subject:(transgenic mouse models)

Dalhousie University

1. Fraser, Leanne M. Locomotor behaviour, emotionality, and cognition in the 3xTg-AD mouse model of Alzheimer's disease: A cross-sectional study.

Degree: PhD, Department of Psychology and Neuroscience, 2013, Dalhousie University

URL: http://hdl.handle.net/10222/28080

► The triple transgenic (3xTg-AD) mouse model of Alzheimer’s disease (AD) possesses three transgenes that lead to the development of amyloid-beta (A?) plaques (APPswe, PS1M146V) and… (more)

▼ The triple transgenic (3xTg-AD) mouse model of Alzheimer’s disease (AD) possesses three transgenes that lead to the development of amyloid-beta (A?) plaques (APPswe, PS1M146V) and neurofibrillary tangles (and tauP301L) (Oddo et al., 2003b). Although the neuropathology of these mice has been extensively studied (Sy et al., 2011), less research has been done to investigate their working memory, emotionality, and locomotor-related behaviour. Using a cross-sectional design, male and female 3xTg-AD mice were compared to control mice (B6129SF2/J) at five ages (2-, 6-, 9-, 12-, and 15-months of age) on a battery of five tests designed to measure: anxiety- and locomotor-related behaviours (open field [OF], elevated plus maze [EPM]); depression (forced swim test [FST]); motor coordination and motor learning (rotarod); and working and reference memory (8-arm radial maze [RAM]). Additionally, the brain tissue of male and female 3xTg-AD and control mice at 2- and 15-months of age was analyzed for the presence of A? plaques and human tauP301L. 3xTg-AD mice were found to travel less and freeze more in both the OF and the EPM, engage in fewer bouts of immobility in the FST, have a longer latency to fall on the rotarod, and make more working and reference memory errors in the RAM than controls. There was no effect of age on performance in any of the tests. Intracellular A? plaques and limited human tau were present in the brain tissue of 2-month old 3xTg-AD mice. At 15-months of age, the brain tissue of 3xTg-AD mice showed extensive intra- and extracellular A? plaques as well as tauP301L staining. The presence of intracellular A? at 2-months of age supports the behavioural differences observed in the 3xTg-AD mice at 2-months of age. However, the lack of progressive behavioural change does not match the increase in neuropathology seen in the brains of the 15-month old 3xTg-AD mice. The results of the present study suggest that while the 3xTg-AD mice display similar neuropathology and some of the behavioural differences seen in individuals with AD, they also exhibit contradictory behaviours; findings that should be taken into consideration for future researchers using 3xTg-AD mice. Advisors/Committee Members: Dr. Wim Crusio (external-examiner), Dr. Simon Sherry (graduate-coordinator), Dr. Jennifer Stamp (thesis-reader), Dr. Kenneth Rockwood (thesis-reader), Dr. Richard E. Brown (thesis-supervisor), Received (ethics-approval), Not Applicable (manuscripts), Not Applicable (copyright-release).

Subjects/Keywords: "Transgenic mice"; "Alzheimer's disease"; "Mouse models"; "Behaviour"; "Memory"; "Motor coordination"

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APA (6^th Edition):

Fraser, L. M. (2013). Locomotor behaviour, emotionality, and cognition in the 3xTg-AD mouse model of Alzheimer's disease: A cross-sectional study. (Doctoral Dissertation). Dalhousie University. Retrieved from http://hdl.handle.net/10222/28080

Chicago Manual of Style (16^th Edition):

Fraser, Leanne M. “Locomotor behaviour, emotionality, and cognition in the 3xTg-AD mouse model of Alzheimer's disease: A cross-sectional study.” 2013. Doctoral Dissertation, Dalhousie University. Accessed March 03, 2021. http://hdl.handle.net/10222/28080.

MLA Handbook (7^th Edition):

Fraser, Leanne M. “Locomotor behaviour, emotionality, and cognition in the 3xTg-AD mouse model of Alzheimer's disease: A cross-sectional study.” 2013. Web. 03 Mar 2021.

Vancouver:

Fraser LM. Locomotor behaviour, emotionality, and cognition in the 3xTg-AD mouse model of Alzheimer's disease: A cross-sectional study. [Internet] [Doctoral dissertation]. Dalhousie University; 2013. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/10222/28080.

Council of Science Editors:

Fraser LM. Locomotor behaviour, emotionality, and cognition in the 3xTg-AD mouse model of Alzheimer's disease: A cross-sectional study. [Doctoral Dissertation]. Dalhousie University; 2013. Available from: http://hdl.handle.net/10222/28080

University College Cork

2. Heimer-McGinn, Victoria. Development and characterization of novel transgenic techniques for the study of neuronal circuitry.

Degree: 2013, University College Cork

URL: http://hdl.handle.net/10468/1251

► Modern neuroscience relies heavily on sophisticated tools that allow us to visualize and manipulate cells with precise spatial and temporal control. Transgenic mouse models, for… (more)

▼ Modern neuroscience relies heavily on sophisticated tools that allow us to visualize and manipulate cells with precise spatial and temporal control. Transgenic mouse models, for example, can be used to manipulate cellular activity in order to draw conclusions about the molecular events responsible for the development, maintenance and refinement of healthy and/or diseased neuronal circuits. Although it is fairly well established that circuits respond to activity-dependent competition between neurons, we have yet to understand either the mechanisms underlying these events or the higher-order plasticity that synchronizes entire circuits. In this thesis we aimed to develop and characterize transgenic mouse models that can be used to directly address these outstanding biological questions in different ways. We present SLICK-H, a Cre-expressing mouse line that can achieve drug-inducible, widespread, neuron-specific manipulations in vivo. This model is a clear improvement over existing models because of its particularly strong, widespread, and even distribution pattern that can be tightly controlled in the absence of drug induction. We also present SLICK-V::Ptox, a mouse line that, through expression of the tetanus toxin light chain, allows long-term inhibition of neurotransmission in a small subset (<1%) of fluorescently labeled pyramidal cells. This model, which can be used to study how a silenced cell performs in a wildtype environment, greatly facilitates the in vivo study of activity-dependent competition in the mammalian brain. As an initial application we used this model to show that tetanus toxin-expressing CA1 neurons experience a 15% - 19% decrease in apical dendritic spine density. Finally, we also describe the attempt to create additional Cre-driven mouse lines that would allow conditional alteration of neuronal activity either by hyperpolarization or inhibition of neurotransmission. Overall, the models characterized in this thesis expand upon the wealth of tools available that aim to dissect neuronal circuitry by genetically manipulating neurons in vivo. Advisors/Committee Members: Young, Paul, SFI.

Subjects/Keywords: Activity-dependent competition; Neuronal circuits; Tetanus toxin; Dendritic spines; Transgenic mouse models; Transgenic mice; Molecular neurobiology; Microbial toxins

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APA (6^th Edition):

Heimer-McGinn, V. (2013). Development and characterization of novel transgenic techniques for the study of neuronal circuitry. (Thesis). University College Cork. Retrieved from http://hdl.handle.net/10468/1251

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):

Heimer-McGinn, Victoria. “Development and characterization of novel transgenic techniques for the study of neuronal circuitry.” 2013. Thesis, University College Cork. Accessed March 03, 2021. http://hdl.handle.net/10468/1251.

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

MLA Handbook (7^th Edition):

Heimer-McGinn, Victoria. “Development and characterization of novel transgenic techniques for the study of neuronal circuitry.” 2013. Web. 03 Mar 2021.

Vancouver:

Heimer-McGinn V. Development and characterization of novel transgenic techniques for the study of neuronal circuitry. [Internet] [Thesis]. University College Cork; 2013. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/10468/1251.

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

Council of Science Editors:

Heimer-McGinn V. Development and characterization of novel transgenic techniques for the study of neuronal circuitry. [Thesis]. University College Cork; 2013. Available from: http://hdl.handle.net/10468/1251

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

University of California – San Diego

3. Nguyen, Annee. Peripheral Neuropathy and Sexual Dimorphism in Prion Disease Mouse Models.

Degree: Biology, 2018, University of California – San Diego

URL: http://www.escholarship.org/uc/item/5hp992p6

► In this study, I characterize peripheral neuropathic phenotypes in F35 mice (knock-out model of prion disease) and 93N mice (novel knock-in model of prion disease)… (more)

Subjects/Keywords: Biology; Pathology; Neurosciences; N-terminus; peripheral neuropathy; prion disease; sexual dimorphism; transgenic mouse models

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APA (6^th Edition):

Nguyen, A. (2018). Peripheral Neuropathy and Sexual Dimorphism in Prion Disease Mouse Models. (Thesis). University of California – San Diego. Retrieved from http://www.escholarship.org/uc/item/5hp992p6

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):

Nguyen, Annee. “Peripheral Neuropathy and Sexual Dimorphism in Prion Disease Mouse Models.” 2018. Thesis, University of California – San Diego. Accessed March 03, 2021. http://www.escholarship.org/uc/item/5hp992p6.

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

MLA Handbook (7^th Edition):

Nguyen, Annee. “Peripheral Neuropathy and Sexual Dimorphism in Prion Disease Mouse Models.” 2018. Web. 03 Mar 2021.

Vancouver:

Nguyen A. Peripheral Neuropathy and Sexual Dimorphism in Prion Disease Mouse Models. [Internet] [Thesis]. University of California – San Diego; 2018. [cited 2021 Mar 03]. Available from: http://www.escholarship.org/uc/item/5hp992p6.

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

Council of Science Editors:

Nguyen A. Peripheral Neuropathy and Sexual Dimorphism in Prion Disease Mouse Models. [Thesis]. University of California – San Diego; 2018. Available from: http://www.escholarship.org/uc/item/5hp992p6

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

4. Palmer, Daniel. Assessment of Visual Sustained Attention and Visual Spatial Integration in the APP/PS1, 5xFAD, and 3xTG Transgenic mouse models of Alzheimer’s disease.

