2005. [cited 2021 Feb 27]. Available from: http://hdl.handle.net/1969.1/2647.

Council of Science Editors:

Villarreal D. Neurotropism of Theiler's murine encephalomyelitis virus. [Masters Thesis]. Texas A&M University; 2005. Available from: http://hdl.handle.net/1969.1/2647

Texas A&M University

19. Lee, Junseok. Mapping and Analyzing the Full Vascular Network in the Mouse Brain at Submicrometer Resolution.

Degree: PhD, Computer Science, 2018, Texas A&M University

URL: http://hdl.handle.net/1969.1/173910

► Mapping the microvascular networks in the brain can lead to significant scientific and clinical insights. The recent advances of high-throughput physical sectioning light microscopy have… (more)

▼ Mapping the microvascular networks in the brain can lead to significant scientific and clinical insights. The recent advances of high-throughput physical sectioning light microscopy have greatly contributed to reducing the gap in neuroimaging between large-scale, low-resolution techniques and small-scale, high-resolution methods. The Brain Networks Laboratory at Texas A&M University developed a serial sectioning microscopy technique called the Knife-Edge Scanning Microscopy (KESM) to section and image the entire mouse brain at submicrometer resolution. The KESM can be used to obtain information about a small animal organ, such as a whole mouse or rat brain, at submicrometer resolution of 0:6 μm 0:7 μm 1:0 μm voxel size. In our effort to map the entire vascular network in the mouse brain, the Brain Networks Laboratory perfused the mouse brain vessels with India ink, and used the KESM to image the prepared brain. However, the image data size of the entire mouse brain from the KESM is about 1.5 TB, and is not easy to handle or analyze. Moreover, the dataset contains unintended noise from the serial sectioning process. Because of these difficulties, previous studies partially analyzed the structure of the mouse brain by manually selecting a small, noise-free portion (volume size under 1000 1000 1000 voxel) in the dataset. In addition to the KESM dataset, there have been studies for vessel reconstruction and analysis of the whole mouse brain at lower resolution or of partial brain regions at submicrometer resolution. However, to the best of our knowledge, there has been no study for vessel reconstruction and analysis of the whole mouse brain at submicrometer resolution. Mapping the microvascular networks in the brain can lead to significant scientific and clinical insights. The recent advances of high-throughput physical sectioning light microscopy have greatly contributed to reducing the gap in neuroimaging between large-scale, low-resolution techniques and small-scale, high-resolution methods. The Brain Networks Laboratory at Texas A&M University developed a serial sectioning microscopy technique called the Knife-Edge Scanning Microscopy (KESM) to section and image the entire mouse brain at submicrometer resolution. The KESM can be used to obtain information about a small animal organ, such as a whole mouse or rat brain, at submicrometer resolution of 0:6 μm x 0:7 μm x 1:0 μm voxel size. In our effort to map the entire vascular network in the mouse brain, the Brain Networks Laboratory perfused the mouse brain vessels with India ink, and used the KESM to image the prepared brain. However, the image data size of the entire mouse brain from the KESM is about 1.5 TB, and is not easy to handle or analyze. Moreover, the dataset contains unintended noise from the serial sectioning process. Because of these difficulties, previous studies partially analyzed the structure of the mouse brain by manually selecting a small, noise-free portion (volume size under 1000 x 1000 x 1000 voxel) in the dataset. In addition to the… Advisors/Committee Members: Choe, Yoonsuck (advisor), Keyser, John (committee member), Schaefer, Scott (committee member), Abbott, Louise (committee member).

Subjects/Keywords: whole mouse brain; cerebral vasculature

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APA (6^th Edition):

Lee, J. (2018). Mapping and Analyzing the Full Vascular Network in the Mouse Brain at Submicrometer Resolution. (Doctoral Dissertation). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/173910

Chicago Manual of Style (16^th Edition):

Lee, Junseok. “Mapping and Analyzing the Full Vascular Network in the Mouse Brain at Submicrometer Resolution.” 2018. Doctoral Dissertation, Texas A&M University. Accessed February 27, 2021. http://hdl.handle.net/1969.1/173910.

MLA Handbook (7^th Edition):

Lee, Junseok. “Mapping and Analyzing the Full Vascular Network in the Mouse Brain at Submicrometer Resolution.” 2018. Web. 27 Feb 2021.

Vancouver:

Lee J. Mapping and Analyzing the Full Vascular Network in the Mouse Brain at Submicrometer Resolution. [Internet] [Doctoral dissertation]. Texas A&M University; 2018. [cited 2021 Feb 27]. Available from: http://hdl.handle.net/1969.1/173910.

