subject:(Transgenic mice)

Rutgers University

1. Anderson, Jeremy, 1993-. Role of notch signaling after traumatic brain injury in a transgenic mouse model.

Degree: PhD, Biomedical Engineering, 2019, Rutgers University

URL: https://rucore.libraries.rutgers.edu/rutgers-lib/61683/

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Traumatic brain injury (TBI) is a leading cause of disability and death in the United States and worldwide. Endogenous neural stem/progenitor cells (NSPCs) in the… (more)

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Traumatic brain injury (TBI) is a leading cause of disability and death in the United States and worldwide. Endogenous neural stem/progenitor cells (NSPCs) in the adult are a potential source for injury recovery. However, much about the response of injury-activated NSPCs is still unknown. Notch signaling is critical for maintaining NSPC status during embryonic development and transiently activated after injury. In the first part of this thesis, the role of Notch signaling after TBI is investigated using a Notch1CR2-GFP transgenic mouse model. During development, GFP mainly marks interneuron progenitor cells. A closed head injury (CHI) in this transgenic mouse was performed to determine the response of injury-activated NSPCs. CHI induces neuroinflammation, cell death, and the expression of typical TBI markers, validating the animal model. In addition, CHI induces cell proliferation in GFP+ cells expressing NSPC markers, e.g., Notch1 and Nestin. A significant higher percentage of GFP+ GABAergic interneurons was observed in the CHI brain, with no significant change in oligodendrocyte lineage between the CHI and sham animal groups. Since injury is known to activate astrogliosis, these results suggest that injury-induced GFP+ NSPCs preferentially differentiate into GABAergic neurons. Our study establishes that Notch1CR2-GFP transgenic mouse is a useful tool for the study of NSPC behavior in vivo after TBI. In the second part of this thesis, the role of Gsx1, a neurogenic transcription factor, on promoting Notch1 expression and neurogenesis is investigated. A lentivirus system is used to deliver Gsx1 at the injury site after closed head injury (CHI) in the Notch1CR2-GFP transgenic mice. We identify that CHI increases GFP+ cell, during the acute phase of TBI and increasingly label neurons during the chronic phase of TBI. Lentivirus-mediated Gsx1 overexpression increases Notch1 expressing cells in the cerebral cortex and hippocampus; these virally transduced cells proliferate and mark NSPCs during the subacute phase of TBI and primarily label glutamatergic neurons during the chronic phase of TBI. The role of Gsx1 promoting Notch signaling and neurogenesis after TBI represents a new therapeutic for the treatment of TBI. Unveiling the potential of NSPCs to TBI (e.g., proliferation and differentiation) will identify new therapeutic strategy for the treatment of brain trauma.

Advisors/Committee Members: Cai, Li (chair), Firestein, Bonnie (internal member), Pang, Zhiping (internal member), Alder, Janet (outside member), School of Graduate Studies.

Subjects/Keywords: Neural stem cells; Transgenic mice

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APA (6^th Edition):

Anderson, Jeremy, 1. (2019). Role of notch signaling after traumatic brain injury in a transgenic mouse model. (Doctoral Dissertation). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/61683/

Chicago Manual of Style (16^th Edition):

Anderson, Jeremy, 1993-. “Role of notch signaling after traumatic brain injury in a transgenic mouse model.” 2019. Doctoral Dissertation, Rutgers University. Accessed January 18, 2021. https://rucore.libraries.rutgers.edu/rutgers-lib/61683/.

MLA Handbook (7^th Edition):

Anderson, Jeremy, 1993-. “Role of notch signaling after traumatic brain injury in a transgenic mouse model.” 2019. Web. 18 Jan 2021.

Vancouver:

Anderson, Jeremy 1. Role of notch signaling after traumatic brain injury in a transgenic mouse model. [Internet] [Doctoral dissertation]. Rutgers University; 2019. [cited 2021 Jan 18]. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/61683/.

Council of Science Editors:

Anderson, Jeremy 1. Role of notch signaling after traumatic brain injury in a transgenic mouse model. [Doctoral Dissertation]. Rutgers University; 2019. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/61683/

University of Hawaii – Manoa

2. Suzuki, Shana T.N. Effects of enhanced muscle growth by myostatin propeptide trangene and dietary fat content on gene expression of adiponectin, adiponectin receptors, PPAR-α and PPAR-γ.

Degree: MS, 2011, University of Hawaii – Manoa

URL: http://hdl.handle.net/10125/20774

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vii, 86 leaves, bound ill. (some col.) 29 cm

Myostatin, a member of the transforming growth factor-β superfamily, is a highly conserved negative regulator of… (more)

Subjects/Keywords: Transgenic mice – Feeding and feeds; Transgenic mice – Endocrinology

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APA (6^th Edition):

Suzuki, S. T. N. (2011). Effects of enhanced muscle growth by myostatin propeptide trangene and dietary fat content on gene expression of adiponectin, adiponectin receptors, PPAR-α and PPAR-γ. (Masters Thesis). University of Hawaii – Manoa. Retrieved from http://hdl.handle.net/10125/20774

Chicago Manual of Style (16^th Edition):

Suzuki, Shana T N. “Effects of enhanced muscle growth by myostatin propeptide trangene and dietary fat content on gene expression of adiponectin, adiponectin receptors, PPAR-α and PPAR-γ.” 2011. Masters Thesis, University of Hawaii – Manoa. Accessed January 18, 2021. http://hdl.handle.net/10125/20774.

MLA Handbook (7^th Edition):

Suzuki, Shana T N. “Effects of enhanced muscle growth by myostatin propeptide trangene and dietary fat content on gene expression of adiponectin, adiponectin receptors, PPAR-α and PPAR-γ.” 2011. Web. 18 Jan 2021.

Vancouver:

Suzuki STN. Effects of enhanced muscle growth by myostatin propeptide trangene and dietary fat content on gene expression of adiponectin, adiponectin receptors, PPAR-α and PPAR-γ. [Internet] [Masters thesis]. University of Hawaii – Manoa; 2011. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/10125/20774.

Council of Science Editors:

Suzuki STN. Effects of enhanced muscle growth by myostatin propeptide trangene and dietary fat content on gene expression of adiponectin, adiponectin receptors, PPAR-α and PPAR-γ. [Masters Thesis]. University of Hawaii – Manoa; 2011. Available from: http://hdl.handle.net/10125/20774

3. Bertin, Eléonore. Étude de l'augmentation du trafic en surface des récepteurs P2X4 de l’ATP à l’aide de nouveaux modèles murins transgéniques : implications dans les processus mnésiques et la sclérose latérale amyotrophique : Study of the increase of P2X4 ATP-gated receptor surface trafficking using novel transgenic murine models : role in memory processes and amyotrophic lateral sclerosis.