Degree: PhD, Department of Psychology, 2017, University of Guelph

URL: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/10148

► In the course of Alzheimer’s Disease (AD) pathology, there is a progressive worsening of cognitive symptoms. One of the important steps in AD research has… (more)

▼ In the course of Alzheimer’s Disease (AD) pathology, there is a progressive worsening of cognitive symptoms. One of the important steps in AD research has been to identify early behavioural symptoms that can be used as markers of further cognitive decline. Previous research with humans has shown that attentional deficits may emerge early in the disease course, prior to memory impairments. It has also been shown that deficits in visual spatial learning are also an early marker of further cognitive decline. While these behaviours have been characterized in humans, there has been very little research looking at attention and visual spatial learning in transgenic mouse models of AD. The goal of these experiments was to systematically characterize attention and visual spatial learning in three of the most used transgenic mouse models of AD. TO assess behaviour, we used newly developed touchscreen equipped operant chambers. We used the APP/PS1, 5xFAD, and 3xTG transgenic mouse models of AD in the current study. We also assessed sex differences by comparing male and female mice performance. To assess attention, we used the 5-choice serial reaction time task (5-CSRTT). Animals were run on the 5-CSRTT at 4, 7, and 10 months of age to look for behavioural changes related to neurological decline. Visual spatial learning was assessed with the paired associate learning (PAL) task at 4 months of age. It was found that 3xTG and 5xFAD transgenic mice show deficits in attention, with the 3xTG mice showing a very early phenotype at 4 months of age. The 3xTG and APP/PS1 male transgenic mice showed a significant impairment in visual spatial learning, while the 5xFAD show significant impairment in the retention of visual spatial memories. Overall, these three transgenic lines show significant differences between strains. This study demonstrates that the cognitive profiles of these transgenic lines are dramatically different, and that researchers should make important considerations when deciding on which strain to use for their research. Advisors/Committee Members: Winters, Boyer (advisor).

Subjects/Keywords: Alzheimer's; Transgenic Mouse Models; Visual Spatial Learning; Attention; 3xTG; 5xFAD; APP/PS1; Touchscreen Operant Chamber

10 more images…

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APA (6^th Edition):

Palmer, D. (2017). Assessment of Visual Sustained Attention and Visual Spatial Integration in the APP/PS1, 5xFAD, and 3xTG Transgenic mouse models of Alzheimer’s disease. (Doctoral Dissertation). University of Guelph. Retrieved from https://atrium.lib.uoguelph.ca/xmlui/handle/10214/10148

Chicago Manual of Style (16^th Edition):

Palmer, Daniel. “Assessment of Visual Sustained Attention and Visual Spatial Integration in the APP/PS1, 5xFAD, and 3xTG Transgenic mouse models of Alzheimer’s disease.” 2017. Doctoral Dissertation, University of Guelph. Accessed March 03, 2021. https://atrium.lib.uoguelph.ca/xmlui/handle/10214/10148.

MLA Handbook (7^th Edition):

Palmer, Daniel. “Assessment of Visual Sustained Attention and Visual Spatial Integration in the APP/PS1, 5xFAD, and 3xTG Transgenic mouse models of Alzheimer’s disease.” 2017. Web. 03 Mar 2021.

Vancouver:

Palmer D. Assessment of Visual Sustained Attention and Visual Spatial Integration in the APP/PS1, 5xFAD, and 3xTG Transgenic mouse models of Alzheimer’s disease. [Internet] [Doctoral dissertation]. University of Guelph; 2017. [cited 2021 Mar 03]. Available from: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/10148.

Council of Science Editors:

Palmer D. Assessment of Visual Sustained Attention and Visual Spatial Integration in the APP/PS1, 5xFAD, and 3xTG Transgenic mouse models of Alzheimer’s disease. [Doctoral Dissertation]. University of Guelph; 2017. Available from: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/10148

Penn State University

5. Yura, Renee E. MEPRIN METALLOPROTEASES MODULATE THE HOST RESPONSE TO ESCHERICHIA COLI .

Degree: 2008, Penn State University

URL: https://submit-etda.libraries.psu.edu/catalog/8602

► Meprin metalloproteases, composed of alpha and/or beta subunits, consist of membrane-bound and secreted forms that are abundantly expressed in kidney and intestinal epithelial cells. They… (more)

▼ Meprin metalloproteases, composed of alpha and/or beta subunits, consist of membrane-bound and secreted forms that are abundantly expressed in kidney and intestinal epithelial cells. They are also expressed in the skin and in certain populations of leukocytes. Meprins have been implicated in several inflammatory diseases, such as renal ischemia, diabetic nephropathy, and inflammatory bowel disease, indicating a role for these enzymes in modulation of the immune response. Prior to the initiation of this work, extensive information about the structure and in vitro behavior of the meprins was known, but little was known about their in vivo roles in immune modulation. These studies are the first to demonstrate a relationship between the inflammatory response and the meprins in both systemic and bladder challenge models. The aim of this work was to determine the role of meprins in the host response to gram-negative uropathic Escherichia coli (E. coli). Initial studies demonstrated marked increases in meprin alpha expression in the urine of women with active urinary tract infections (UTIs), implicating meprin involvement in the host response to bacterial infections. To examine further the role of meprins in the host response to UTI, meprin alpha knockout (alphaKO) and wild-type (WT) mice were challenged with a transurethral inoculation of uropathic E. coli. In this localized model of inflammation, bladder myeloperoxidase (MPO) activity, bladder weight, and bladder permeability were significantly less in alphaKO compared to WT mice after induction of UTI. These data indicate that meprin A is pro-inflammatory, contributing to leukocyte infiltration, edema, and epithelial damage. To determine whether the action of meprin A was the result of a direct interaction with E. coli, extensive in vitro studies were carried out. Meprin A did not decrease the binding of E. coli to bladder cells in culture, nor did it degrade the pili that are responsible for the attachment of E. coli to the bladder epithelium. No evidence of direct interactions between meprin A and E. coli has been found, indicating that the differential response observed in meprin alphaKO mice in comparison to WT is indirect and likely involves the immune system. A large component of the immune response to E. coli is directed toward lipopolysaccharide (LPS) in the bacterial cell wall. Therefore, the responses of meprin alphaKO, meprin beta knockout (betaKO), meprin alphabeta double knockout (alphabetaKO), and WT mice after intraperitoneal (i.p.) LPS challenge were examined. Genotype-specific differences in response to LPS were observed as early as 1 h after challenge with 2.5 mg/kg i.p. E. coli LPS. Meprin alphaKO mice displayed a decreased systemic response to LPS compared to WT mice and meprin betaKO mice, as indicated by lower blood urea nitrogen (BUN) levels, lower serum TNFalpha levels, and less severe hypothermia, implicating meprin in modulation of the host immune response to endotoxin. These data are consistent with those from UTI studies,… Advisors/Committee Members: Judith S Bond, Committee Chair/Co-Chair, Sarah Bronson, Committee Member, Robert G Levenson, Committee Member, Andrea Manni, Committee Member, W. Brian Reeves, Committee Member.

Subjects/Keywords: meprins; metalloproteases; lipopolysaccharide; urinary tract infection; transgenic mouse models

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APA (6^th Edition):

Yura, R. E. (2008). MEPRIN METALLOPROTEASES MODULATE THE HOST RESPONSE TO ESCHERICHIA COLI . (Thesis). Penn State University. Retrieved from https://submit-etda.libraries.psu.edu/catalog/8602

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):

Yura, Renee E. “MEPRIN METALLOPROTEASES MODULATE THE HOST RESPONSE TO ESCHERICHIA COLI .” 2008. Thesis, Penn State University. Accessed March 03, 2021. https://submit-etda.libraries.psu.edu/catalog/8602.

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

MLA Handbook (7^th Edition):

Yura, Renee E. “MEPRIN METALLOPROTEASES MODULATE THE HOST RESPONSE TO ESCHERICHIA COLI .” 2008. Web. 03 Mar 2021.

Vancouver:

Yura RE. MEPRIN METALLOPROTEASES MODULATE THE HOST RESPONSE TO ESCHERICHIA COLI . [Internet] [Thesis]. Penn State University; 2008. [cited 2021 Mar 03]. Available from: https://submit-etda.libraries.psu.edu/catalog/8602.

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

Council of Science Editors:

Yura RE. MEPRIN METALLOPROTEASES MODULATE THE HOST RESPONSE TO ESCHERICHIA COLI . [Thesis]. Penn State University; 2008. Available from: https://submit-etda.libraries.psu.edu/catalog/8602

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

University of Oxford

6. Anwar, Sabina Zareen. Functional characterisation of synuclein-based novel genetic mouse models.

Degree: PhD, 2011, University of Oxford

URL: http://ora.ox.ac.uk/objects/uuid:b14fc29e-2bc8-4a31-865b-f4ec0e0f6f2c ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.558207

► Synucleins are highly conserved presynaptic proteins with unknown function. α-synuclein plays a key role regulating dopamine homeostasis and is intimately involved in Parkinson’s disease (PD)… (more)

▼ Synucleins are highly conserved presynaptic proteins with unknown function. α-synuclein plays a key role regulating dopamine homeostasis and is intimately involved in Parkinson’s disease (PD) pathogenesis. However, the normal/pathological role of α-synuclein remains unidentified. Studies exploring its function are limited as current transgenic mouse models do not fully recapitulate PD pathology. This thesis reports the functional characterisation of two novel synuclein-based mouse models. I report the molecular and functional characterisation of transgenic mouse lines with wild-type or A30P-mutant human α-synuclein genomic locus carried within a bacterial artificial chromosome. SNCA-A30P+Snca-/- mice exhibited a highly physiologically relevant expression pattern of the transgene, including expression in the substantia nigra pars compacta (SNpc) and a specific, age-related loss of TH+ cells in the SNpc, the key region of preferential cell loss in PD, compared with non-transgenic Snca -/- littermate controls. Analysis of dopamine signalling using fast-scan cyclic voltammetry (FCV) showed young adult SNCA-A30P+Snca-/- mice had an approximately 20% lower evoked extracellular dopamine concentration ([DA]o) compared with non-transgenic Snca -/- littermate controls, a decrease specific to the dorsal striatum. This difference diminished with age and could not be attributed to changes in dopamine reuptake/content. I detail the behavioural and neurochemical phenotype in mice lacking all three synucleins (α/β/γ). Functional compensation between synucleins emphasises the importance of studying their effects by removing all three proteins simultaneously. Triple-null mice exhibited hyperactivity in a novel environment reminiscent of a hyperdopaminergic-like phenotype, but showed no phenotype in anxiety or motor related tests. FCV revealed synuclein triple-null mice had a two-fold increase in [DA]o, specific to the dorsal striatum and not attributable to changes in dopamine reuptake/content, changes in striatal nicotinic receptor activity nor calcium-dependent changes in dopamine exocytosis. Together, the analysis from these two novel mouse models reveal synucleins play an important role in altering synaptic function in the dorsal striatum (the region selectively affected in PD) and contributes to growing evidence suggesting synucleins are negative regulators of synaptic dopamine release.