Council of Science Editors:

Lee J. Mapping and Analyzing the Full Vascular Network in the Mouse Brain at Submicrometer Resolution. [Doctoral Dissertation]. Texas A&M University; 2018. Available from: http://hdl.handle.net/1969.1/173910

McMaster University

20. Lai, Jonathan. Neurodevelopmental Outcomes in the Fragile X Mouse.

Degree: PhD, 2015, McMaster University

URL: http://hdl.handle.net/11375/17209

►

Fragile X Syndrome (FXS) is a neurodevelopmental disorder and the most common heritable single gene cause of Autism Spectrum Disorder (ASD). The Fragile X (FMR1-KO)… (more)

▼

Fragile X Syndrome (FXS) is a neurodevelopmental disorder and the most common heritable single gene cause of Autism Spectrum Disorder (ASD). The Fragile X (FMR1-KO) mouse model has been used to understand the pathophysiology of the disease. However, the majority of studies have been done in adult mice and early life outcomes have yet to be explored. Therefore, in order to contribute to the knowledge of the neurodevelopmental processes associated with brain disorders, this thesis examines postnatal outcomes in the Fragile X Mouse Model: early life behaviours, the developmental trajectory of a set of ASD risk genes, and neuroanatomical phenotype. The first study examined ultrasonic vocalizations in pups and showed a transient increase in calls in FMR1-KO mice. To understand the relationship between early life behaviours, the second study examined outcomes in the pre-pubertal period in these mice when challenged with lipopolysaccharide and maternal separation. The results showed genotype and treatment interactions affecting sexually dimorphic behavioural outcomes and developmental milestones. In the third study, possible underpinnings of behavioural differences were explored by examining mRNA expression of the neuroligins and neurexins. In FMR1-KO mice, changes were transient and sex-specific, suggesting these as molecular effectors in the disease. Lastly, using structural brain imaging, the fourth study examined regional volume differences that may be related to behavioural differences. Differences in regions affected in FXS patients were observed and genetic background was shown to affect the neuroanatomical phenotype. Overall, this thesis demonstrates that the FXS model recapitulates some outcomes in other ASD mouse models and shows that this single gene has multiple interactions with sex, strain, and postnatal challenge which manifests at specific ages at molecular, brain structure and behavioural levels. This work contributes to the efforts elucidating the neurobiology of ASD and reverse translation approaches to identify therapeutic targets for neurodevelopment disorders.

Dissertation

Doctor of Philosophy (PhD)

Autism spectrum disorder (ASD) is a diagnosis based on observed behaviours: impaired communication and repetitive actions. However, there are genetic and other behavioural differences in ASD patients that are not shared among the group. It is important to tease apart this group since current treatments for ASD do not target the biological problems or the core impairments. This thesis focuses on Fragile X Syndrome, the leading genetic condition that results in ASD in order to understand the biological basis of ASD. Using a mouse model, compared to healthy mice, these studies report changes in behaviours, in the size of different brain regions, and in molecules involved in connecting brain cells during development. These findings shed light on the molecular story underlying ASD. By understanding the nature of influences on the developing brain, the type and timing of interventions can be designed to…

Advisors/Committee Members: Foster, Jane, Neuroscience.

Subjects/Keywords: brain development; genetic mouse model

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APA (6^th Edition):

Lai, J. (2015). Neurodevelopmental Outcomes in the Fragile X Mouse. (Doctoral Dissertation). McMaster University. Retrieved from http://hdl.handle.net/11375/17209

Chicago Manual of Style (16^th Edition):

Lai, Jonathan. “Neurodevelopmental Outcomes in the Fragile X Mouse.” 2015. Doctoral Dissertation, McMaster University. Accessed February 27, 2021. http://hdl.handle.net/11375/17209.

MLA Handbook (7^th Edition):

Lai, Jonathan. “Neurodevelopmental Outcomes in the Fragile X Mouse.” 2015. Web. 27 Feb 2021.

Vancouver:

Lai J. Neurodevelopmental Outcomes in the Fragile X Mouse. [Internet] [Doctoral dissertation]. McMaster University; 2015. [cited 2021 Feb 27]. Available from: http://hdl.handle.net/11375/17209.

Council of Science Editors:

Lai J. Neurodevelopmental Outcomes in the Fragile X Mouse. [Doctoral Dissertation]. McMaster University; 2015. Available from: http://hdl.handle.net/11375/17209

McMaster University

21. Chaudhary, Roopali. OVEREXPRESSION OF THE TRANSCRIPTION FACTOR KAISO IN MURINE INTESTINES INDUCES INFLAMMATION.

Degree: 2015, McMaster University

URL: http://hdl.handle.net/11375/17215

►

Since the discovery of the p120ctn binding partner, Kaiso, a BTB/POZ transcription factor, several studies have implicated the protein in both development and tumourigenesis. Most… (more)

Subjects/Keywords: Mouse intestine; Inflamamtion; Kaiso; Transgenics

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APA (6^th Edition):

Chaudhary, R. (2015). OVEREXPRESSION OF THE TRANSCRIPTION FACTOR KAISO IN MURINE INTESTINES INDUCES INFLAMMATION. (Thesis). McMaster University. Retrieved from http://hdl.handle.net/11375/17215

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Chaudhary, Roopali. “OVEREXPRESSION OF THE TRANSCRIPTION FACTOR KAISO IN MURINE INTESTINES INDUCES INFLAMMATION.” 2015. Thesis, McMaster University. Accessed February 27, 2021. http://hdl.handle.net/11375/17215.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Chaudhary, Roopali. “OVEREXPRESSION OF THE TRANSCRIPTION FACTOR KAISO IN MURINE INTESTINES INDUCES INFLAMMATION.” 2015. Web. 27 Feb 2021.