Degree: Docteur es, Neurosciences, 2019, Bordeaux

URL: http://www.theses.fr/2019BORD0341

► La signalisation purinergique ainsi que l'augmentation en surface des récepteurs ionotropiques P2X4 activé par l'ATP sont exacerbés dans divers troubles du SNC dont la sclérose… (more)

▼ La signalisation purinergique ainsi que l'augmentation en surface des récepteurs ionotropiques P2X4 activé par l'ATP sont exacerbés dans divers troubles du SNC dont la sclérose latérale amyotrophique (SLA). Le récepteur P2X4 a une expression étendue dans le système nerveux central (SNC) au niveau des neurones et des cellules gliales ainsi que dans divers types cellulaires périphériques. Une question clé concernant le rôle de la signalisation purinergique dans la physiologie et la physiopathologie est la fonction de l'augmentation du nombre de récepteurs P2X4 en surface observée dans différents types cellulaires de manière spécifique.Pour élucider les fonctions cellulaires spécifiques du récepteur P2X4 dans un contexte pathologique, une lignée de souris transgéniques conditionnelle (P2X4mCherryIN floxée) a été créée permettant la substitution du motif d'internalisation de P2X4 par la protéine fluorescente mCherry, sous la dépendance de la Cre recombinase, empêchant ainsi l'endocytose constitutive du récepteur P2X4. Nous avons validé et caractérisé deux lignées de souris knock-in (KI) exprimant le récepteur mutant d'internalisation P2X4mCherryIN dans les neurones excitateurs du cerveau antérieur (CamK2) ou dans toutes les cellules exprimant le récepteur P2X4 de façon native (CMV). Comme attendu, la substitution génétique du récepteur P2X4 sauvage par le mutant P2X4mCherryIN dans les deux modèles de souris knock-in n'altère pas la distribution ni la localisation subcellulaire du récepteur P2X4 mais conduit à une augmentation accrue de son expression en surface de manière cellule-spécifique. D’un point de vue fonctionnel, ces modèles ont permis de démontrer que l'augmentation du récepteur P2X4 à la surface des neurones excitateurs diminue l'anxiété et altère la mémoire en raison de la modulation de la plasticité synaptique dans la région CA1 de l'hippocampe.Dans le but élucider l'implication du récepteur P2X4 dans la pathogenèse de la SLA, nous avons croisé le nouveau modèle de souris KI CMV (ou P2X4KI) généré exprimant le récepteur P2X4 augmenté en surface dans toutes les cellules qui expriment nativement le récepteur P2X4 ou bien un modèle de souris transgénique délétée pour le gène p2x4 (P2X4KO) avec le modèle murin de SLA le plus couramment utilisé portant la mutation SOD1-G93A humaine (SOD1) pour la génération de souris double-transgénqiues SOD1:P2X4KI et SOD1 :P2X4KO. De manière intéressante, l'ablation du récepteur P2X4 ainsi que l'expression du mutant d'internalisation chez les souris SOD1 ont un impact significatif et positif sur les performances motrices et la survie des animaux, ce qui révèle un rôle actif bien que complexe des récepteurs P2X4 dans la progression de la SLA. Chez les souris SOD1, l'expression de P2X4 dans la moelle épinière (ME), est initialement limitée au MN puis augmente au niveau de la microglie pendant la phase symptomatique, et le récepteur P2X4 joue un rôle double sur l'expression des marqueurs d''inflammation pendant la progression de la maladie. Parallèlement, l'expression à la surface… Advisors/Committee Members: Boué-Grabot, Eric (thesis director).

Subjects/Keywords: Souris transgéniques; Sla; Als; Transgenic mice

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

APA (6^th Edition):

Bertin, E. (2019). Étude de l'augmentation du trafic en surface des récepteurs P2X4 de l’ATP à l’aide de nouveaux modèles murins transgéniques : implications dans les processus mnésiques et la sclérose latérale amyotrophique : Study of the increase of P2X4 ATP-gated receptor surface trafficking using novel transgenic murine models : role in memory processes and amyotrophic lateral sclerosis. (Doctoral Dissertation). Bordeaux. Retrieved from http://www.theses.fr/2019BORD0341

Chicago Manual of Style (16^th Edition):

Bertin, Eléonore. “Étude de l'augmentation du trafic en surface des récepteurs P2X4 de l’ATP à l’aide de nouveaux modèles murins transgéniques : implications dans les processus mnésiques et la sclérose latérale amyotrophique : Study of the increase of P2X4 ATP-gated receptor surface trafficking using novel transgenic murine models : role in memory processes and amyotrophic lateral sclerosis.” 2019. Doctoral Dissertation, Bordeaux. Accessed January 18, 2021. http://www.theses.fr/2019BORD0341.

MLA Handbook (7^th Edition):

Bertin, Eléonore. “Étude de l'augmentation du trafic en surface des récepteurs P2X4 de l’ATP à l’aide de nouveaux modèles murins transgéniques : implications dans les processus mnésiques et la sclérose latérale amyotrophique : Study of the increase of P2X4 ATP-gated receptor surface trafficking using novel transgenic murine models : role in memory processes and amyotrophic lateral sclerosis.” 2019. Web. 18 Jan 2021.

Vancouver:

Bertin E. Étude de l'augmentation du trafic en surface des récepteurs P2X4 de l’ATP à l’aide de nouveaux modèles murins transgéniques : implications dans les processus mnésiques et la sclérose latérale amyotrophique : Study of the increase of P2X4 ATP-gated receptor surface trafficking using novel transgenic murine models : role in memory processes and amyotrophic lateral sclerosis. [Internet] [Doctoral dissertation]. Bordeaux; 2019. [cited 2021 Jan 18]. Available from: http://www.theses.fr/2019BORD0341.

Council of Science Editors:

Bertin E. Étude de l'augmentation du trafic en surface des récepteurs P2X4 de l’ATP à l’aide de nouveaux modèles murins transgéniques : implications dans les processus mnésiques et la sclérose latérale amyotrophique : Study of the increase of P2X4 ATP-gated receptor surface trafficking using novel transgenic murine models : role in memory processes and amyotrophic lateral sclerosis. [Doctoral Dissertation]. Bordeaux; 2019. Available from: http://www.theses.fr/2019BORD0341

East Carolina University

4. Kirsanov, Oleksandr. ANALYSIS OF TRANSGENIC MOUSE MODELS TO STUDY MAMMALIAN SPERMATOGONIA.

Degree: MS, MS-Biomedical Science, 2018, East Carolina University

URL: http://hdl.handle.net/10342/6969

► Spermatogenesis in the mammalian testis results in the daily production of millions of spermatozoa. This developmental process is founded upon the actions of a small… (more)

Subjects/Keywords: Spermatogonia; Animals; Mice, Transgenic; Mammals; Spermatogenesis

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APA (6^th Edition):

Kirsanov, O. (2018). ANALYSIS OF TRANSGENIC MOUSE MODELS TO STUDY MAMMALIAN SPERMATOGONIA. (Masters Thesis). East Carolina University. Retrieved from http://hdl.handle.net/10342/6969

Chicago Manual of Style (16^th Edition):

Kirsanov, Oleksandr. “ANALYSIS OF TRANSGENIC MOUSE MODELS TO STUDY MAMMALIAN SPERMATOGONIA.” 2018. Masters Thesis, East Carolina University. Accessed January 18, 2021. http://hdl.handle.net/10342/6969.

MLA Handbook (7^th Edition):

Kirsanov, Oleksandr. “ANALYSIS OF TRANSGENIC MOUSE MODELS TO STUDY MAMMALIAN SPERMATOGONIA.” 2018. Web. 18 Jan 2021.

Vancouver:

Kirsanov O. ANALYSIS OF TRANSGENIC MOUSE MODELS TO STUDY MAMMALIAN SPERMATOGONIA. [Internet] [Masters thesis]. East Carolina University; 2018. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/10342/6969.

Council of Science Editors:

Kirsanov O. ANALYSIS OF TRANSGENIC MOUSE MODELS TO STUDY MAMMALIAN SPERMATOGONIA. [Masters Thesis]. East Carolina University; 2018. Available from: http://hdl.handle.net/10342/6969

University of Manitoba

5. Yeganeh, Behzad. Characterization of lung adenocarcinoma in transgenic mice overexpressing calreticulin under control of the Tie-2 promoter.