Subjects/Keywords: 616.83307; Medical Sciences; Neuroscience; Neurogenetics; Parkinsons disease; synuclein; alpha-synuclein; dopamine; basal ganglia; fast-scan cyclic voltammetry; transgenic mouse models

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

APA (6^th Edition):

Anwar, S. Z. (2011). Functional characterisation of synuclein-based novel genetic mouse models. (Doctoral Dissertation). University of Oxford. Retrieved from http://ora.ox.ac.uk/objects/uuid:b14fc29e-2bc8-4a31-865b-f4ec0e0f6f2c ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.558207

Chicago Manual of Style (16^th Edition):

Anwar, Sabina Zareen. “Functional characterisation of synuclein-based novel genetic mouse models.” 2011. Doctoral Dissertation, University of Oxford. Accessed March 03, 2021. http://ora.ox.ac.uk/objects/uuid:b14fc29e-2bc8-4a31-865b-f4ec0e0f6f2c ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.558207.

MLA Handbook (7^th Edition):

Anwar, Sabina Zareen. “Functional characterisation of synuclein-based novel genetic mouse models.” 2011. Web. 03 Mar 2021.

Vancouver:

Anwar SZ. Functional characterisation of synuclein-based novel genetic mouse models. [Internet] [Doctoral dissertation]. University of Oxford; 2011. [cited 2021 Mar 03]. Available from: http://ora.ox.ac.uk/objects/uuid:b14fc29e-2bc8-4a31-865b-f4ec0e0f6f2c ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.558207.

Council of Science Editors:

Anwar SZ. Functional characterisation of synuclein-based novel genetic mouse models. [Doctoral Dissertation]. University of Oxford; 2011. Available from: http://ora.ox.ac.uk/objects/uuid:b14fc29e-2bc8-4a31-865b-f4ec0e0f6f2c ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.558207

University of New South Wales

7. Jeet, Varinder. Development and characterisation of a transgenic mouse model to investigate the mechanisms and treatment options for Androgen independent metastatic prostate cancer.

Degree: Clinical School - Prince of Wales Hospital, 2009, University of New South Wales

URL: http://handle.unsw.edu.au/1959.4/44578 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:7875/SOURCE1?view=true

► Currently, there are no preclinical immunocompetent mouse models that adequately represent all stages of prostate cancer (PC) especially, androgen depletion independent (ADI) and bone metastatic… (more)

▼ Currently, there are no preclinical immunocompetent mouse models that adequately represent all stages of prostate cancer (PC) especially, androgen depletion independent (ADI) and bone metastatic PC. The best characterized, Transgenic Adenocarcinoma of the Mouse Prostate (TRAMP) model is logistically a difficult model for in vivo assessments and it does not adequately represent all stages of PC. Therefore, the aim of this study was to broaden the TRAMP model to include ADI and bone metastatic PC. Three ADI sublines were derived from androgen-sensitive (AS) TRAMP C1 (TC1) and TRAMP C2 (TC2) parental lines in vitro by dihydrotestosterone (TC1-T5 and TC2-T5) deprivation and in vivo by growing in TRAMP female mice (TC1-F1). The new sublines showed several characteristic features of ADI-PC 1.) faster growth rates in vitro and in vivo 2.) increased invasiveness 3.) androgen depletion independence in vitro and in vivo 4.) variable expression of androgen receptor 5.) downregulation of metastasis suppressor genes, E-cadherin and KAI-1. Genetic and molecular studies of ADI sublines showed alteration of genes representing major cancer related pathways. ADI TC1-T5, that displayed the most aggressive phenotype/genotype was selected to expand the TRAMP model to represent PC metastases Metastatic ability of TC1-T5 to migrate to bone and other soft tissues after intracardiac injections was shown in contrast to AS TC1 cells. Bone metastatic lesions displayed both osteoblastic and osteolytic features in multiple locations. Additionally, unlike AS TC1, the TC1-T5 tumours were able to grow with 100% incidence in the prostate and as lungs pseudometastases. The ADI PC lines were used to explore Aurora Kinases (AKs) as therapeutic targets for ADI PC. Compared to TC1, ADI-TC1-T5 cells showed a significant upregulation of AK-A and AK-B and their downstream regulators, survivin and phosphorylated-histone H3. Enhanced sensitivity of TC1-T5 to AK inhibitor VX680 functionally validated this and together with docetaxel led to enhanced efficacy which correlated with implication of AK-A/B in development of docetaxel-resistance. Thus, TRAMP model now represents ADI-PC that can grow in the bone, lungs and in the prostate; a significant step towards a well rounded preclinical model with greater clinical relevance. Advisors/Committee Members: Khatri, Aparajita, Clinical School - Prince of Wales Hospital, Faculty of Medicine, UNSW, Russell, Pamela J, Clinical School - Prince of Wales Hospital, Faculty of Medicine, UNSW.

Subjects/Keywords: Androgen independent PCa; Prostate Cancer; Transgenic Mouse Models

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APA (6^th Edition):

Jeet, V. (2009). Development and characterisation of a transgenic mouse model to investigate the mechanisms and treatment options for Androgen independent metastatic prostate cancer. (Doctoral Dissertation). University of New South Wales. Retrieved from http://handle.unsw.edu.au/1959.4/44578 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:7875/SOURCE1?view=true

Chicago Manual of Style (16^th Edition):

Jeet, Varinder. “Development and characterisation of a transgenic mouse model to investigate the mechanisms and treatment options for Androgen independent metastatic prostate cancer.” 2009. Doctoral Dissertation, University of New South Wales. Accessed March 03, 2021. http://handle.unsw.edu.au/1959.4/44578 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:7875/SOURCE1?view=true.

MLA Handbook (7^th Edition):

Jeet, Varinder. “Development and characterisation of a transgenic mouse model to investigate the mechanisms and treatment options for Androgen independent metastatic prostate cancer.” 2009. Web. 03 Mar 2021.

Vancouver:

Jeet V. Development and characterisation of a transgenic mouse model to investigate the mechanisms and treatment options for Androgen independent metastatic prostate cancer. [Internet] [Doctoral dissertation]. University of New South Wales; 2009. [cited 2021 Mar 03]. Available from: http://handle.unsw.edu.au/1959.4/44578 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:7875/SOURCE1?view=true.

Council of Science Editors:

Jeet V. Development and characterisation of a transgenic mouse model to investigate the mechanisms and treatment options for Androgen independent metastatic prostate cancer. [Doctoral Dissertation]. University of New South Wales; 2009. Available from: http://handle.unsw.edu.au/1959.4/44578 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:7875/SOURCE1?view=true

8. Jung, Sophie. Agents infectieux et rupture de tolérance lymphocytaire B : étude des processus de maturation d'affinité et de différenciation plasmocytaire au cours d'une infection bactérienne dans un nouveau modèle knock-in autoréactif : Infectious agents and B cell tolerance breakdown : study of affinity maturation and plasma-cell differentiation processes during bacterial infection in a new autoreactive knock-in mouse model.

Degree: Docteur es, Aspects moléculaires et cellulaires de la biologie, 2013, Université de Strasbourg

URL: http://www.theses.fr/2013STRAJ067

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Les maladies auto-immunes, qui touchent plus de 5% de la population, sont induites par une perte de la tolérance aux antigènes du Soi. Ces pathologies,… (more)

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Les maladies auto-immunes, qui touchent plus de 5% de la population, sont induites par une perte de la tolérance aux antigènes du Soi. Ces pathologies, généralement multifactorielles, résultent de l’effet combiné de plusieurs allèles de susceptibilité et de différents facteurs environnementaux. Les agents infectieux ont été tout particulièrement incriminés, mais les mécanismes en jeu restent encore mal élucidés. Les lymphocytes B, qui jouent un rôle central dans la pathogénie de nombreuses maladies auto-immunes, sont susceptibles d’être activés selon différents mécanismes au cours d’un processus infectieux et cette activation peut englober des cellules autoréactives. On ne sait cependant pas si cette activation peut entraîner la production d’auto-anticorps pathogènes de forte affinité et d’isotype IgG à partir du pool de cellules productrices d’auto-anticorps naturels de faible affinité, qui sont présentes de façon constitutive dans le répertoire B de l’individu sain. Nous avons mis au point un nouveau modèle murin knock-in pour des lymphocytes B présentant une affinité intermédiaire pour leur auto-antigène, la protéine HEL2X mutée (Hen-Egg Lysozyme). Ce modèle autoréactif d’affinité intermédiaire SWHEL X HEL2X, élaboré sur un fond génétique non autoimmun, permet de suivre le processus de maturation d’affinité des cellules B anti-HEL en présence de leur auto-antigène HEL2X au cours de l’infection chronique par la bactérie Borrelia burgdorferi. L’infection induit au niveau ganglionnaire une prolifération ainsi qu’une activation lymphocytaire B incluant des cellules anergiques. Certains clones autoréactifs sont capables de gagner les centres germinatifs ganglionnaires, de commuter vers l’isotype IgG et présentent des mutations somatiques au niveau de la région variable de la chaîne lourde de leur immunoglobuline, dans la zone d’interaction avec HEL2X, indiquant un processus de sélection par l’auto-antigène. Malgré un taux augmenté d’auto-anticorps d’isotype IgM, ces animaux ne produisent pas de plasmocytes capables de sécréter des auto-anticorps d’isotype IgG. Nos observations suggèrent l’existence de mécanismes de tolérance périphérique intrinsèques mis en place en particulier au niveau du centre germinatif. Un premier point de contrôle va éliminer les lymphocytes B autoréactifs ayant commuté de classe et présentant des mutations somatiques leur conférant une affinité augmentée pour l’auto-antigène tandis qu’un second point de contrôle va empêcher la différenciation en plasmocytes IgG+.Chez l’individu non prédisposé génétiquement, des mécanismes pourraient ainsi permettre de prévenir le développement d’une auto-immunité pathogène au cours d’un épisode infectieux.