Vancouver:

Chaudhary R. OVEREXPRESSION OF THE TRANSCRIPTION FACTOR KAISO IN MURINE INTESTINES INDUCES INFLAMMATION. [Internet] [Thesis]. McMaster University; 2015. [cited 2021 Feb 27]. Available from: http://hdl.handle.net/11375/17215.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Chaudhary R. OVEREXPRESSION OF THE TRANSCRIPTION FACTOR KAISO IN MURINE INTESTINES INDUCES INFLAMMATION. [Thesis]. McMaster University; 2015. Available from: http://hdl.handle.net/11375/17215

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

North Carolina State University

22. Summers, Caroline Rueda. Modulation of Inflammatory Responses by Green and Black Tea in LPS-induced RAW 264.7 Cells.

Degree: MS, Nutrition, 2010, North Carolina State University

URL: http://www.lib.ncsu.edu/resolver/1840.16/6332

► Recently, the World Health Organization estimated that chronic diseases are responsible for 46% of disease occurrence and 59% of all deaths worldwide. Growing evidence suggests… (more)

▼ Recently, the World Health Organization estimated that chronic diseases are responsible for 46% of disease occurrence and 59% of all deaths worldwide. Growing evidence suggests that increasing chronic disease incidence is dependent upon several factors, including inadequate consumption of antioxidant-rich fruits and vegetables and chronic inflammation. Many researchers have previously investigated potential health benefits associated with consuming plant-based foods, and the ability of these foods to prevent or suppress the pathologies linked to chronic diseases. Specifically, plant-based bioactive compounds called polyphenols have been widely studied, and show promise as a therapeutic agent against chronic diseases. Tea is produced from the leaves of the Camellia sinensis plant and, aside from water, is the most popular beverage in the world. Green tea, black tea, and oolong tea are the three major types of commercially produced tea. Black tea comprises over 75% of global tea production and consumption, followed by green tea at approximately 20%, and oolong tea at less than 2%. For centuries, tea has been known for its health effects. It has historically been used as a medicine in China and Japan. Tea polyphenols are particularly thought to have chemopreventive and cardioprotective effects due to their antioxidant and anti-inflammatory properties. Previous in vitro and animal studies have analyzed the anti-inflammatory activity of polyphenols, and the specific mechanisms by which these compounds suppress inflammation. But, to our knowledge, few studies have investigated teaâ€™s anti-inflammatory capacity as a whole food, or compared the potential anti-inflammatory effects of different tea types. Therefore, the objectives of the following study were to evaluate total phenol content in green tea (GT) and black tea (BT); to assess viability of cells exposed to GT, BT, and LPS; and to measure the modulation of inflammatory responses in lipopolysaccharide (LPS)-induced RAW 264.7 mouse macrophages by GT and BT. We predicted that GT and BT would differentially modulate inflammation because of differences in composition. First, the total phenolic content in commercially produced GT and BT was measured using the Folin-Ciocalteu method. Freshly prepared GT had a significantly higher phenolic content than freshly prepared BT (1317.1 + 6.0 GAE, 918.9 + 10.7 GAE). Stored at -80Â° C, the phenolic content of GT and BT significantly increased at one month (1770.0 + 35.2 GAE, 1124.0 + 19.1 GAE) and two months post-preparation (1587.2 + 21.5 GAE, 1003.2 + 8.6 GAE), then decreased at 3 months post-preparation (1407.8 + 13.4 GAE, 941.8 + 0.5 GAE) (p < 0.05). The second goal of our study was to assess viability in RAW 264.7 cells treated with GT, BT, and LPS. Viability was colorimetrically determined by the Trypan Blue assay and by measured absorbance values from the MTT assay. The GT, BT, and LPS treatments did not produce a cytotoxic effect, and cell viability values for each treatment were not significantly… Advisors/Committee Members: Dr. Brenda P. Alston-Mills, Committee Member (advisor), Dr. Jonathan C. Allen, Committee Co-Chair (advisor), Dr. Gabriel Keith Harris, Committee Chair (advisor).

Subjects/Keywords: LPS; tea; mouse macrophage; inflammation

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APA (6^th Edition):

Summers, C. R. (2010). Modulation of Inflammatory Responses by Green and Black Tea in LPS-induced RAW 264.7 Cells. (Thesis). North Carolina State University. Retrieved from http://www.lib.ncsu.edu/resolver/1840.16/6332

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Summers, Caroline Rueda. “Modulation of Inflammatory Responses by Green and Black Tea in LPS-induced RAW 264.7 Cells.” 2010. Thesis, North Carolina State University. Accessed February 27, 2021. http://www.lib.ncsu.edu/resolver/1840.16/6332.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Summers, Caroline Rueda. “Modulation of Inflammatory Responses by Green and Black Tea in LPS-induced RAW 264.7 Cells.” 2010. Web. 27 Feb 2021.