Degree: Biochemistry and Medical Genetics, 2010, University of Manitoba

URL: http://hdl.handle.net/1993/4239

► Calreticulin (CRT) is a multifunctional Ca2+ dependent chaperone protein, which is localized to the endoplasmic reticulum and plays many important biological roles. In addition to… (more)

▼ Calreticulin (CRT) is a multifunctional Ca2+ dependent chaperone protein, which is localized to the endoplasmic reticulum and plays many important biological roles. In addition to its critical role in cardiovascular development, CRT has been reported to be important for cell migration, adhesion and apoptosis. A few studies have also suggested different roles for exogenous CRT in angiogenesis and tumor growth however no direct evidence for the role of endogenous CRT in these processes is available. To study the in vivo role of CRT in angiogenesis and vascular development, we generated a transgenic mouse overexpressing CRT under the control of the Tie2 promoter (referred to as Tie2-CRT) which is active in both endothelial cells and hematopoietic stem cells (HSCs). The main phenotype of these mice is an increased incidence of lung tumors. These tumors have been characterized according to their histochemical properties as being adenocarcinoma with a Surfactant Protein-C positive (SP-CPos) and Clara Cell Protein negative (CC10Neg) phenotype suggesting an alveolar origin for these tumors. We observed that during the early stages of tumor formation, the lungs show signs of increased inflammation as evidenced by congestion, reddish discoloration and the accumulation of inflammatory cells. We have also identified that the early stage tumors contain cells that express exogenous CRT and HSC markers including CD133, Sca-1, and c-Kit. As the tumor progresses to a fully developed adenocarcinoma, these cells lose the expression of exogenous CRT and HSCs markers and gain an alveolar type II phenotype (SP-CPos). In vitro evaluation of tumor progression using lung tumor cells from Tie2-CRT mice demonstrated a differentiation dependent expression of HSC markers by tumor cells supporting the hypothesis that HSCs might be the cells of origin for the lung tumors observed in Tie2-CRT mice. In summary, the results from this study provide evidence that lung tumors from the Tie2-CRT mice are non-epithelial in origin and that the undifferentiated population of tumor cells have HSC characteristics. After differentiation, these cells lose their stem cell phenotype and acquire an epithelial phenotype. This study is the first to examine the potential link between CRT and lung cancer development. Advisors/Committee Members: Mesaeli, Nasrin (Biochemistry and Medical Genetics) (supervisor), Murphy, Leigh(Biochemistry and Medical Genetics) Wigle, Jeffrey (Biochemistry and Medical Genetics) Myal, Yvonne (Pathology) Opas, Michal (University of Toronto) (examiningcommittee).

Subjects/Keywords: Molecular Biology; Lung Cancer; Transgenic mice; Calreticulin

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APA (6^th Edition):

Yeganeh, B. (2010). Characterization of lung adenocarcinoma in transgenic mice overexpressing calreticulin under control of the Tie-2 promoter. (Thesis). University of Manitoba. Retrieved from http://hdl.handle.net/1993/4239

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):

Yeganeh, Behzad. “Characterization of lung adenocarcinoma in transgenic mice overexpressing calreticulin under control of the Tie-2 promoter.” 2010. Thesis, University of Manitoba. Accessed January 18, 2021. http://hdl.handle.net/1993/4239.

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

MLA Handbook (7^th Edition):

Yeganeh, Behzad. “Characterization of lung adenocarcinoma in transgenic mice overexpressing calreticulin under control of the Tie-2 promoter.” 2010. Web. 18 Jan 2021.

Vancouver:

Yeganeh B. Characterization of lung adenocarcinoma in transgenic mice overexpressing calreticulin under control of the Tie-2 promoter. [Internet] [Thesis]. University of Manitoba; 2010. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/1993/4239.

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

Council of Science Editors:

Yeganeh B. Characterization of lung adenocarcinoma in transgenic mice overexpressing calreticulin under control of the Tie-2 promoter. [Thesis]. University of Manitoba; 2010. Available from: http://hdl.handle.net/1993/4239

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

University of Newcastle

6. Guo, Su Tang. The role of inositol polyphosphate 4-phosphatase II (INPP4B) in the pathogeneis of colon ccancer.

Degree: PhD, 2018, University of Newcastle

URL: http://hdl.handle.net/1959.13/1386333

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Research Doctorate - Doctor of Philosophy (PhD)

Colon cancer is one of the most common and deadly malignancies. Despite recent advances in early diagnosis and… (more)

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Research Doctorate - Doctor of Philosophy (PhD)

Colon cancer is one of the most common and deadly malignancies. Despite recent advances in early diagnosis and the development of novel treatment approaches, the overall survival of patients with metastatic colon cancers remains disappointing. Lots of investigations have discovered some pathways important during the initiation and progression of CRC. These include the WNT, RAS−MAPK, PI3K, TGF-β, P53 and DNA mismatch-repair pathways. But Aberrant activation of the phosphatidylinositol 3-kinase (PI3K) pathway is of particular importance in CRC development, progression and resistance to treatment, since many common genetic and epigenetic anomalies in the disease, such as amplification of epidermal growth factor receptor, activating mutations of KRAS and loss of phosphate and tensin homolog deleted on chromosome 10 (PTEN), converge on activation of PI3K signaling. Lipid and protein kinases promote PI3K signaling, whereas lipid and protein phosphatases suppress PI3K signaling (Manning and Toker, 2017; Newton and Trotman, 2014). Activation of PI3K signaling is negatively regulated by three classes of inositol polyphosphate phosphatases. (Rodgers et al., 2017). The inositol polyphosphate 3-phosphatase (3-phosphatase) PTEN dephosphorylates the 3-position of PI(3,4,5)P3 to generate PI(4,5)P2 (Gericke et al., 2013; Kurokawa et al., 2012), whereas 5-phosphatases, such as Src homology 2-containing inositol 5- phosphatase (SHIP) and phosphatidylinositol 4,5-bisphosphate 5-phosphatase (PIB5PA)/proline-rich inositol polyphosphate phosphatase (PIPP) dephosphorylate the 5-position to produce PI(3,4)P2 (Park et al., 2001). The latter is in turn subjected to dephosphorylation by inositol polyphosphate 4-phosphatase type I (INPP4A) and type II (INPP4B) at the 4-position to generate PI(3)P, thus terminating PI3K signaling. During the past decades, INPP4B has been well established to be a tumor suppressor in a number of cancers. However, we have found that it is frequently upregulated in human colon cancer cells. Silencing of INPP4B blocks activation of Akt and serum- and glucocorticoid-regulated kinase 3 (SGK3), inhibits colon cancer cell proliferation and retards colon cancer xenograft growth. Conversely, overexpression of INPP4B increases proliferation and triggers anchorage-independent growth of normal colon epithelial cells. Moreover, we demonstrate that the effect of INPP4B on Akt and SGK3 is associated with inactivation of phosphate and tensin homolog through its protein phosphatase activity and that the increase in INPP4B is due to Ets-1-mediated transcriptional upregulation in colon cancer cells. To further consolidate the result, two genetically modified mouse model were generated by CRISP/CAS9 technique. The INPP4B^+/-; VillinCre^+/- mouse strain in which INPP4B expression limited to colon epithelium display increased proliferation potential than wild-type mice. Moreover, these mice appeared to be more sensitive to Colitis induced by Dextran Sulfate Sodium…

Advisors/Committee Members: University of Newcastle. Faculty of Health & Medicine, School of Biomedical Sciences and Pharmacy.

Subjects/Keywords: INPP4B; colon cancer; pten; transgenic mice

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APA (6^th Edition):

Guo, S. T. (2018). The role of inositol polyphosphate 4-phosphatase II (INPP4B) in the pathogeneis of colon ccancer. (Doctoral Dissertation). University of Newcastle. Retrieved from http://hdl.handle.net/1959.13/1386333

Chicago Manual of Style (16^th Edition):

Guo, Su Tang. “The role of inositol polyphosphate 4-phosphatase II (INPP4B) in the pathogeneis of colon ccancer.” 2018. Doctoral Dissertation, University of Newcastle. Accessed January 18, 2021. http://hdl.handle.net/1959.13/1386333.