Autoimmune diseases, affecting more than 5% of the population, reflect a loss of tolerance to selfantigens. These multifactorial diseases result from the combined effect of several susceptibility alleles and different environmental factors. Infectious agents have been particularly incriminated but there is no clear understanding of the underlying…

Advisors/Committee Members: Korganow, Anne-Sophie (thesis director).

Subjects/Keywords: Auto-immunité; Lymphocyte B; Infection bactérienne; Modèles murins transgéniques; Tolérance lymphocytaire B; Autoimmunity; B lymphocyte; Bacterial infection; Transgenic mouse models; B cell tolerance; 571.96; 572.8; 616.97

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

APA (6^th Edition):

Jung, S. (2013). Agents infectieux et rupture de tolérance lymphocytaire B : étude des processus de maturation d'affinité et de différenciation plasmocytaire au cours d'une infection bactérienne dans un nouveau modèle knock-in autoréactif : Infectious agents and B cell tolerance breakdown : study of affinity maturation and plasma-cell differentiation processes during bacterial infection in a new autoreactive knock-in mouse model. (Doctoral Dissertation). Université de Strasbourg. Retrieved from http://www.theses.fr/2013STRAJ067

Chicago Manual of Style (16^th Edition):

Jung, Sophie. “Agents infectieux et rupture de tolérance lymphocytaire B : étude des processus de maturation d'affinité et de différenciation plasmocytaire au cours d'une infection bactérienne dans un nouveau modèle knock-in autoréactif : Infectious agents and B cell tolerance breakdown : study of affinity maturation and plasma-cell differentiation processes during bacterial infection in a new autoreactive knock-in mouse model.” 2013. Doctoral Dissertation, Université de Strasbourg. Accessed March 03, 2021. http://www.theses.fr/2013STRAJ067.

MLA Handbook (7^th Edition):

Jung, Sophie. “Agents infectieux et rupture de tolérance lymphocytaire B : étude des processus de maturation d'affinité et de différenciation plasmocytaire au cours d'une infection bactérienne dans un nouveau modèle knock-in autoréactif : Infectious agents and B cell tolerance breakdown : study of affinity maturation and plasma-cell differentiation processes during bacterial infection in a new autoreactive knock-in mouse model.” 2013. Web. 03 Mar 2021.

Vancouver:

Jung S. Agents infectieux et rupture de tolérance lymphocytaire B : étude des processus de maturation d'affinité et de différenciation plasmocytaire au cours d'une infection bactérienne dans un nouveau modèle knock-in autoréactif : Infectious agents and B cell tolerance breakdown : study of affinity maturation and plasma-cell differentiation processes during bacterial infection in a new autoreactive knock-in mouse model. [Internet] [Doctoral dissertation]. Université de Strasbourg; 2013. [cited 2021 Mar 03]. Available from: http://www.theses.fr/2013STRAJ067.

Council of Science Editors:

Jung S. Agents infectieux et rupture de tolérance lymphocytaire B : étude des processus de maturation d'affinité et de différenciation plasmocytaire au cours d'une infection bactérienne dans un nouveau modèle knock-in autoréactif : Infectious agents and B cell tolerance breakdown : study of affinity maturation and plasma-cell differentiation processes during bacterial infection in a new autoreactive knock-in mouse model. [Doctoral Dissertation]. Université de Strasbourg; 2013. Available from: http://www.theses.fr/2013STRAJ067

9. Franks, Sarah Elizabeth. The Importance of the Insulin-like Growth Factor Signaling Pathway in Lung Cancer and the Potential of its Components as Therapeutic Targets.

Degree: PhD, Department of Biomedical Sciences, 2015, University of Guelph

URL: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/8860

► Lung cancer is the leading cause of cancer-related mortalities worldwide. Despite the introduction of new therapeutics, there has been very little improvement in survival for… (more)

▼ Lung cancer is the leading cause of cancer-related mortalities worldwide. Despite the introduction of new therapeutics, there has been very little improvement in survival for patients with advanced stage disease. The insulin-like growth factor (IGF) system is frequently activated in lung cancer and the type I insulin-like growth factor receptor (IGF-IR) has emerged as a potential therapeutic target. However, clinical trials to date have had limited success and it is clear that a more thorough understanding of the IGF-system is required to improve clinical efficacy in targeting this pathway. Here we show that treatment with a dual inhibitor that targets the IGF-IR and the insulin receptor decreased proliferation and survival of lung cancer cells, which was mediated by inhibition of Akt signaling. Furthermore, use of the dual inhibitor enhanced the effects of low doses of platinum therapeutics in lung cancer cells. Akt is an important mediator of IGF-IR signaling and is currently under investigation as a therapeutic target in its own right. Akt exists as three isoforms (Akt1-3), which were previously thought to be largely redundant in activity; however, recent evidence indicates that they have unique functions. In order to investigate the specific roles of Akt isoforms in lung tumorigenesis our lab used a previously developed tissue-specific, inducible transgenic mouse model of lung cancer. In these mice, IGF-IR overexpression in type II alveolar cells is sufficient to induce the formation of nodular adenomas and adenocarcinomas. By combining these transgenic mice with isoform specific Akt knockout mice, we were able to determine if the lack of a single Akt isoform was sufficient to disrupt lung tumorigenesis. Akt1 deficiency was sufficient to decrease IGF-IR-mediated lung tumor development resulting in fewer surface tumors and a lower tumor burden but having no influence in tumor histology. In contrast, Akt2 deficient mice had an increase in tumor burden as well as a change in tumor histology. These mice had diffuse tumor tissue throughout their lungs as tumors did not maintain nodular growth. Therefore, Akt isoforms have unique roles in IGF-IR mediated lung tumorigenesis, which should be reflected in the design and implementation of Akt-targeting therapeutics. Advisors/Committee Members: Moorehead, Roger (advisor).

Subjects/Keywords: Lung Cancer; The type I insulin-like growth factor receptor (IGF-IR); Akt Isoforms (Akt1 and Akt2); Transgenic Mouse Models; Kruppel-like factor 5 (KLF5)

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APA (6^th Edition):

Franks, S. E. (2015). The Importance of the Insulin-like Growth Factor Signaling Pathway in Lung Cancer and the Potential of its Components as Therapeutic Targets. (Doctoral Dissertation). University of Guelph. Retrieved from https://atrium.lib.uoguelph.ca/xmlui/handle/10214/8860

Chicago Manual of Style (16^th Edition):

Franks, Sarah Elizabeth. “The Importance of the Insulin-like Growth Factor Signaling Pathway in Lung Cancer and the Potential of its Components as Therapeutic Targets.” 2015. Doctoral Dissertation, University of Guelph. Accessed March 03, 2021. https://atrium.lib.uoguelph.ca/xmlui/handle/10214/8860.

MLA Handbook (7^th Edition):

Franks, Sarah Elizabeth. “The Importance of the Insulin-like Growth Factor Signaling Pathway in Lung Cancer and the Potential of its Components as Therapeutic Targets.” 2015. Web. 03 Mar 2021.

Vancouver:

Franks SE. The Importance of the Insulin-like Growth Factor Signaling Pathway in Lung Cancer and the Potential of its Components as Therapeutic Targets. [Internet] [Doctoral dissertation]. University of Guelph; 2015. [cited 2021 Mar 03]. Available from: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/8860.

Council of Science Editors:

Franks SE. The Importance of the Insulin-like Growth Factor Signaling Pathway in Lung Cancer and the Potential of its Components as Therapeutic Targets. [Doctoral Dissertation]. University of Guelph; 2015. Available from: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/8860

University of Connecticut

10. Perrino, Peter. Reanalysis of the Usher syndrome type 2 carrier as “phenotype-free”.

Degree: MS, Psychological Sciences, 2019, University of Connecticut

URL: https://opencommons.uconn.edu/gs_theses/1326

Subjects/Keywords: Auditory processing disorder; transgenic mouse models; neurodevelopmental disorders; USH2A; rapid auditory processing

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

APA (6^th Edition):

Perrino, P. (2019). Reanalysis of the Usher syndrome type 2 carrier as “phenotype-free”. (Masters Thesis). University of Connecticut. Retrieved from https://opencommons.uconn.edu/gs_theses/1326

Chicago Manual of Style (16^th Edition):

Perrino, Peter. “Reanalysis of the Usher syndrome type 2 carrier as “phenotype-free”.” 2019. Masters Thesis, University of Connecticut. Accessed March 03, 2021. https://opencommons.uconn.edu/gs_theses/1326.