Vancouver:

Summers CR. Modulation of Inflammatory Responses by Green and Black Tea in LPS-induced RAW 264.7 Cells. [Internet] [Thesis]. North Carolina State University; 2010. [cited 2021 Feb 27]. Available from: http://www.lib.ncsu.edu/resolver/1840.16/6332.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Summers CR. Modulation of Inflammatory Responses by Green and Black Tea in LPS-induced RAW 264.7 Cells. [Thesis]. North Carolina State University; 2010. Available from: http://www.lib.ncsu.edu/resolver/1840.16/6332

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

23. Dingle, Yu-Ting Liu. In Vitro Modeling of the Central Nervous System: Towards Optimized Cell-based Therapies.

Degree: PhD, Biomedical Engineering, 2015, Brown University

URL: https://repository.library.brown.edu/studio/item/bdr:419530/

► Cell-based therapy is a promising treatment option for central nervous system (CNS) disease and injury, but therapy strategies require optimization to achieve clinical improvement. The… (more)

▼ Cell-based therapy is a promising treatment option for central nervous system (CNS) disease and injury, but therapy strategies require optimization to achieve clinical improvement. The primary motivation of this thesis is to gain knowledge of in vitro neuronal differentiation of stem cells and to develop three-dimensional (3D) culture models to investigate stem cell transplantation to the CNS. The first study in this thesis addressed the heterogeneity of mouse embryonic stem cell-derived dopamine neurons. In vitro, the percentage of calbindin+ subtype of DA neurons was higher than the calretinin+ subtype, which was a similar trend to in vivo. In addition, dopamine neuron subtype generation in vitro was not governed by exogenous sonic hedgehog and fibroblast growth factor 8. In the second study, we developed a scaffold-free, 3D neural spheroid culture using primary rat cerebral cortex cells. Cortical cells in agarose hydrogels containing round-bottom microwells self-assembled into spheroids. The 3D neural spheroids recapitulated key in vivo-like features including 3D neuronal and astroglial network formation, extracellular matrix production, electrical activity, circuitry formation via excitatory and inhibitory synapses, and brain-like mechanical properties. These physiologically relevant characteristics make these spheroids an effective in vitro model for the CNS. In the third study, we expanded the 3D culture technique to develop an in vitro model for stem cell transplantation to the CNS. To represent the host CNS tissue in vitro, trampoline-shaped 3D microtissues were fabricated using cortical cells. Neural stem cells (NSCs) in the form of spheroids were placed in the center of the CNS host trampoline microtissues, and NSC behavior in this transplantation model construct was monitored. In a proof-of-concept experiment, we utilized this model to test the effect of fibroblast growth factor 2 on NSC migration. Based on the microtissue characterization results, this 3D in vitro transplantation model has the potential to generate more translatable results than 2D co-culture platforms. These works together contribute to a deeper understanding of in vitro generation of neurons and provide a novel in vitro 3D engineered CNS model for the investigation of cell-based therapies. Advisors/Committee Members: Hoffman-Kim, Diane (Director), Morgan, Jeffrey (Reader), Darling, Eric (Reader), Coulombe, Kareen (Reader), Kaplan, David (Reader).

Subjects/Keywords: mouse embryonic stem cells

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APA (6^th Edition):

Dingle, Y. L. (2015). In Vitro Modeling of the Central Nervous System: Towards Optimized Cell-based Therapies. (Doctoral Dissertation). Brown University. Retrieved from https://repository.library.brown.edu/studio/item/bdr:419530/

Chicago Manual of Style (16^th Edition):

Dingle, Yu-Ting Liu. “In Vitro Modeling of the Central Nervous System: Towards Optimized Cell-based Therapies.” 2015. Doctoral Dissertation, Brown University. Accessed February 27, 2021. https://repository.library.brown.edu/studio/item/bdr:419530/.

MLA Handbook (7^th Edition):

Dingle, Yu-Ting Liu. “In Vitro Modeling of the Central Nervous System: Towards Optimized Cell-based Therapies.” 2015. Web. 27 Feb 2021.

Vancouver:

Dingle YL. In Vitro Modeling of the Central Nervous System: Towards Optimized Cell-based Therapies. [Internet] [Doctoral dissertation]. Brown University; 2015. [cited 2021 Feb 27]. Available from: https://repository.library.brown.edu/studio/item/bdr:419530/.