MLA Handbook (7^th Edition):

Guo, Su Tang. “The role of inositol polyphosphate 4-phosphatase II (INPP4B) in the pathogeneis of colon ccancer.” 2018. Web. 18 Jan 2021.

Vancouver:

Guo ST. The role of inositol polyphosphate 4-phosphatase II (INPP4B) in the pathogeneis of colon ccancer. [Internet] [Doctoral dissertation]. University of Newcastle; 2018. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/1959.13/1386333.

Council of Science Editors:

Guo ST. The role of inositol polyphosphate 4-phosphatase II (INPP4B) in the pathogeneis of colon ccancer. [Doctoral Dissertation]. University of Newcastle; 2018. Available from: http://hdl.handle.net/1959.13/1386333

Columbia University

7. Abrams, Jeffrey. Dysfunctional Sodium Channels and Arrhythmogenesis: Insights into the Molecular Regulation of Cardiac Sodium Channels Using Transgenic Mice.

Degree: 2017, Columbia University

URL: https://doi.org/10.7916/D86Q28NQ

► Proper functioning of the voltage gated sodium channel, NaV1.5, is essential for maintenance of normal cardiac electrophysiological properties. Changes to the biophysical properties of sodium… (more)

▼ Proper functioning of the voltage gated sodium channel, NaV1.5, is essential for maintenance of normal cardiac electrophysiological properties. Changes to the biophysical properties of sodium channels can take many forms and can affect the peak component of current carried during phase zero of the action potential; the “persistent” or “late” current component conducted during the repolarizing phases of the action potential; the availability of the channel as seen by changes in window current; and the kinetics of channel transitions between closed, opened and inactivated states. Mutations in NaV1.5 that alter these parameters of channel function are linked to a number of cardiac diseases including arrhythmias such as atrial fibrillation. In addition, mutations in many of the auxiliary proteins that form part of the sodium channel macromolecular complex have likewise been associated with diseases of the heart. Mutations in regions of the sodium channel responsible for interactions with these auxiliary proteins have also been linked to various dysfunctional cardiac states. Indeed, a large number of disease causing mutations are localized to the C-terminal domain of NaV1.5, a hotspot for interacting proteins. Using a transgenic mouse model, we show that expression of a mutant sodium channel with gain-of-function properties conferring increased persistent current, is sufficient to cause both structural and electrophysiological abnormalities in the heart driving the development of spontaneous and prolonged episodes of atrial fibrillation. The sustained and spontaneous atrial arrhythmias, an unusual if not unique phenotype in mice, enabled explorations of mechanisms of atrial fibrillation using in vivo (telemetry), ex vivo (optical voltage mapping), and in vitro (cellular electrophysiology) techniques. Since persistent sodium current was the driver of the structural and electrophysiological abnormalities leading to atrial fibrillation, we subsequently pursued studies exploring the mechanisms of persistent sodium current. Prior work of heterologously expressed sodium channels identified calmodulin as a regulator of persistent current. Mutation of the calmodulin binding site in the C-terminus of the cardiac sodium channel caused increased persistent current when the channel was expressed heterologously. The role of calmodulin in the regulation of the sodium channel in cardiomyocytes has not been definitively determined. We created transgenic mice expressing human sodium channels harboring a mutation of the calmodulin binding site. Using whole cell patch clamping, we found, in contrast to previously reported findings, that ablation of the calmodulin binding site did not induce increased persistent sodium current. Instead, loss of calmodulin binding stabilized the inactivated state by shifting the V50 for steady-state inactivation in the hyperpolarizing direction. Furthermore, loss of calmodulin binding sped up the transition to the inactivated state demonstrated by a significantly shortened tau of…

Subjects/Keywords: Biophysics; Sodium channels; Transgenic mice; Electrophysiology

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APA (6^th Edition):

Abrams, J. (2017). Dysfunctional Sodium Channels and Arrhythmogenesis: Insights into the Molecular Regulation of Cardiac Sodium Channels Using Transgenic Mice. (Doctoral Dissertation). Columbia University. Retrieved from https://doi.org/10.7916/D86Q28NQ

Chicago Manual of Style (16^th Edition):

Abrams, Jeffrey. “Dysfunctional Sodium Channels and Arrhythmogenesis: Insights into the Molecular Regulation of Cardiac Sodium Channels Using Transgenic Mice.” 2017. Doctoral Dissertation, Columbia University. Accessed January 18, 2021. https://doi.org/10.7916/D86Q28NQ.

MLA Handbook (7^th Edition):

Abrams, Jeffrey. “Dysfunctional Sodium Channels and Arrhythmogenesis: Insights into the Molecular Regulation of Cardiac Sodium Channels Using Transgenic Mice.” 2017. Web. 18 Jan 2021.

Vancouver:

Abrams J. Dysfunctional Sodium Channels and Arrhythmogenesis: Insights into the Molecular Regulation of Cardiac Sodium Channels Using Transgenic Mice. [Internet] [Doctoral dissertation]. Columbia University; 2017. [cited 2021 Jan 18]. Available from: https://doi.org/10.7916/D86Q28NQ.

Council of Science Editors:

Abrams J. Dysfunctional Sodium Channels and Arrhythmogenesis: Insights into the Molecular Regulation of Cardiac Sodium Channels Using Transgenic Mice. [Doctoral Dissertation]. Columbia University; 2017. Available from: https://doi.org/10.7916/D86Q28NQ

George Mason University

8. Bozzelli, P. Lorenzo. The Effects That Dietary Manipulations of Zinc and Copper Have on Nest Building, Zinc Transporter and Glial Fibrillary Acidic Protein Expression in a Transgenic Mouse Model of Alzheimer’s Disease .

Degree: 2014, George Mason University

URL: http://hdl.handle.net/1920/9077

► The role of essential trace elements, such as zinc and copper, in Alzheimer’s disease (AD) has received much attention in the last decade. Zinc (Zn)… (more)

▼ The role of essential trace elements, such as zinc and copper, in Alzheimer’s disease (AD) has received much attention in the last decade. Zinc (Zn) and copper (Cu) are involved in many biological processes. Amyloid-β (Aβ) interacts with these metal ions, sequesters them, and causes an intracellular decrease in Zn and Cu. In this study, we characterize nest building ability, zinc transporter 3 (ZnT3) and glial fibrillary acidic protein (GFAP) expression in wildtype (WT) and transgenic (J20) mice in one of three dietary conditions: regular lab water (LW) with a copper-control (CC) diet (LW/CC); regular LW with a copper-deficient (CD) diet (LW/CD); or lab water enhanced with 10 ppm ZnCO3 with the CC diet (Zn/CC). Based on previous work from our laboratory, Zn-enhanced water was shown to induce behavioral deficits, but when Cu was added to the Zn drinking water, the behavioral deficits were abrogated. Other studies however have shown that Cu-deficiency may be beneficial in AD. We sought out to evaluate what mechanisms may be involved in Zn supplementation and whether or not there would be similar results between the two manipulated diets. Surprisingly, J20 mice significantly outperformed WT mice in the nesting assay, but in only the LW/CC condition. Males outperformed females on the nesting assay, but again this was significant in only the LW/CC group (p<.05). ZnT3 levels were not observed to be different based on genotype, but diet did induce higher expression of ZnT3 (p<.10), with the Zn/CC group expressing the highest and the control LW/CC group expressing the least amount (p<.05). GFAP levels were less consistent but the manipulated diets induced higher expression of GFAP (p < .10). Also, the only genotypic difference was observed in the control LW/CC which shows that the manipulated diets made the WT mice take on a J20 profile. These data warrant further investigation into the role of dietary Zn and Cu therapeutics. Advisors/Committee Members: Flinn, Jane M (advisor).