MLA Handbook (7^th Edition):

Perrino, Peter. “Reanalysis of the Usher syndrome type 2 carrier as “phenotype-free”.” 2019. Web. 03 Mar 2021.

Vancouver:

Perrino P. Reanalysis of the Usher syndrome type 2 carrier as “phenotype-free”. [Internet] [Masters thesis]. University of Connecticut; 2019. [cited 2021 Mar 03]. Available from: https://opencommons.uconn.edu/gs_theses/1326.

Council of Science Editors:

Perrino P. Reanalysis of the Usher syndrome type 2 carrier as “phenotype-free”. [Masters Thesis]. University of Connecticut; 2019. Available from: https://opencommons.uconn.edu/gs_theses/1326

East Carolina University

11. Nopparat, Jongdee. [Delta]-catenin: implications in prostate cancer progression.

Degree: PhD, Anatomy and Cell Biology, 2014, East Carolina University

URL: http://hdl.handle.net/10342/4436

► Prostate cancer (PCa) is the most commonly diagnosed cancer and the second most common cause of cancer death among men in the US. Due to… (more)

▼ Prostate cancer (PCa) is the most commonly diagnosed cancer and the second most common cause of cancer death among men in the US. Due to the advances in research, the ability to detect and cure PCa has improved and led to significant reductions in PCa patients' mortality. Therefore, determining and understanding specific molecular mechanisms involved in PCa progression is a pivotal step towards the potentially better and more accurate diagnosis and intervention of PCa in the future. [Delta]-catenin is a unique armadillo (Arm) domain containing protein in that it is neural specific and primarily expressed in the brain. However, [delta]-catenin alterations have been implicated in pathogenesis ranging from neuronal deficits, genetic disorders, to cancers. In particular, [delta]-catenin expression is shown to increase in primary human prostatic adenocarcinomas corresponding with PCa progression. Although overexpressed [delta]-catenin in PCa has been reported over a decade ago, few studies have been undertaken to identify how [delta]-catenin promotes PCa progression and what other significant molecules are relevant to its expression. Studies presented in this dissertation explore the effects of a truncated variant of [delta]-catenin involved in promoting PCa using both in vitro PCa culture systems and in vivo mouse models of PCa. Additionally, we aim to test the hypothesis that [delta]-catenin mutations promote PCa progression by interacting with multiple cancer-specific pathways including Î²-catenin/LEF-1-mediated transcription and HIF-1Î±. Information presented in this dissertation demonstrates that ectopic [delta]-catenin gene is susceptible to mutagenesis when overexpressed in PCa cells, CWR22Rv-1 and PC-3, leading to sequence disruptions predicting functional alterations. It is shown that PCa cells overexpressing mutant [delta]-catenin increase Î²-catenin translocation to the nucleus and HIF-1Î±; expression when cultured under glucose deprived condition. These results suggest that [delta]-catenin mutations provide a survival advantage upon overgrowth and glucose deprivation over the control cells. Furthermore, we demonstrate that [delta]-catenin mutations promote tumor development in mouse prostate with probasin promoter (ARRâ‚‚PB)-driven, prostate specific expression of Myc oncogene. Additional investigations indicate that [delta]-catenin mutations in Myc transgenic mice not only promote Î²-catenin expression leading to dramatically elevated Myc expression but HIF-1Î±; is also increased in a [delta]-catenin gene-dosage dependent manner. Overall, we reveal that the introduction Î²-catenin mutations is an important step in metabolic adaptation by modulating Î²-catenin and HIF-1Î±; signaling in order to magnify its tumor promoting effect Advisors/Committee Members: Chen, Yan-Hua (advisor).

Subjects/Keywords: Biology, Molecular; [Delta]-catenin; Glucose deprivation; Prostate – Cancer; Somatic mutations; Transgenic mouse models; Î´-catenin; Molecular biology; Prostatic Neoplasms – diagnosis; Catenins – metabolism; Adenocarcinomas – diagnosis

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APA (6^th Edition):

Nopparat, J. (2014). [Delta]-catenin: implications in prostate cancer progression. (Doctoral Dissertation). East Carolina University. Retrieved from http://hdl.handle.net/10342/4436

Chicago Manual of Style (16^th Edition):

Nopparat, Jongdee. “[Delta]-catenin: implications in prostate cancer progression.” 2014. Doctoral Dissertation, East Carolina University. Accessed March 03, 2021. http://hdl.handle.net/10342/4436.

MLA Handbook (7^th Edition):

Nopparat, Jongdee. “[Delta]-catenin: implications in prostate cancer progression.” 2014. Web. 03 Mar 2021.

Vancouver:

Nopparat J. [Delta]-catenin: implications in prostate cancer progression. [Internet] [Doctoral dissertation]. East Carolina University; 2014. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/10342/4436.

Council of Science Editors:

Nopparat J. [Delta]-catenin: implications in prostate cancer progression. [Doctoral Dissertation]. East Carolina University; 2014. Available from: http://hdl.handle.net/10342/4436

12. Πετράκης, Ιωάννης. Μηχανισμοί νεφρικής βλάβης στην οικογενή αμυλοειδική πολυνευροπάθεια.

Degree: 2014, University of Crete (UOC); Πανεπιστήμιο Κρήτης

URL: http://hdl.handle.net/10442/hedi/38838

► Introduction: Familial Amyloid Polyneuropathy (FAP) has been first described 60 years ago. Nowadays consists one of the commonest forms of hereditary amyloidosis. It is inherited… (more)

▼ Introduction: Familial Amyloid Polyneuropathy (FAP) has been first described 60 years ago. Nowadays consists one of the commonest forms of hereditary amyloidosis. It is inherited through the autosomal dominant way of transmittance. Clinical features vary, but the dominant one is polyneuropathy due to small nerve fibers insult. Till present all FAP patients carry spot mutations of transthyretin gene and present amyloid deposition in various tissues. Renal amyloid deposition and renal injury has been a not so common feature in FAP patients. As far as FAP pathogenesis is concerned oligomeric non-fibrilar transthyretin species induce apoptosis, increase pro-inflammatory cytokines and induce oxidative stress within target tissues.Scope: The present study had the intention to examine mechanisms of renal insult in FAP animal models. It specifically examined urinary albumin excretion (UAE) in FAP animal models. Furthermore it examined the way with which various components of the slit diaphragm (nephrin and podocin), podocyte number, mRNA levels of WT1, glomerular basement membrane (GBM) thickness, foot process width (FPW), change due to partial shortage of Hsf-1. In addition it examined, the effect of different environmental conditions in TTRV30M glomerular deposition, TTRV30M renal gene expression, TTRV30M podocytic localization, as well as caspase 3 activation. Furthermore sex impact under the administration of rapamycin in tissue TTRV30M deposition was examined. Glomerular levels of bax/bcl-2 were examined in relation to transgenic mice gender.Materials and Methods: Transgenic animals (C57Bl/6-Tg(6.0 TTRMet30)15Imeg –hTTRV30M, CARD, Kumamoto Japan) were used for experimentation. Oviduct transfer of cryopreserved embryos was performed. Young animals (10-16 months old), and Old animals (16-21) with or without TTRVal30Met gene were used for 24 hrs urinary collection. UAE was normalized over body weight (BW) of laboratory animals. UAE was examined with the use of ELISA (Bethyl laboratories). Logarithmic transformation of data was performed and test Chi square was used for statistical analysis. Statistical analysis was performed with SPSS 19 (IBM) software. Pearson’s R was used for correlation analysis. Statistical significance was set at .05. In addition in an animal group 8 months old rapamycin (0.4 mg/kg BW) was administered i.p for 2 months. In this group urinary collections were performed. The kidneys were acutely frozen in liquid nitrogen. Five μm thick cryosections were fixed with paraformaldehyde solution 4% and were incubated with rabbit anti-human transthyretin antibody (DAKO), bax anti mouse antibody (Abcam), bcl-2 anti mouse antibody (Abcam). Renal tissue was further stained for PAS, Silver Stain, Masson, Congo Red (CR) and H&E. Confocal microscopy was utilized for analyzing immunofluorescence sections (Leica, SP). Leica confocal software was used for image analysis. Data were examined for normality. In case of non normality logarithmic transformation was performed. Statistical significance was set at .05 and was…

Subjects/Keywords: Τρανσθυρετίνη; Ποδοκύτταρα; Αμυλοείδωση; Διαγονιδιακά μοντέλα νεφρικής νόσου; Περιβαλλοντική επίδραση; Μηχανισμοί νεφρικής βλάβης; Transthyretin; Podocytes; Amyloidosis; Transgenic mouse models of renal disease; Environmental interaction; Mechanisms of renal insult

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APA (6^th Edition):

Πετράκης, . �. (2014). Μηχανισμοί νεφρικής βλάβης στην οικογενή αμυλοειδική πολυνευροπάθεια. (Thesis). University of Crete (UOC); Πανεπιστήμιο Κρήτης. Retrieved from http://hdl.handle.net/10442/hedi/38838

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):

Πετράκης, Ιωάννης. “Μηχανισμοί νεφρικής βλάβης στην οικογενή αμυλοειδική πολυνευροπάθεια.” 2014. Thesis, University of Crete (UOC); Πανεπιστήμιο Κρήτης. Accessed March 03, 2021. http://hdl.handle.net/10442/hedi/38838.

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

MLA Handbook (7^th Edition):

Πετράκης, Ιωάννης. “Μηχανισμοί νεφρικής βλάβης στην οικογενή αμυλοειδική πολυνευροπάθεια.” 2014. Web. 03 Mar 2021.

Vancouver:

Πετράκης �. Μηχανισμοί νεφρικής βλάβης στην οικογενή αμυλοειδική πολυνευροπάθεια. [Internet] [Thesis]. University of Crete (UOC); Πανεπιστήμιο Κρήτης; 2014. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/10442/hedi/38838.