Council of Science Editors:

Dingle YL. In Vitro Modeling of the Central Nervous System: Towards Optimized Cell-based Therapies. [Doctoral Dissertation]. Brown University; 2015. Available from: https://repository.library.brown.edu/studio/item/bdr:419530/

Purdue University

24. Umapathi, Udayan. Realization And Evaluation Of A 3-Degrees-Of-Freedom Mouse Model.

Degree: MS, Electrical and Computer Engineering, 2014, Purdue University

URL: http://docs.lib.purdue.edu/open_access_theses/387

► Kinesiology research has shown that translation and rotation are inseparable actions in the real world. Motivated by this fact, this thesis explores a model… (more)

Subjects/Keywords: Applied sciences; 3-degrees-of- freedom mouse; Intertial mouse; Mouse; Rotational mouse; Computer Engineering; Electrical and Computer Engineering

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Umapathi, U. (2014). Realization And Evaluation Of A 3-Degrees-Of-Freedom Mouse Model. (Thesis). Purdue University. Retrieved from http://docs.lib.purdue.edu/open_access_theses/387

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Umapathi, Udayan. “Realization And Evaluation Of A 3-Degrees-Of-Freedom Mouse Model.” 2014. Thesis, Purdue University. Accessed February 27, 2021. http://docs.lib.purdue.edu/open_access_theses/387.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Umapathi, Udayan. “Realization And Evaluation Of A 3-Degrees-Of-Freedom Mouse Model.” 2014. Web. 27 Feb 2021.

Vancouver:

Umapathi U. Realization And Evaluation Of A 3-Degrees-Of-Freedom Mouse Model. [Internet] [Thesis]. Purdue University; 2014. [cited 2021 Feb 27]. Available from: http://docs.lib.purdue.edu/open_access_theses/387.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Umapathi U. Realization And Evaluation Of A 3-Degrees-Of-Freedom Mouse Model. [Thesis]. Purdue University; 2014. Available from: http://docs.lib.purdue.edu/open_access_theses/387

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Brigham Young University

25. Chronis, Rhonda Nicole. Comparison of Cytokine Expression and Bacterial Growth During Periparturient and Mid Lactation Mastitis in a Mouse Model.

Degree: MS, 2017, Brigham Young University

URL: https://scholarsarchive.byu.edu/cgi/viewcontent.cgi?article=7847&context=etd

► Clinical cases of bovine mastitis are most severe in the early stages of lactation. The causes of this increased propensity for severe mastitis during early… (more)

Subjects/Keywords: mastitis; periparturient; mouse model; Microbiology

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APA (6^th Edition):

Chronis, R. N. (2017). Comparison of Cytokine Expression and Bacterial Growth During Periparturient and Mid Lactation Mastitis in a Mouse Model. (Masters Thesis). Brigham Young University. Retrieved from https://scholarsarchive.byu.edu/cgi/viewcontent.cgi?article=7847&context=etd

Chicago Manual of Style (16^th Edition):

Chronis, Rhonda Nicole. “Comparison of Cytokine Expression and Bacterial Growth During Periparturient and Mid Lactation Mastitis in a Mouse Model.” 2017. Masters Thesis, Brigham Young University. Accessed February 27, 2021. https://scholarsarchive.byu.edu/cgi/viewcontent.cgi?article=7847&context=etd.

MLA Handbook (7^th Edition):

Chronis, Rhonda Nicole. “Comparison of Cytokine Expression and Bacterial Growth During Periparturient and Mid Lactation Mastitis in a Mouse Model.” 2017. Web. 27 Feb 2021.

Vancouver:

Chronis RN. Comparison of Cytokine Expression and Bacterial Growth During Periparturient and Mid Lactation Mastitis in a Mouse Model. [Internet] [Masters thesis]. Brigham Young University; 2017. [cited 2021 Feb 27]. Available from: https://scholarsarchive.byu.edu/cgi/viewcontent.cgi?article=7847&context=etd.

Council of Science Editors:

Chronis RN. Comparison of Cytokine Expression and Bacterial Growth During Periparturient and Mid Lactation Mastitis in a Mouse Model. [Masters Thesis]. Brigham Young University; 2017. Available from: https://scholarsarchive.byu.edu/cgi/viewcontent.cgi?article=7847&context=etd

University of California – San Francisco

26. Halpern, Benjamin. Effect of Macrophage Activity and Age on Periodontal Disease in a Mouse Model.

Degree: Oral and Craniofacial Sciences, 2019, University of California – San Francisco

URL: http://www.escholarship.org/uc/item/3zz6b97g

► Background: Periodontal disease is an inflammatory disease that increases in prevalence with increasing age. The elderly demonstrate an elevated and dysregulated inflammatory response. Macrophages act… (more)