Subjects/Keywords: ZnT3; transgenic mice; biometals; Alzheimer's disease

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APA (6^th Edition):

Bozzelli, P. L. (2014). The Effects That Dietary Manipulations of Zinc and Copper Have on Nest Building, Zinc Transporter and Glial Fibrillary Acidic Protein Expression in a Transgenic Mouse Model of Alzheimer’s Disease . (Thesis). George Mason University. Retrieved from http://hdl.handle.net/1920/9077

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):

Bozzelli, P Lorenzo. “The Effects That Dietary Manipulations of Zinc and Copper Have on Nest Building, Zinc Transporter and Glial Fibrillary Acidic Protein Expression in a Transgenic Mouse Model of Alzheimer’s Disease .” 2014. Thesis, George Mason University. Accessed January 18, 2021. http://hdl.handle.net/1920/9077.

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

MLA Handbook (7^th Edition):

Bozzelli, P Lorenzo. “The Effects That Dietary Manipulations of Zinc and Copper Have on Nest Building, Zinc Transporter and Glial Fibrillary Acidic Protein Expression in a Transgenic Mouse Model of Alzheimer’s Disease .” 2014. Web. 18 Jan 2021.

Vancouver:

Bozzelli PL. The Effects That Dietary Manipulations of Zinc and Copper Have on Nest Building, Zinc Transporter and Glial Fibrillary Acidic Protein Expression in a Transgenic Mouse Model of Alzheimer’s Disease . [Internet] [Thesis]. George Mason University; 2014. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/1920/9077.

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

Council of Science Editors:

Bozzelli PL. The Effects That Dietary Manipulations of Zinc and Copper Have on Nest Building, Zinc Transporter and Glial Fibrillary Acidic Protein Expression in a Transgenic Mouse Model of Alzheimer’s Disease . [Thesis]. George Mason University; 2014. Available from: http://hdl.handle.net/1920/9077

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

9. Rojas, José-Manuel. Identification of novel immunogenic HLA-DR-restricted peptides from tumour-associated antigens.

Degree: PhD, 2003, Nottingham Trent University

URL: http://irep.ntu.ac.uk/id/eprint/40993/ ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.273771

► CD4⁺ T cells play a central role in antitumour immunity; not only do they provide help for the development of CTL recognising tumour antigens but… (more)

▼ CD4⁺ T cells play a central role in antitumour immunity; not only do they provide help for the development of CTL recognising tumour antigens but they can also enhance antitumour responses via indirect cytotoxic mechanisms at the tumour site. Since CD4⁺ T cells recognise the antigen in the form of peptides presented on MHC class II molecules, attention has been focused in the recent years on the identification of these peptides derived from tumour antigens. Therefore the aim of this study was to identify novel immunogenic peptides derived from tumour antigens where presentation was restricted to human MHC class II HLA-DR1 and/or HLADR4 molecules. The adopted strategy consisted in predicting peptides from the tumour antigens p53, gp100 and bcr-abl(b3a2) using computer-assisted algorithms, and immunisation of HLA-DR1 transgenic mice with these peptides in order to assess their immunogenicity. Immunogenic peptides in transgenic mice were then tested in human in in vitro T cell sensitisation assays. To determine peptide immunogenicity in mice, a method was optimised using the reported I-Ak-restricted peptides HEL46-61 and HEL119-132. This model was then successfully established in HLA-DR1 transgenic mice with the model peptide HA307-319. Proliferative responses and IFN-γ production were observed when the splenocytes of HLA-DR1 transgenic mice were re-presented in vitro with the HA307-319 peptide used in immunisation. Dendritic cells (DC) were shown to be better antigen presenting cells (APC) than syngeneic splenocytes in proliferation assays; thus DC were subsequently used as APC in all experiments. Further characterisation of DC, generated from bone marrow precursors by culture with GM-CSF, demonstrated that day 8 non-adherent cells matured with LPS were optimal for antigen presentation in this experimental setting. Immunisation of HLA-DR1 transgenic mice with predicted peptides from p53, gp100 and bcr-abl (b3a2) resulted in HLA-DR1-restricted responses for two novel p53 peptides (p53 63-77 and p53 108-122) and two bcr-abl peptides (bcr-abl GFK11 and bcr-abl ATG18). Responses were also observed to two novel gp100 peptides (gpl00 194-208 and gp100 566-580). This study demonstrated that HLA-DR-restricted responses to novel peptides can be obtained in HLA-DR1 transgenic mice. Furthermore, proliferative responses to p53 63-77 in a HLA-DR1⁺ donor, to gp100 566-580 in another HLA-DR1⁺ donor, and to p53 108-122 in two HLA-DR4⁺ donors demonstrated that these peptides were also immunogenic in human assays. Collectively, these results indicated that peptide immunisation of HLA-DR1 transgenic mice could facilitate the identification of novel immunogenic HLA-DR-restricted peptides from tumour antigens, that allow us to understand further the role of CD4⁺ in antitumour immunity and improve cancer immunotherapeutic strategies.

Subjects/Keywords: 616; Transgenic mice

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APA (6^th Edition):

Rojas, J. (2003). Identification of novel immunogenic HLA-DR-restricted peptides from tumour-associated antigens. (Doctoral Dissertation). Nottingham Trent University. Retrieved from http://irep.ntu.ac.uk/id/eprint/40993/ ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.273771

Chicago Manual of Style (16^th Edition):

Rojas, José-Manuel. “Identification of novel immunogenic HLA-DR-restricted peptides from tumour-associated antigens.” 2003. Doctoral Dissertation, Nottingham Trent University. Accessed January 18, 2021. http://irep.ntu.ac.uk/id/eprint/40993/ ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.273771.

MLA Handbook (7^th Edition):

Rojas, José-Manuel. “Identification of novel immunogenic HLA-DR-restricted peptides from tumour-associated antigens.” 2003. Web. 18 Jan 2021.

Vancouver:

Rojas J. Identification of novel immunogenic HLA-DR-restricted peptides from tumour-associated antigens. [Internet] [Doctoral dissertation]. Nottingham Trent University; 2003. [cited 2021 Jan 18]. Available from: http://irep.ntu.ac.uk/id/eprint/40993/ ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.273771.

Council of Science Editors:

Rojas J. Identification of novel immunogenic HLA-DR-restricted peptides from tumour-associated antigens. [Doctoral Dissertation]. Nottingham Trent University; 2003. Available from: http://irep.ntu.ac.uk/id/eprint/40993/ ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.273771

Montana State University

10. Orr, Miranda Ethel. Mouse and stem cell models of frontotemporal dementia.

Degree: PhD, College of Letters & Science, 2012, Montana State University

URL: https://scholarworks.montana.edu/xmlui/handle/1/1994

► Alzheimer's disease (AD) is the most prevalent brain disease in the United States, and an escalating health concern. AD patient brains acquire hallmark protein aggregates,… (more)