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

Council of Science Editors:

Πετράκης �. Μηχανισμοί νεφρικής βλάβης στην οικογενή αμυλοειδική πολυνευροπάθεια. [Thesis]. University of Crete (UOC); Πανεπιστήμιο Κρήτης; 2014. Available from: http://hdl.handle.net/10442/hedi/38838

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

13. Ha, Michael Neul. In Vitro and In Vivo Studies with Measles Virus and its Interaction with the Mouse Innate Immune System.

Degree: 2012, University of Toronto

URL: http://hdl.handle.net/1807/32725

►

Measles is one of the most contagious diseases known to mankind. Despite the availability of a safe and effective vaccine, approximately 164,000 measles-related deaths were… (more)

▼

Measles is one of the most contagious diseases known to mankind. Despite the availability of a safe and effective vaccine, approximately 164,000 measles-related deaths were recorded in 2008. The inherent restricted host tropism of MV means that the development of authentic rodent models will be a valuable research tool in testing new vaccines and antivirals. In addition to the receptor requirement, mouse innate immunity has been shown to inhibit MV growth. In this thesis, the contributions of several key components of the mouse innate immune system on the inhibition of MV replication were examined. The transcription factor interferon regulatory factor 3 (IRF3), which normally plays a key role in mediating innate immune signaling, contributed relatively little in inhibiting MV replication both in vitro and in vivo. In contrast, the JAK/STAT pathway and the double-stranded RNA inducible protein kinase, PKR, played more important roles in controlling virus replication. The resurgence of measles in areas where the virus was once thought to be eradicated makes the development of anti-MV treatments essential. Concurrent to the development of an animal model to better study its pathogenesis, we wanted to look at the effect of MV inhibitors on its replication. The MV fusion inhibitor, carbobenzoxy-D-phenylalanine-L-phenylalanine-glycine (ZfFG), was developed in the past to study fusion; however, its mechanism of action has not yet been elucidated. To examine this, spontaneous ZfFG-resistant mutants were generated and characterized. Mutations were found in the HRB region of the fusion (F) protein, and when these were modeled using published paramyxovirus F crystal structures, data suggested that ZfFG targeted a small pocket present between the head and stalk regions of its pre-fusion conformation. An authentic mouse model of measles developed from findings in this study may allow for in vivo efficacy testing of ZfFG in the future.

PhD

Advisors/Committee Members: Richardson, Christopher Donald, Medical Biophysics.

Subjects/Keywords: molecular biology; virology; paramyxovirus; measles; innate immunity; mouse models; transgenic mouse; fusion; fusion inhibitor; FIP; IRF3; microbiology; ZfFG; plasmacytoid dendritic cell; mouse embryonic fibroblast; receptor; 0720

…128 Figure II. Transgenic mouse expressing vaccinia virus E3L… …131 Appendix II: Generation of transgenic mouse which… …64 Figure 3.1. Verification of SLAM/IRF3KO mouse… …Figure 4.5. Computer generated models of ZfFG resistant mutants… …Mitochondrial antiviral signaling MCMV Mouse cytomegalovirus MCP Membrane cofactor protein MDA…

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APA (6^th Edition):

Ha, M. N. (2012). In Vitro and In Vivo Studies with Measles Virus and its Interaction with the Mouse Innate Immune System. (Doctoral Dissertation). University of Toronto. Retrieved from http://hdl.handle.net/1807/32725

Chicago Manual of Style (16^th Edition):

Ha, Michael Neul. “In Vitro and In Vivo Studies with Measles Virus and its Interaction with the Mouse Innate Immune System.” 2012. Doctoral Dissertation, University of Toronto. Accessed March 03, 2021. http://hdl.handle.net/1807/32725.

MLA Handbook (7^th Edition):

Ha, Michael Neul. “In Vitro and In Vivo Studies with Measles Virus and its Interaction with the Mouse Innate Immune System.” 2012. Web. 03 Mar 2021.

Vancouver:

Ha MN. In Vitro and In Vivo Studies with Measles Virus and its Interaction with the Mouse Innate Immune System. [Internet] [Doctoral dissertation]. University of Toronto; 2012. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/1807/32725.

Council of Science Editors:

Ha MN. In Vitro and In Vivo Studies with Measles Virus and its Interaction with the Mouse Innate Immune System. [Doctoral Dissertation]. University of Toronto; 2012. Available from: http://hdl.handle.net/1807/32725

14. Ito-Smith, Kristine M. Characterization of Caytaxin Protein in Animal Models of Cerebellar Dysfunction.

Degree: PhD, Cellular and Molecular Biology, 2012, University of Michigan

URL: http://hdl.handle.net/2027.42/95992

► Over 150,000 Americans have been diagnosed with ataxia, however most are untreatable due to yet-unknown etiologies. The work described within this dissertation aims to expand… (more)

▼ Over 150,000 Americans have been diagnosed with ataxia, however most are untreatable due to yet-unknown etiologies. The work described within this dissertation aims to expand current knowledge regarding ataxia and the brain by elucidating the function of Caytaxin, a neuronal protein that is essential for nervous system processes. Caytaxin is encoded by the Atcay/ATCAY gene and is highly conserved. Two mutations in ATCAY, a splice and a non-synonymous exon variant, are associated with the rare hereditary disease Cayman ataxia in humans. Mutations in the murine ortholog Atcay have been identified as the cause of marked motor defects in four ataxic and dystonic mouse lines. While the function of Caytaxin has not been fully characterized, several lines of evidence and the data contained in this dissertation suggest that Caytaxin is required for maintaining nervous system processes. In Chapter II, we discuss the generation of novel anti-Caytaxin monoclonal antibodies and their use in characterizing endogenous Caytaxin expression in wild type and Atcay mutant mice, and in humanized ATCAY transgenic lines. Caytaxin protein is absent from brain tissues in the two severely ataxic jittery and sidewinder lines, and markedly decreased in the mildly ataxic/dystonic hesitant line, indicating a correlation between Caytaxin expression and disease severity. Biochemical analysis reveals that Caytaxin is expressed as three protein isoforms, two of which originate from different conserved methionine translation start sites. Phenotypic analysis of transgenic ATCAY mouse lines suggests a conserved physiological function between the human and mouse Caytaxin orthologs as expression of wild type human Caytaxin rescues the ataxic phenotype in mutant sidewinder and jittery mice. In Chapter III, we report preliminary data obtained from transgenic mouse lines generated to recapitulate the human Cayman ataxia mutations. We reveal that the splice mutation results in a protein truncation, but fails to completely abrogate Caytaxin function, indicating the possibility that both Cayman ataxia mutations may act synergistically to cause disease. Our characterization of Caytaxin protein and its expression in mouse models of cerebellar dysfunction presents novel methods for accurate assessment of how Caytaxin maintains normal nervous system function, thus providing insight into other forms of ataxia. Advisors/Committee Members: Burmeister, Margit (committee member), Hortsch, Michael (committee member), Umemori, Hisashi (committee member), Shakkottai, Vikram (committee member), Lieberman, Andrew P. (committee member), Paulson, Henry L. (committee member).

Subjects/Keywords: Ataxia; Cayman Ataxia; Transgenic Mouse Models; Alternative Translation; Caytaxin; Atcay/ATCAY; Molecular, Cellular and Developmental Biology; Science

…heterozygote, wild type hesitant heterozygote, wild type Transgenic mouse, positive for the transgene… …Transgenic mouse, negative for the transgene Transgenic line, ATCAY exon 9 mutation Transgenic line… …Caytaxin remains poorly understood. Four mouse models and one rat model have been identified to… …mAb) specific for the Caytaxin protein as well as transgenic mouse lines expressing… …lines, wild type and Atcay mouse mutants, and transgenic ATCAY mouse lines. These analyses…

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APA (6^th Edition):

Ito-Smith, K. M. (2012). Characterization of Caytaxin Protein in Animal Models of Cerebellar Dysfunction. (Doctoral Dissertation). University of Michigan. Retrieved from http://hdl.handle.net/2027.42/95992

Chicago Manual of Style (16^th Edition):

Ito-Smith, Kristine M. “Characterization of Caytaxin Protein in Animal Models of Cerebellar Dysfunction.” 2012. Doctoral Dissertation, University of Michigan. Accessed March 03, 2021. http://hdl.handle.net/2027.42/95992.

MLA Handbook (7^th Edition):

Ito-Smith, Kristine M. “Characterization of Caytaxin Protein in Animal Models of Cerebellar Dysfunction.” 2012. Web. 03 Mar 2021.

Vancouver:

Ito-Smith KM. Characterization of Caytaxin Protein in Animal Models of Cerebellar Dysfunction. [Internet] [Doctoral dissertation]. University of Michigan; 2012. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/2027.42/95992.

Council of Science Editors:

Ito-Smith KM. Characterization of Caytaxin Protein in Animal Models of Cerebellar Dysfunction. [Doctoral Dissertation]. University of Michigan; 2012. Available from: http://hdl.handle.net/2027.42/95992

15. Dey, Joyoti. Understanding the role of the Sonic Hedgehog signaling pathway in cerebellar development and medulloblastoma genesis.