▼ Background: Periodontal disease is an inflammatory disease that increases in prevalence with increasing age. The elderly demonstrate an elevated and dysregulated inflammatory response. Macrophages act as a key regulator of inflammation. The study aim was to evaluate the extent to which age-related changes and chemical inhibition in the macrophage affect periodontal disease in a mouse model. Methods: Old (24 month) and young (3 month) mice were utilized for this study. Periodontal status was examined in mice at baseline. Periodontal disease was induced via Porphyromonas gingivalis (P. gingivalis) inoculated ligatures in old and young mice for 7 days. A second cohort had disease induced for 7 days, followed by ligature removal, and recovery for 7 additional days. Half the mice in each induction or recovery group were treated with Pexidartinib (PLX), which inhibits macrophage recruitment. Linear bone loss, alveolar bone volume, and macrophage quantification were examined by t test.Results: PLX successfully inhibited macrophage numbers in all treatment groups. The young periodontal disease group had significantly more vertical bone loss (0.234±0.024mm) compared to the young periodontal disease PLX group (0.140±0.023mm)(p≤0.001) and less alveolar bone volume (0.460±0.016BV/TV) compared to the young periodontal disease PLX group (0.586±0.004BV/TV)(p≤0.001). The old periodontal disease group exhibited no difference in vertical bone loss (0.242±0.025mm) compared to the old periodontal disease PLX group (0.238±0.032mm)(p=0.825) and significantly less alveolar bone volume (0.536±0.030BV/TV) compared to the old periodontal disease PLX group (0.614±0.030BV/TV)(p≤0.01). The young recovery control group trended towards less vertical bone loss (0.170±0.020mm) compared to the young recovery + PLX group (0.190±0.011mm)(p=0.055) and had no difference in alveolar bone volume (0.557±0.015 BV/TV) compared to the young recovery PLX group (0.545±0.011 BV/TV)(p=0.131). The old recovery control group exhibited no difference in vertical bone loss (0.241±0.019mm) compared to the old recovery PLX group (0.218±0.035mm)(p=0.187) and had significantly less alveolar bone volume (0.567±0.021BV/TV) compared to the old recovery PLX group (0.617±0.023BV/TV)(p≤0.01).Conclusion:PLX prevents periodontal disease induction in old and young groups and improves recovery in older age groups. The difference in response during recovery could suggest that there are age related changes in the macrophage that affect disease progression.

Subjects/Keywords: Biochemistry; Age; Macrophage; Mouse; Periodontitis

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Halpern, B. (2019). Effect of Macrophage Activity and Age on Periodontal Disease in a Mouse Model. (Thesis). University of California – San Francisco. Retrieved from http://www.escholarship.org/uc/item/3zz6b97g

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Halpern, Benjamin. “Effect of Macrophage Activity and Age on Periodontal Disease in a Mouse Model.” 2019. Thesis, University of California – San Francisco. Accessed February 27, 2021. http://www.escholarship.org/uc/item/3zz6b97g.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Halpern, Benjamin. “Effect of Macrophage Activity and Age on Periodontal Disease in a Mouse Model.” 2019. Web. 27 Feb 2021.

Vancouver:

Halpern B. Effect of Macrophage Activity and Age on Periodontal Disease in a Mouse Model. [Internet] [Thesis]. University of California – San Francisco; 2019. [cited 2021 Feb 27]. Available from: http://www.escholarship.org/uc/item/3zz6b97g.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Halpern B. Effect of Macrophage Activity and Age on Periodontal Disease in a Mouse Model. [Thesis]. University of California – San Francisco; 2019. Available from: http://www.escholarship.org/uc/item/3zz6b97g

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Toronto

27. Minty, Gillian Eleanor Summersgill. The Role of TLR3 in the Development of Lupus-like Autoimmunity in B6.NZBc13 Mice.

Degree: 2013, University of Toronto

URL: http://hdl.handle.net/1807/43245

►

The New Zealand Black (NZB) mouse chromosome 13 (c13) is linked to development of autoimmunity. B6 mice containing a portion of NZBc13 (B6.NZBc13 (c13)) develop… (more)

Subjects/Keywords: Autoimmunity; mouse model; SLE; 0982

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APA (6^th Edition):

Minty, G. E. S. (2013). The Role of TLR3 in the Development of Lupus-like Autoimmunity in B6.NZBc13 Mice. (Masters Thesis). University of Toronto. Retrieved from http://hdl.handle.net/1807/43245

Chicago Manual of Style (16^th Edition):

Minty, Gillian Eleanor Summersgill. “The Role of TLR3 in the Development of Lupus-like Autoimmunity in B6.NZBc13 Mice.” 2013. Masters Thesis, University of Toronto. Accessed February 27, 2021. http://hdl.handle.net/1807/43245.

MLA Handbook (7^th Edition):

Minty, Gillian Eleanor Summersgill. “The Role of TLR3 in the Development of Lupus-like Autoimmunity in B6.NZBc13 Mice.” 2013. Web. 27 Feb 2021.

Vancouver:

Minty GES. The Role of TLR3 in the Development of Lupus-like Autoimmunity in B6.NZBc13 Mice. [Internet] [Masters thesis]. University of Toronto; 2013. [cited 2021 Feb 27]. Available from: http://hdl.handle.net/1807/43245.

Council of Science Editors:

Minty GES. The Role of TLR3 in the Development of Lupus-like Autoimmunity in B6.NZBc13 Mice. [Masters Thesis]. University of Toronto; 2013. Available from: http://hdl.handle.net/1807/43245

28. Bogni, Caroline. Développement de thérapies géniques pour les myopathies congénitales : Development of gene thérapies for congenital myopathies.