▼ Alzheimer's disease (AD) is the most prevalent brain disease in the United States, and an escalating health concern. AD patient brains acquire hallmark protein aggregates, referred to as senile A beta plaques and neurofibrillary tangles (NFTs), that coincide with brain cell loss and dementia. A subset of AD patients carry mutant genes. Our understanding of AD largely relies on model systems that express these gene variants. Mice engineered to express AD-mutant human genes develop A beta plaques, but fail to develop the tau-containing NFTs or cell loss. Mutant tau variants are required to induce NFTs and neuronal loss in mice, but AD patients carry normal tau genes. The inability of mouse tau to become a pathogenic protein in the presence of AD-mutant gene variants, and the general insufficiency of the current systems to recapitulate AD, inspired the research described here. To determine if species differences between mouse and human tau inhibit the progression of AD in mice, I utilized a well-characterized mouse model of a related disease, frontotemporal dementia (FTD). FTD mice carry mutant human tau and develop NFTs and cell loss. I ablated mouse tau in FTD mice and looked for signs of more severe pathology. I compared the FTD mice, with and without mouse tau, to FTD mice with and without wild type human tau to investigate potential tau species-specific differences. My studies indicated that wild type tau, mouse or human, dampened the pathological effects of FTD tau implying a general, not mouse-specific, effect of normal tau protein. Our data suggest that unknown factors, distinct from endogenous mouse tau, contribute to the inability of mice to model AD. The recent interest in patient-specific stem cell (SC) models to study disease necessitates a thorough evaluation of their ability to recapitulate key characteristics of disease, reproducibility, and longevity. I generated and characterized brain SC cultures from FTD fetal mice and compared them to those generated from mice with normal human tau. Significant genotype associated differences were discovered in the SC system and later verified in adult mice to reinforce the potential of patient-specific SC models to study disease. Advisors/Committee Members: Chairperson, Graduate Committee: George A. Carlson. (advisor).

Subjects/Keywords: Dementia.; Alzheimer's disease.; Stem cells.; Transgenic mice.

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APA (6^th Edition):

Orr, M. E. (2012). Mouse and stem cell models of frontotemporal dementia. (Doctoral Dissertation). Montana State University. Retrieved from https://scholarworks.montana.edu/xmlui/handle/1/1994

Chicago Manual of Style (16^th Edition):

Orr, Miranda Ethel. “Mouse and stem cell models of frontotemporal dementia.” 2012. Doctoral Dissertation, Montana State University. Accessed January 18, 2021. https://scholarworks.montana.edu/xmlui/handle/1/1994.

MLA Handbook (7^th Edition):

Orr, Miranda Ethel. “Mouse and stem cell models of frontotemporal dementia.” 2012. Web. 18 Jan 2021.

Vancouver:

Orr ME. Mouse and stem cell models of frontotemporal dementia. [Internet] [Doctoral dissertation]. Montana State University; 2012. [cited 2021 Jan 18]. Available from: https://scholarworks.montana.edu/xmlui/handle/1/1994.

Council of Science Editors:

Orr ME. Mouse and stem cell models of frontotemporal dementia. [Doctoral Dissertation]. Montana State University; 2012. Available from: https://scholarworks.montana.edu/xmlui/handle/1/1994

University of Hong Kong

11. Ng, Chun-pong. The role of Densin-180 on mouse behavior and synaptic protein distribution.

Degree: 2013, University of Hong Kong

URL: http://hdl.handle.net/10722/249861

► Lrrc7 (Leucine Rich Repeat Containing 7) encodes Densin-180, a scaffold protein located in the postsynaptic density of excitatory synapses. A transgenic mouse line with disruption… (more)

▼ Lrrc7 (Leucine Rich Repeat Containing 7) encodes Densin-180, a scaffold protein located in the postsynaptic density of excitatory synapses. A transgenic mouse line with disruption of Lrrc7 by the transgene displayed severe abnormalities, including intensive fighting with littermates, anxious and attack during handling, and death at weaning due to dehydration. Homozygous females did not nurse their babies. As the transgene was not expressed and there was almost a complete loss of expression of Densin-180 in the mutant brain, the behavioral defects might be due to molecular abnormalities in excitatory synapses induced by the deficiency of Densin-180. Also, to reduce injury due to fighting caused by mutant mice, a colored transparent plastic house and paper nesting strips were used to enhance the nursing condition in the home cage. Surprisingly, fighting was no longer observed. Therefore, the first objective of this study was to analyze the behavioral and biochemical defects in Densin-180 mutants, and then to examine the effect of environmental enrichment (EE) on these defects in the mutants. The ultimate hope is to rescue the abnormalities displayed in Densin-180 mutants. The behavioral assessments confirmed that Lrrc7 mutants were anxious as illustrated in three independent tests for the level of anxiety: Open field, elevated plus maze and light-dark box. Also, the sucrose preference test suggested anhedonia-like behavior in Lrrc7 mutants. Interestingly, the Lrrc7 mutants displayed a normal social interaction in three-chamber test, but reduced aggressiveness in one-chamber test. At the cellular level, the reduced levels of Calcium/calmodulin-dependent kinase II (CamKII) α and NMDA receptor subunit 2B (Nr2B) in the synaptosomal fraction of mutant cortex was consistent with the scaffold role of Densin-180. Furthermore, the reduction of neurite length and breadth in primary hippocampal neurons isolated from mutant embryos suggested that loss of Densin-180 affected early neurite development. Taken together, the data not only consolidated the scaffold role of Densin-180 in the synapse, but also revealed an important function of Densin-180 in neurite development. With the above-mentioned EE protocol, the difference in the levels of both CamKIIα and Nr2B were no longer observed in the mutant from western analysis. Concerning their behavior, enrichment was capable to rescue the anhedonia-like behavior, but it did not reduce the anxiety level of the mutant mice. Exploration and locomotion were increased in both wild-type (WT) and mutant mice in the open field and light-dark box. Even though EE did not exert any effect on the anxiety-like behavior, the beneficial influence of EE on the general well-being of Lrrc7 mouse mutants and their littermates was remarkable. To conclude, Lrrc7 mutants exhibited excessive fighting with littermates before weaning. Behavioral tests of adult mice showed that homozygous mutant mice had increased anxiety but might have lost the aggressiveness. Loss of Densin-180 impaired neurite…

Subjects/Keywords: Transgenic mice - Behavior

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APA (6^th Edition):

Ng, C. (2013). The role of Densin-180 on mouse behavior and synaptic protein distribution. (Thesis). University of Hong Kong. Retrieved from http://hdl.handle.net/10722/249861

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):

Ng, Chun-pong. “The role of Densin-180 on mouse behavior and synaptic protein distribution.” 2013. Thesis, University of Hong Kong. Accessed January 18, 2021. http://hdl.handle.net/10722/249861.

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

MLA Handbook (7^th Edition):

Ng, Chun-pong. “The role of Densin-180 on mouse behavior and synaptic protein distribution.” 2013. Web. 18 Jan 2021.

Vancouver:

Ng C. The role of Densin-180 on mouse behavior and synaptic protein distribution. [Internet] [Thesis]. University of Hong Kong; 2013. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/10722/249861.

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

Council of Science Editors:

Ng C. The role of Densin-180 on mouse behavior and synaptic protein distribution. [Thesis]. University of Hong Kong; 2013. Available from: http://hdl.handle.net/10722/249861

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

University of Hong Kong

12. Chan, Sing-kwok. Mouse preproendothelin-1 gene: transgenic mouse models to study tissue-specific and developmental expression andregulation.

Degree: 1998, University of Hong Kong

URL: http://hdl.handle.net/10722/35179

Subjects/Keywords: Transgenic mice.; Endothelins.

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APA (6^th Edition):

Chan, S. (1998). Mouse preproendothelin-1 gene: transgenic mouse models to study tissue-specific and developmental expression andregulation. (Thesis). University of Hong Kong. Retrieved from http://hdl.handle.net/10722/35179

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):

Chan, Sing-kwok. “Mouse preproendothelin-1 gene: transgenic mouse models to study tissue-specific and developmental expression andregulation.” 1998. Thesis, University of Hong Kong. Accessed January 18, 2021. http://hdl.handle.net/10722/35179.