Degree: PhD, 2012, University of Washington

URL: http://hdl.handle.net/1773/20238

► Medulloblastoma is a developmental cancer of the cerebellum. It continues to be the most common pediatric brain cancer associated with dire survival and impaired quality… (more)

▼ Medulloblastoma is a developmental cancer of the cerebellum. It continues to be the most common pediatric brain cancer associated with dire survival and impaired quality of life. In order to develop therapeutic interventions, it is necessary to bridge the gaps in knowledge about cerebellar development and understand how aberrations in developmental pathways lead to cancer. The Sonic hedgehog pathway (Shh) plays a pivotal role in cerebellar development and mutations leading to hyperactive signaling cause medulloblastoma. Although the fundamentals of the pathway mechanics are known, and have led to the development of mouse models to study the human disease, there are critical questions that remain to be answered. Based on pathway signatures medulloblastomas are categorized into subgroups, Shh-driven being one such subgroup. However there is significant heterogeneity even among Shh-driven medulloblastomas that necessitates understanding key differences between the various mutations and differential regulation of downstream effectors. Through the characterization of a novel mouse model of medulloblastoma, SmoA2 and comparative analyses with the existing SmoA1 model, I have demonstrated salient molecular and cellular differences between two activating mutations in the same region of a single gene. While the SmoA1 mutation leads to medulloblastoma in adult mice, in addition to cancer, the SmoA2 mutation causes severe defects early in cerebellar development. The transcriptional profiles downstream of these two mutations and biological processes affected are distinct. An unexpected finding from the SmoA2 model is the preservation of normal cerebellar function despite a completely disrupted cytoarchitecture challenging the notion that stereotypical organization of the cerebellum is critical for its function. My second aim was to identify molecules that interact with the Shh pathway in development and disease. Toward this goal, I discovered a previously unknown expression pattern of MyoD in the proliferative phase of the developing cerebellum as well as in mouse medulloblastoma. MyoD, a myogenic differentiation factor has been known to be exclusive to the skeletal muscle lineage. I demonstrate MyoD functions as a novel haploinsufficient tumor suppressor in the context of medulloblastoma with potential clinical significance. Advisors/Committee Members: Olson, James M (advisor).

Subjects/Keywords: cerebellar development; medulloblastoma; MyoD; neurooncology; Sonic hedgehog signaling; transgenic mouse models; Molecular biology; Oncology; Developmental biology; Molecular and cellular biology

…through lineage tracing and genetic analyses in mouse models of medulloblastoma… …atlas that has generated more than 600 transgenic mouse lines expressing Enhanced Green… …expression and function can lead to cancer and neuropathological conditions. Mouse models of… …the existing mouse models recapitulating this subtype (Hatten and Roussel, 2011)… …Wechsler-Reya, 2011). These mouse models have provided critical information about…

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APA (6^th Edition):

Dey, J. (2012). Understanding the role of the Sonic Hedgehog signaling pathway in cerebellar development and medulloblastoma genesis. (Doctoral Dissertation). University of Washington. Retrieved from http://hdl.handle.net/1773/20238

Chicago Manual of Style (16^th Edition):

Dey, Joyoti. “Understanding the role of the Sonic Hedgehog signaling pathway in cerebellar development and medulloblastoma genesis.” 2012. Doctoral Dissertation, University of Washington. Accessed March 03, 2021. http://hdl.handle.net/1773/20238.

MLA Handbook (7^th Edition):

Dey, Joyoti. “Understanding the role of the Sonic Hedgehog signaling pathway in cerebellar development and medulloblastoma genesis.” 2012. Web. 03 Mar 2021.

Vancouver:

Dey J. Understanding the role of the Sonic Hedgehog signaling pathway in cerebellar development and medulloblastoma genesis. [Internet] [Doctoral dissertation]. University of Washington; 2012. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/1773/20238.

Council of Science Editors:

Dey J. Understanding the role of the Sonic Hedgehog signaling pathway in cerebellar development and medulloblastoma genesis. [Doctoral Dissertation]. University of Washington; 2012. Available from: http://hdl.handle.net/1773/20238

16. Λέκκα, Ευτυχία. Πειραματικά μοντέλα ανοσοθεραπείας HER-2/neu θετικών όγκων.

Degree: 2009, National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ)

URL: http://hdl.handle.net/10442/hedi/23771

► Overexpression of the HER-2/neu oncogene by a significant number of human carcinomas has been associated with more aggressive disease. Despite its high oncogenic potential, HER2/neu… (more)

▼ Overexpression of the HER-2/neu oncogene by a significant number of human carcinomas has been associated with more aggressive disease. Despite its high oncogenic potential, HER2/neu oncoprotein has been considered as a promising target for cancer therapeutics as it has been proven to be immunogenic in vivo inducing specific CTL and IgG responses in a considerable subset of patients with HER-2/neu positive breast cancer. Moreover, various MHC class I- and class II-binding peptides from the HER-2/neu sequence were also able to elicit in vitro tumor reactive CTL and T helper (Th) responses, respectively. However, synthetic peptides corresponding to HER-2/neu immunogenic epitopes have greatly failed to function as therapeutic vaccines in phase I/II trials. Due to the fact that HER-2/neu is a self-protein, tolerance mechanisms may provide a serious obstacle towards the development of efficient anti-tumor responses in vivo. In order to circumvent tolerance against the HER-2/neu protein, several approaches have been invented and applied in preclinical models, resulting in more persistent and efficient antitumor responses. However, in parallel with studies aiming at improving the effectiveness of a vaccine, it has been considered essential to identify novel immunogenic CTL epitopes, aiming at providing insight into the design of more efficacious peptide-based treatment modalities. This study describes a novel HLA-A*0201-restricted epitope, encompassing amino acids 828-836 (residues QIAKGMSYL), which is naturally presented by various HER-2/neu⁺ tumor cell lines. HER-2/neu(828-836), [HER-2(9₈₂₈)], possesses two anchor residues and stabilized HLA-A*0201 on T2 cells in a concentration-dependent class I binding assay. This peptide was stable for 3.5h in an off-kinetics assay. HER-2(9₈₂₈) was found to be immunogenic in HLAA*0201 transgenic (HHD) mice inducing peptide-specific and functionally potent CTL and lasting anti-tumor immunity. Most important, using HLA-A*0201 pentamer analysis we could detect increased ex vivo frequencies of CD8⁺ T lymphocytes specifically recognizing HER2(9₈₂₈) in eight out of twenty HLA-A*0201⁺ HER-2/neu⁺ breast cancer patients. Moreover, HER2(9₈₂₈)-specific human CTL recognized the tumor cell line SKOV3.A2 as well as the primary RS.A2.1.DR1 tumor cell line both expressing HER-2/neu and HLA-A*0201. Finally, therapeutic vaccination with HER-2(9₈₂₈) in HHD mice was proven effective against established transplantable ALC.A2.1.HER tumors, inducing complete tumor regression in 50% of mice. Our data encourage further exploitation of HER-2(9₈₂₈) as a promising candidate for peptide-based cancer vaccines. The necessity of CD4 T-cell help to generate and sustain MHC class I–restricted CD8 T-cell responses has led to the identification of a new MHC class II–restricted epitope derived from the human HER-2/neu protein, namely HER-2(15₈₂₂). This helper 15-mer peptide, which exhibits a very strong binding score with the HLA-DRB1*0101 (HLA-DR1) molecule (according to the SYFPEITHI database) encompasses the amino acid…

Subjects/Keywords: Ογκοπρωτεΐνη HER/2-neu; Πεπτιδικά εμβόλια; Διαγονιδιακά πειραματόζωα; Κυτταροτοξικά Τ λεμφοκύτταρα; Καρκίνος μαστού; HER-2/neu oncoprotein; Peptide vaccines; Transgenic mouse models; Cytotoxic T lymphocytes; Breast cancer

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

APA (6^th Edition):

Λέκκα, . �. (2009). Πειραματικά μοντέλα ανοσοθεραπείας HER-2/neu θετικών όγκων. (Thesis). National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ). Retrieved from http://hdl.handle.net/10442/hedi/23771

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):

Λέκκα, Ευτυχία. “Πειραματικά μοντέλα ανοσοθεραπείας HER-2/neu θετικών όγκων.” 2009. Thesis, National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ). Accessed March 03, 2021. http://hdl.handle.net/10442/hedi/23771.

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

MLA Handbook (7^th Edition):

Λέκκα, Ευτυχία. “Πειραματικά μοντέλα ανοσοθεραπείας HER-2/neu θετικών όγκων.” 2009. Web. 03 Mar 2021.

Vancouver:

Λέκκα �. Πειραματικά μοντέλα ανοσοθεραπείας HER-2/neu θετικών όγκων. [Internet] [Thesis]. National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ); 2009. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/10442/hedi/23771.

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

Council of Science Editors:

Λέκκα �. Πειραματικά μοντέλα ανοσοθεραπείας HER-2/neu θετικών όγκων. [Thesis]. National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ); 2009. Available from: http://hdl.handle.net/10442/hedi/23771

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

17. Zhong, Jia. Exploring the Three-Dimensional Regional Myocardial Function in Transgenic Mouse Models of Cardiac Diseases using Novel MR Tissue Tracking Techniques.

Degree: PhD, Biomedical Engineering, 2009, Case Western Reserve University School of Graduate Studies

URL: http://rave.ohiolink.edu/etdc/view?acc_num=case1247260314

► The advent of the genomic age is revolutionizing the experimental cardiovascular research irreversibly. Dissecting molecular switches that control the changes of cardiac physiology with… (more)

▼ The advent of the genomic age is revolutionizing the experimental cardiovascular research irreversibly. Dissecting molecular switches that control the changes of cardiac physiology with transgenic mouse models has proven to offer important insights into the control of cardiac function. The integration of novel MR tissue tracking techqniques with these genetically manipulated mice may allow comprehensive characterization of contractile dysfunction non-invasively at the earliest diseased stages, thus facilitate our understanding of the pathogenesis of human cardiac diseases. In the current thesis, we aimed at developing fast and accurate MR tissue tracking techniques and applying them for the assessment of ventricular function in transgenic mouse models of cardiac diseases. First, spatial modulation of magnetization (SPAMM) tagging was implemented in the mouse heart; and a 3D SPAMM tagging analysis method was developed based on harmonic phase (HARP) and homogeneous strain analysis. Using this 3D tagging analysis method, longitudinal strain and circumferential-longitudinal shear was quantified in addition to the 2D ventricular wall strain. Second, to improve the limited tagging resolution of existing SPAMM techniques, a HARP-based high-resolution tagging analysis method was proposed in mouse. The utility of such method was demostrated by quantifying the transmural heterogeneity of the left ventricle. Third, a 2D multi-phase displacement encoding with stimulated echoes (DENSE) imaging and analysis method was developed which allows direct and automatic Lagrangian strain quantification with high spatial and temporal resolution. Additionally, the utility of this multi-phase DENSE method was demonstrated in mouse both at baseline and with high workload. Functional enhancement was identified upon dobutamine stimulation both at the global and the regional levels. Fourth, for the evaluation of longitudinal wall motion within the short axis (SA) plane, 2D multi-phase DENSE imaging method was extended to the third dimension. Last, the application of MR tagging and DENSE methods was investigated in diabetic mouse hearts with cardiac-specific GLUT1-overexpression. Normalized cardiac function was found in diabetic mice with enhanced glucose metabolism through GLUT1-overexpression. Our results demonstrated the capability of MR tagging and DENSE in delineating left ventricular function in the mouse heart. Advisors/Committee Members: YU, XIN (Committee Chair).