Degree: Docteur es, Sciences de la vie et de la santé, 2019, Université Paris-Saclay (ComUE)

URL: http://www.theses.fr/2019SACLE038

► Les myopathies congénitales sont des maladies génétiques rares touchant les muscles qui ne possèdent pour le moment pas de traitement curatif. Elles se manifestent par… (more)

▼ Les myopathies congénitales sont des maladies génétiques rares touchant les muscles qui ne possèdent pour le moment pas de traitement curatif. Elles se manifestent par une hypotonie et une faiblesse musculaire généralisée pouvant entrainer le décès précoce des patients. Parmi elles, on retrouve la myopathie à némaline (NEM3) causée par des mutations dans le gène de l'alpha-actine (ACTA1) et la myopathie myotubulaire (XLMTM) liée à MTM1, qui se caractérisent respectivement du point de vue histopathologique par la présence d'agrégats protéiques et de noyaux en position centrale dans les fibres musculaires, et dont les mécanismes physiopathologiques sont encore mal connus.Dans ce projet de thèse, j'ai étudié la physiopathologie de la NEM3 grâce à l'analyse du transcriptome des muscles du modèle murin porteur de la mutation p.H40Y dans Acta1 (KI(Acta1)H40Y). Ainsi, plusieurs voies de signalisation ont été révélées comme étant dérégulées, notamment celles contrôlant la masse musculaire et la transmission synaptique. J'ai analysé la morphologie et fonction des jonctions neuromusculaires (JNM) et mis en évidence une fragmentation de celles-ci, associée à des altérations ultrastructurales et moléculaires, et une fatigabilité accrue du muscle mutant lors d'une stimulation nerveuse électrophysiologique répétée, ce qui pourrait ouvrir des perspectives de traitement pharmacologique. Parallèlement, j'ai aussi exploré des stratégies de thérapie génique pour cette myopathie. Mes résultats ont montré que l'administration intramusculaire et intraveineuse de virus adéno-associés recombinants (AAVr) exprimant le transgène ACTA1 sous le promoteur de la desmine ou du cytomégalovirus n'a pas permis d'améliorer le phénotype des souris KI(Acta1)H40Y. Ainsi, j'ai mis au point une autre approche consistant à réduire l'expression de l'ARN messager d'Acta1 et sélectionné in vitro des séquences siARN ayant la meilleure spécificité pour l'allèle muté. L'injection intramusculaire de vecteurs AAV exprimant des shARN ciblant le transcrit d'Acta1 muté chez le modèle murin n'a cependant pas montré de signes d'amélioration de la pathologie, mais plutôt une importante réaction immunitaire. Mes résultats indiquent donc qu'une optimisation de ces stratégies de thérapie génique sera nécessaire pour corriger la maladie.D'autre part, dans le contexte de la myopathie myotubulaire, j'ai participé au développement d'une approche thérapeutique visant à diminuer le niveau d'expression de la dynamine 2 dans les cellules musculaires en utilisant des oligonucléotides antisens (vivo-morpholinos). Des mutations dans le gène de la dynamine 2 (DNM2) sont responsables de la forme autosomique dominante de myopathie centronucléaire et la neuropathie de Charcot-Marie-Tooth de type DI-CMT2B; de plus, la surexpression de DNM2 est impliquée dans le mécanisme physiopathologique de la myopathie myotubulaire. Nous avons montré que l'administration intramusculaire de vivo-morpholinos chez le modèle murin de XLMTM (KO-Mtm1) permet d'améliorer la pathologie, avec une augmentation de… Advisors/Committee Members: Buj-Bello, Ana (thesis director).

Subjects/Keywords: Modèle murin; Mouse model

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APA (6^th Edition):

Bogni, C. (2019). Développement de thérapies géniques pour les myopathies congénitales : Development of gene thérapies for congenital myopathies. (Doctoral Dissertation). Université Paris-Saclay (ComUE). Retrieved from http://www.theses.fr/2019SACLE038

Chicago Manual of Style (16^th Edition):

Bogni, Caroline. “Développement de thérapies géniques pour les myopathies congénitales : Development of gene thérapies for congenital myopathies.” 2019. Doctoral Dissertation, Université Paris-Saclay (ComUE). Accessed February 27, 2021. http://www.theses.fr/2019SACLE038.

MLA Handbook (7^th Edition):

Bogni, Caroline. “Développement de thérapies géniques pour les myopathies congénitales : Development of gene thérapies for congenital myopathies.” 2019. Web. 27 Feb 2021.

Vancouver:

Bogni C. Développement de thérapies géniques pour les myopathies congénitales : Development of gene thérapies for congenital myopathies. [Internet] [Doctoral dissertation]. Université Paris-Saclay (ComUE); 2019. [cited 2021 Feb 27]. Available from: http://www.theses.fr/2019SACLE038.