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

MLA Handbook (7^th Edition):

Chan, Sing-kwok. “Mouse preproendothelin-1 gene: transgenic mouse models to study tissue-specific and developmental expression andregulation.” 1998. Web. 18 Jan 2021.

Vancouver:

Chan S. Mouse preproendothelin-1 gene: transgenic mouse models to study tissue-specific and developmental expression andregulation. [Internet] [Thesis]. University of Hong Kong; 1998. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/10722/35179.

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

Council of Science Editors:

Chan S. Mouse preproendothelin-1 gene: transgenic mouse models to study tissue-specific and developmental expression andregulation. [Thesis]. University of Hong Kong; 1998. Available from: http://hdl.handle.net/10722/35179

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

University of Cambridge

13. Myelnikov, Dmitriy. Transforming mice : technique and communication in the making of transgenic animals, 1974-1988.

Degree: PhD, 2015, University of Cambridge

URL: https://doi.org/10.17863/CAM.16164 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.678957

Subjects/Keywords: 500; transgenic animals; transgenic mice

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APA (6^th Edition):

Myelnikov, D. (2015). Transforming mice : technique and communication in the making of transgenic animals, 1974-1988. (Doctoral Dissertation). University of Cambridge. Retrieved from https://doi.org/10.17863/CAM.16164 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.678957

Chicago Manual of Style (16^th Edition):

Myelnikov, Dmitriy. “Transforming mice : technique and communication in the making of transgenic animals, 1974-1988.” 2015. Doctoral Dissertation, University of Cambridge. Accessed January 18, 2021. https://doi.org/10.17863/CAM.16164 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.678957.

MLA Handbook (7^th Edition):

Myelnikov, Dmitriy. “Transforming mice : technique and communication in the making of transgenic animals, 1974-1988.” 2015. Web. 18 Jan 2021.

Vancouver:

Myelnikov D. Transforming mice : technique and communication in the making of transgenic animals, 1974-1988. [Internet] [Doctoral dissertation]. University of Cambridge; 2015. [cited 2021 Jan 18]. Available from: https://doi.org/10.17863/CAM.16164 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.678957.

Council of Science Editors:

Myelnikov D. Transforming mice : technique and communication in the making of transgenic animals, 1974-1988. [Doctoral Dissertation]. University of Cambridge; 2015. Available from: https://doi.org/10.17863/CAM.16164 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.678957

Central Connecticut State University

14. Lanza, Janna R., 1976-. Abnormal apoptosis in sterile mshi/mshi mutant mice / Janna R. Lanza.

Degree: Department of Biological Sciences, 2004, Central Connecticut State University

URL: http://content.library.ccsu.edu/u?/ccsutheses,1520

► Infertility is a common problem, affecting approximately 10% of all couples attempting to conceive (Watson et al., 1998). Although numerous potential causes of human infertility… (more)

Subjects/Keywords: Transgenic mice; Mice – Infertility

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APA (6^th Edition):

Lanza, Janna R., 1. (2004). Abnormal apoptosis in sterile mshi/mshi mutant mice / Janna R. Lanza. (Thesis). Central Connecticut State University. Retrieved from http://content.library.ccsu.edu/u?/ccsutheses,1520

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):

Lanza, Janna R., 1976-. “Abnormal apoptosis in sterile mshi/mshi mutant mice / Janna R. Lanza.” 2004. Thesis, Central Connecticut State University. Accessed January 18, 2021. http://content.library.ccsu.edu/u?/ccsutheses,1520.

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

MLA Handbook (7^th Edition):

Lanza, Janna R., 1976-. “Abnormal apoptosis in sterile mshi/mshi mutant mice / Janna R. Lanza.” 2004. Web. 18 Jan 2021.

Vancouver:

Lanza, Janna R. 1. Abnormal apoptosis in sterile mshi/mshi mutant mice / Janna R. Lanza. [Internet] [Thesis]. Central Connecticut State University; 2004. [cited 2021 Jan 18]. Available from: http://content.library.ccsu.edu/u?/ccsutheses,1520.

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

Council of Science Editors:

Lanza, Janna R. 1. Abnormal apoptosis in sterile mshi/mshi mutant mice / Janna R. Lanza. [Thesis]. Central Connecticut State University; 2004. Available from: http://content.library.ccsu.edu/u?/ccsutheses,1520

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

Central Connecticut State University

15. Ye, Naiqing. Interleukin 20 receptor a (il20ra) is not the molecular basis of the mouse male sterility and histoincompatibility (mshi) mutation.

Degree: Department of Biomolecular Sciences, 2006, Central Connecticut State University

URL: http://content.library.ccsu.edu/u?/ccsutheses,976

► The male sterility and histoincompatibility mutant, mshi, results from a recessive mutation that arose spontaneously in the BALB/cBy inbred mouse strain. Using a 402-member BALB/cBy-mshi/mshi… (more)

Subjects/Keywords: Mice – Infertility; Transgenic mice

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APA (6^th Edition):

Ye, N. (2006). Interleukin 20 receptor a (il20ra) is not the molecular basis of the mouse male sterility and histoincompatibility (mshi) mutation. (Thesis). Central Connecticut State University. Retrieved from http://content.library.ccsu.edu/u?/ccsutheses,976

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):

Ye, Naiqing. “Interleukin 20 receptor a (il20ra) is not the molecular basis of the mouse male sterility and histoincompatibility (mshi) mutation.” 2006. Thesis, Central Connecticut State University. Accessed January 18, 2021. http://content.library.ccsu.edu/u?/ccsutheses,976.

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

MLA Handbook (7^th Edition):

Ye, Naiqing. “Interleukin 20 receptor a (il20ra) is not the molecular basis of the mouse male sterility and histoincompatibility (mshi) mutation.” 2006. Web. 18 Jan 2021.

Vancouver:

Ye N. Interleukin 20 receptor a (il20ra) is not the molecular basis of the mouse male sterility and histoincompatibility (mshi) mutation. [Internet] [Thesis]. Central Connecticut State University; 2006. [cited 2021 Jan 18]. Available from: http://content.library.ccsu.edu/u?/ccsutheses,976.

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

Council of Science Editors:

Ye N. Interleukin 20 receptor a (il20ra) is not the molecular basis of the mouse male sterility and histoincompatibility (mshi) mutation. [Thesis]. Central Connecticut State University; 2006. Available from: http://content.library.ccsu.edu/u?/ccsutheses,976

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

Central Connecticut State University

16. Lu, Yi-Chien. Interleukin 20 receptor (IL20RA) is not the gene disrupted by the male sterility and histoincompatibility (mshi) mutation in mice.

Degree: Department of Biomolecular Sciences, 2004, Central Connecticut State University

URL: http://content.library.ccsu.edu/u?/ccsutheses,1026

► The recessive male sterility and histoincompatibility mutation (mshi) in the mouse generates pleiotropic effects on graft transplantation and male reproduction. Previous analysis of backcross mice… (more)

Subjects/Keywords: Mice – Infertility; Transgenic mice

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APA (6^th Edition):

Lu, Y. (2004). Interleukin 20 receptor (IL20RA) is not the gene disrupted by the male sterility and histoincompatibility (mshi) mutation in mice. (Thesis). Central Connecticut State University. Retrieved from http://content.library.ccsu.edu/u?/ccsutheses,1026

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):

Lu, Yi-Chien. “Interleukin 20 receptor (IL20RA) is not the gene disrupted by the male sterility and histoincompatibility (mshi) mutation in mice.” 2004. Thesis, Central Connecticut State University. Accessed January 18, 2021. http://content.library.ccsu.edu/u?/ccsutheses,1026.