Subjects/Keywords: Biomedical Research; Engineering; transgenic mouse models; cardiac diseases; spatial modulation of magnetization (SPAMM) tagging; harmonic phase (HARP); displacement encoding with stimulated echoes (DENSE); strain; regional myocardial function

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

APA (6^th Edition):

Zhong, J. (2009). Exploring the Three-Dimensional Regional Myocardial Function in Transgenic Mouse Models of Cardiac Diseases using Novel MR Tissue Tracking Techniques. (Doctoral Dissertation). Case Western Reserve University School of Graduate Studies. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=case1247260314

Chicago Manual of Style (16^th Edition):

Zhong, Jia. “Exploring the Three-Dimensional Regional Myocardial Function in Transgenic Mouse Models of Cardiac Diseases using Novel MR Tissue Tracking Techniques.” 2009. Doctoral Dissertation, Case Western Reserve University School of Graduate Studies. Accessed March 03, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=case1247260314.

MLA Handbook (7^th Edition):

Zhong, Jia. “Exploring the Three-Dimensional Regional Myocardial Function in Transgenic Mouse Models of Cardiac Diseases using Novel MR Tissue Tracking Techniques.” 2009. Web. 03 Mar 2021.

Vancouver:

Zhong J. Exploring the Three-Dimensional Regional Myocardial Function in Transgenic Mouse Models of Cardiac Diseases using Novel MR Tissue Tracking Techniques. [Internet] [Doctoral dissertation]. Case Western Reserve University School of Graduate Studies; 2009. [cited 2021 Mar 03]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=case1247260314.

Council of Science Editors:

Zhong J. Exploring the Three-Dimensional Regional Myocardial Function in Transgenic Mouse Models of Cardiac Diseases using Novel MR Tissue Tracking Techniques. [Doctoral Dissertation]. Case Western Reserve University School of Graduate Studies; 2009. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=case1247260314

Leiden University

18. Kara, F. Monitoring Alzheimer's disease in transgenic mice with ultra high field magnetic resonance imaging.

Degree: 2013, Leiden University

URL: http://hdl.handle.net/1887/22736

► While aging remains one of the most significant risk factors for development of Alzheimer disease (AD), increasing evidence strongly points to the potential roles… (more)

Subjects/Keywords: 17.6 T; Alzheimer's disease; Transverse relaxation time; Blood flow alterations; Transgenic mouse models of AD; Corpus callosum; Ultra high magnetic field; Magnetic resonance imaging

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

APA (6^th Edition):

Kara, F. (2013). Monitoring Alzheimer's disease in transgenic mice with ultra high field magnetic resonance imaging. (Doctoral Dissertation). Leiden University. Retrieved from http://hdl.handle.net/1887/22736

Chicago Manual of Style (16^th Edition):

Kara, F. “Monitoring Alzheimer's disease in transgenic mice with ultra high field magnetic resonance imaging.” 2013. Doctoral Dissertation, Leiden University. Accessed March 03, 2021. http://hdl.handle.net/1887/22736.

MLA Handbook (7^th Edition):

Kara, F. “Monitoring Alzheimer's disease in transgenic mice with ultra high field magnetic resonance imaging.” 2013. Web. 03 Mar 2021.

Vancouver:

Kara F. Monitoring Alzheimer's disease in transgenic mice with ultra high field magnetic resonance imaging. [Internet] [Doctoral dissertation]. Leiden University; 2013. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/1887/22736.

Council of Science Editors:

Kara F. Monitoring Alzheimer's disease in transgenic mice with ultra high field magnetic resonance imaging. [Doctoral Dissertation]. Leiden University; 2013. Available from: http://hdl.handle.net/1887/22736

Johannes Gutenberg Universität Mainz

19. Steiner, Michel-Alexander. Transgenic mice as a tool for depression research: examples from the endocannabinoid and the corticotropin-releasing hormone system.

Degree: 2007, Johannes Gutenberg Universität Mainz

URL: http://ubm.opus.hbz-nrw.de/volltexte/2008/1583/

►

Major depression belongs to the most serious and widespread psychiatric disorders in today’s society. There is a great need for the delineation of the underlying… (more)

▼

Major depression belongs to the most serious and widespread psychiatric disorders in today’s society. There is a great need for the delineation of the underlying molecular mechanisms as well as for the identification of novel targets for its treatment. In this thesis, transgenic mice of the endocannabinoid and the corticotropin-releasing hormone (CRH) system were investigated to determine the putative role of these systems for depression-like phenotypes in mice. In the first part of the thesis, we found that the endocannabinoid system was prominently involved in a brain region-specific and temporally controlled manner in acute as well as in chronic stress processing. Genetic deletion in combination with pharmacological intervention revealed the importance of a fully functional endocannabinoid system for efficient neuroendocrine and behavioral stress coping. Accordingly, cannabinoid type 1 (CB1) receptor-deficient mice displayed several depression-like symptoms and molecular alterations, including “behavioral despair”, stress hormone hypersecretion and decreased glucocorticoid receptor and brain-derived neurotrophic factor expression in the hippocampus. However, the endocannabinoid system was dispensable for the efficacy of currently used antidepressant drugs. To facilitate future endocannabinoid research, a transgenic mouse was generated, which overexpressed the CB1 receptor protein fused to a fluorescent protein. In the second part of the thesis, conditional brain region-specific CRH overexpressing mice were evaluated as a model for pathological chronic CRH hyperactivation. Mutant mice showed aberrant neuroendocrine and behavioral stress coping and hyperarousal due to CRH-induced activation of the noradrenergic system in the brain. Mutant mice appeared to share similarities with naturally occurring endogenous CRH activation in wild-type mice and were sensitive to acute pharmacological blockade of CRH receptor type 1 (CRH-R1). Thus, CRH overexpressing mice serve as an ideal in vivo tool to evaluate the efficacy of novel CRH-R1 antagonists. Together, these findings highlight the potential of transgenic mice for the understanding of certain endo-phenotypes (isolated symptoms) of depression and their molecular correlates.

Depressionen gehören zu den schwerwiegendsten und am weitesten verbreiteten psychiatrischen Erkrankungen in unserer heutigen Gesellschaft. Die Erfoschung der zu Grunde liegenden molekularen Mechanismen und die Identifizierung neuer Zielmoleküle für die Behandlung ist unbedingt erforderlich. In dieser Doktorarbeit wurden transgene Mäuse des Endocannabinoid- und des „Corticotropin-releasing hormone“ (Corticotropin freisetzendes Hormon) (CRH)-Systems eingehend untersucht, um die Rolle dieser Systeme für die Ausbildung depressionsähnlicher Phänotypen in der Maus zu charakterisieren. Im ersten Teil der Arbeit konnte gezeigt werden, dass das Endocannabinoid-System in einer hirnregionspezifischen und zeitlich kontrollierten Weise von herausragender Bedeutung für die akute und chronische…

Subjects/Keywords: Transgene Mäuse, Endocannabinoid-System, CRH, Depression, Angst, Tiermodell, Stress, HPA Achse; Transgenic mice, endocannabinoid system, CRH, CRF, depression, anxiety, mouse models, stress, HPA axis; Chemistry and allied sciences

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

APA (6^th Edition):

Steiner, M. (2007). Transgenic mice as a tool for depression research: examples from the endocannabinoid and the corticotropin-releasing hormone system. (Doctoral Dissertation). Johannes Gutenberg Universität Mainz. Retrieved from http://ubm.opus.hbz-nrw.de/volltexte/2008/1583/

Chicago Manual of Style (16^th Edition):

Steiner, Michel-Alexander. “Transgenic mice as a tool for depression research: examples from the endocannabinoid and the corticotropin-releasing hormone system.” 2007. Doctoral Dissertation, Johannes Gutenberg Universität Mainz. Accessed March 03, 2021. http://ubm.opus.hbz-nrw.de/volltexte/2008/1583/.

MLA Handbook (7^th Edition):

Steiner, Michel-Alexander. “Transgenic mice as a tool for depression research: examples from the endocannabinoid and the corticotropin-releasing hormone system.” 2007. Web. 03 Mar 2021.

Vancouver:

Steiner M. Transgenic mice as a tool for depression research: examples from the endocannabinoid and the corticotropin-releasing hormone system. [Internet] [Doctoral dissertation]. Johannes Gutenberg Universität Mainz; 2007. [cited 2021 Mar 03]. Available from: http://ubm.opus.hbz-nrw.de/volltexte/2008/1583/.

Council of Science Editors:

Steiner M. Transgenic mice as a tool for depression research: examples from the endocannabinoid and the corticotropin-releasing hormone system. [Doctoral Dissertation]. Johannes Gutenberg Universität Mainz; 2007. Available from: http://ubm.opus.hbz-nrw.de/volltexte/2008/1583/

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Open Access Theses and Dissertations