Council of Science Editors:

Bogni C. Développement de thérapies géniques pour les myopathies congénitales : Development of gene thérapies for congenital myopathies. [Doctoral Dissertation]. Université Paris-Saclay (ComUE); 2019. Available from: http://www.theses.fr/2019SACLE038

University of Toronto

29. Carias, Marc. Comparison of Radiofrequency Coil Configurations for Multiple Mouse Magnetic Resonance Imaging.

Degree: 2013, University of Toronto

URL: http://hdl.handle.net/1807/42700

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Multiple-mouse MRI (MMMRI) accelerates biomedical research by imaging multiple mice simultaneously. To date, MMMRI has been explored in three ways: shielded transmit-receive coils, shielded transmits… (more)

Subjects/Keywords: Radiofrequency Coil; Mouse MRI; 0760

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Carias, M. (2013). Comparison of Radiofrequency Coil Configurations for Multiple Mouse Magnetic Resonance Imaging. (Masters Thesis). University of Toronto. Retrieved from http://hdl.handle.net/1807/42700

Chicago Manual of Style (16^th Edition):

Carias, Marc. “Comparison of Radiofrequency Coil Configurations for Multiple Mouse Magnetic Resonance Imaging.” 2013. Masters Thesis, University of Toronto. Accessed February 27, 2021. http://hdl.handle.net/1807/42700.

MLA Handbook (7^th Edition):

Carias, Marc. “Comparison of Radiofrequency Coil Configurations for Multiple Mouse Magnetic Resonance Imaging.” 2013. Web. 27 Feb 2021.

Vancouver:

Carias M. Comparison of Radiofrequency Coil Configurations for Multiple Mouse Magnetic Resonance Imaging. [Internet] [Masters thesis]. University of Toronto; 2013. [cited 2021 Feb 27]. Available from: http://hdl.handle.net/1807/42700.

Council of Science Editors:

Carias M. Comparison of Radiofrequency Coil Configurations for Multiple Mouse Magnetic Resonance Imaging. [Masters Thesis]. University of Toronto; 2013. Available from: http://hdl.handle.net/1807/42700

University of Colorado

30. Maranjian, Kayla Jean. Mechanical and material property changes in bone with experimental diabetes: a murine model.

Degree: MS, Mechanical Engineering, 2011, University of Colorado

URL: https://scholar.colorado.edu/mcen_gradetds/28

► Over 23 million people in the United States are plagued by diabetes mellitus. Studies have shown that those with diabetes have a higher occurrence… (more)

▼ Over 23 million people in the United States are plagued by diabetes mellitus. Studies have shown that those with diabetes have a higher occurrence of bone fractures than those without the disease, but risk factors associated with diabetes account for only a portion of these fractures (Schwartz 2003; Vestergaard 2006). This implies that there are properties of diabetic bones that account for this increase in fractures. Research has been performed on the bone mineral density (BMD) of those with and without diabetes. However, studying this singular property of bones does not fully explain the increase in bone fractures in the diabetic population. Additionally, this research has yielded inconclusive results: some studies show that diabetes leads to an increase in BMD while others show a decrease in this property (Krakauer et al. 1995; Retzepi & Donos 2010). The objective of this study is to analyze the effect of experimental diabetes on bone properties in mice. This relationship is explored through analyzing different mouse strains to determine a potential genetic link, kidney removal to mimic the effects of nephropathy, and an LXR agonist to explore a potential diabetes treatment. We hypothesize that diabetes will negatively impact bone properties across multiple strains of mice, kidney removal will further degrade bone properties and the LXR agonist will improve some of the negative bone effects that diabetes causes. In general, STZ-induced diabetes was accompanied by decreases in physical and compositional bone properties in both strains of mice. Kidney removal and treatment with an LXR-agonist had little to no effects on these bone properties. Kidney removal was performed in skeletally mature mice; this old age may have contributed to the lack of effects. Similarly, the LXR agonist was administered over a short time period, and the detrimental effects from the diabetes were not able to be overcome. The data presented here provides evidence that experimentally-induced diabetes corresponds with a decrease in bone properties and nephropathy. While LXR agonists hold promise for mitigating bone property changes in diabetes, further analysis is required to determine their potential effects. Advisors/Committee Members: Virginia L. Ferguson, Mark Rentschler, Karen, King.

Subjects/Keywords: Biomedical; Bone; Mouse; Mechanical Engineering

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Maranjian, K. J. (2011). Mechanical and material property changes in bone with experimental diabetes: a murine model. (Masters Thesis). University of Colorado. Retrieved from https://scholar.colorado.edu/mcen_gradetds/28

Chicago Manual of Style (16^th Edition):

Maranjian, Kayla Jean. “Mechanical and material property changes in bone with experimental diabetes: a murine model.” 2011. Masters Thesis, University of Colorado. Accessed February 27, 2021. https://scholar.colorado.edu/mcen_gradetds/28.

MLA Handbook (7^th Edition):

Maranjian, Kayla Jean. “Mechanical and material property changes in bone with experimental diabetes: a murine model.” 2011. Web. 27 Feb 2021.

Vancouver:

Maranjian KJ. Mechanical and material property changes in bone with experimental diabetes: a murine model. [Internet] [Masters thesis]. University of Colorado; 2011. [cited 2021 Feb 27]. Available from: https://scholar.colorado.edu/mcen_gradetds/28.

Council of Science Editors:

Maranjian KJ. Mechanical and material property changes in bone with experimental diabetes: a murine model. [Masters Thesis]. University of Colorado; 2011. Available from: https://scholar.colorado.edu/mcen_gradetds/28

Open Access Theses and Dissertations