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

MLA Handbook (7^th Edition):

Lu, Yi-Chien. “Interleukin 20 receptor (IL20RA) is not the gene disrupted by the male sterility and histoincompatibility (mshi) mutation in mice.” 2004. Web. 18 Jan 2021.

Vancouver:

Lu Y. Interleukin 20 receptor (IL20RA) is not the gene disrupted by the male sterility and histoincompatibility (mshi) mutation in mice. [Internet] [Thesis]. Central Connecticut State University; 2004. [cited 2021 Jan 18]. Available from: http://content.library.ccsu.edu/u?/ccsutheses,1026.

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

Council of Science Editors:

Lu Y. Interleukin 20 receptor (IL20RA) is not the gene disrupted by the male sterility and histoincompatibility (mshi) mutation in mice. [Thesis]. Central Connecticut State University; 2004. Available from: http://content.library.ccsu.edu/u?/ccsutheses,1026

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

Hong Kong University of Science and Technology

17. Yeung, Rigil Kent LIFS. Gabrb2 knockout mice displayed schizophrenia-like and comorbid phenotypes with GABAergic interneuron-astrocyte-microglia dysregulation and neuroinflammation.

Degree: 2018, Hong Kong University of Science and Technology

URL: http://repository.ust.hk/ir/Record/1783.1-92991 ; https://doi.org/10.14711/thesis-991012615863503412 ; http://repository.ust.hk/ir/bitstream/1783.1-92991/1/th_redirect.html

► Intronic polymorphisms of the GABA_A receptor β₂ subunit gene (GABRB2) were earlier associated with schizophrenia, deficit of gene expression, different electrophysiological properties of the long… (more)

Subjects/Keywords: GABA ; Receptors ; Neurobehavioral disorders ; Transgenic mice ; Messenger RNA ; Mice as laboratory animals

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APA (6^th Edition):

Yeung, R. K. L. (2018). Gabrb2 knockout mice displayed schizophrenia-like and comorbid phenotypes with GABAergic interneuron-astrocyte-microglia dysregulation and neuroinflammation. (Thesis). Hong Kong University of Science and Technology. Retrieved from http://repository.ust.hk/ir/Record/1783.1-92991 ; https://doi.org/10.14711/thesis-991012615863503412 ; http://repository.ust.hk/ir/bitstream/1783.1-92991/1/th_redirect.html

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):

Yeung, Rigil Kent LIFS. “Gabrb2 knockout mice displayed schizophrenia-like and comorbid phenotypes with GABAergic interneuron-astrocyte-microglia dysregulation and neuroinflammation.” 2018. Thesis, Hong Kong University of Science and Technology. Accessed January 18, 2021. http://repository.ust.hk/ir/Record/1783.1-92991 ; https://doi.org/10.14711/thesis-991012615863503412 ; http://repository.ust.hk/ir/bitstream/1783.1-92991/1/th_redirect.html.

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

MLA Handbook (7^th Edition):

Yeung, Rigil Kent LIFS. “Gabrb2 knockout mice displayed schizophrenia-like and comorbid phenotypes with GABAergic interneuron-astrocyte-microglia dysregulation and neuroinflammation.” 2018. Web. 18 Jan 2021.

Vancouver:

Yeung RKL. Gabrb2 knockout mice displayed schizophrenia-like and comorbid phenotypes with GABAergic interneuron-astrocyte-microglia dysregulation and neuroinflammation. [Internet] [Thesis]. Hong Kong University of Science and Technology; 2018. [cited 2021 Jan 18]. Available from: http://repository.ust.hk/ir/Record/1783.1-92991 ; https://doi.org/10.14711/thesis-991012615863503412 ; http://repository.ust.hk/ir/bitstream/1783.1-92991/1/th_redirect.html.

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

Council of Science Editors:

Yeung RKL. Gabrb2 knockout mice displayed schizophrenia-like and comorbid phenotypes with GABAergic interneuron-astrocyte-microglia dysregulation and neuroinflammation. [Thesis]. Hong Kong University of Science and Technology; 2018. Available from: http://repository.ust.hk/ir/Record/1783.1-92991 ; https://doi.org/10.14711/thesis-991012615863503412 ; http://repository.ust.hk/ir/bitstream/1783.1-92991/1/th_redirect.html

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

18. Κατσιμπούλας, Μιχαήλ. Ο ρόλος των ενδοκανναβινοειδών στην αθηροσκλήρωση: πειραματική μελέτη.

Degree: 2013, National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ)

URL: http://hdl.handle.net/10442/hedi/38033

► Introduction: The newly discovered endocannabinoid system contributes tothe physiological regulation of energy balance, food intake and lipid and glucosemetabolism through both central and peripheral effects.… (more)

▼ Introduction: The newly discovered endocannabinoid system contributes tothe physiological regulation of energy balance, food intake and lipid and glucosemetabolism through both central and peripheral effects. The cannabinoids exerttheir pharmacologic action through the interaction with the specific receptors CB1and CB2, while the presence of another receptor is questionable (CB3). The formerreceptors are primarily distributed to the brain and adipose tissue but they are alsofound in the myocardium, vascular endothelium and sympathetic nerve terminals.Apart from their well-known psycho-active properties, novel data have risenconcerning the role of endocannabinoids in cardiovascular system. Underlyingmechanisms of cardiovascular cannabinoid actions may involve not only activationof cannabinoid receptors on peripheral nerves, but also signalling via receptorslocated in the vascular wall. Previous clinical trials reported that the CB1 receptorblocker, rimonabant, had significant effects on lipid parameters and severalcardiovascular risk factors. The influence of that antagonist on body composition,food consumption and metabolic agents has been recently investigated in rodentmodels and human beings. All data indicate a sustained weight loss and anincreased rate of smoking cessation. In particular central blockade decreases foodintake, while peripheral antagonism decreases abdominal fat, triglycerides, sd-LDL,CRP and insulin resistance. Besides this, CB1 receptor antagonist increasesremarkably HDL and adiponectin. Taken all together, it seems that CB1 receptorantagonist exerts multiple anti-atherogenic effects. Finally it remains unclearwhether receptor signalling via endocannabinoids regulates chronic subclinicalinflammation ongoing during atherosclerosis development. Now it’s essential toinvestigate the underlying mechanisms and the influence of these novelpharmaceutical compounds in the treatment of atherosclerosis.Aim: The aim of this study is to investigate the effects of a multi-factorialintervention of canabinnoid receptor antagonist and exercise program on anatherosclerotic animal model. For this purpose we used an animal model, prone toatherosclerosis, and we examined the pharmaceutical+exercise-induced changes inthe cellular and extracellular components, MMPs and TIMPs within theatherosclerotic plaque. Experimental design: Prospective, randomized, controlled, interventionalstudy.Setting: Center of Experimental Surgery, Foundation of BiomedicalResearch, Academy of Athens.Subjects: Male apoE-/- C57BL/6J knockout mice.Methods: At the age of 8 weeks, all mice were randomly assigned to thefollowing groups: a) Control group of atherosclerosis (Co, N=25), b) Exercisegroup (Ex, N=15), c) Rimonabant group (R, N=15), d) Rimonabant + Exercisegroup (REx, N=15). All groups were fed atherogenic, high-fat, diet for 16 weeksand at the end of the 16th week 10 male of Co group were euthanatized. Theremaining mice received normal, low-fat, diet for additional 6 weeks. During thistime period groups Ex and REx underwent an…

Subjects/Keywords: Αθηροσκλήρωση; Ενδοκανναβινοειδή; Άσκηση; Μύες; Διαγονιδιακοί μύες; Αναστολέας; Atherosclerosis; Endocannabinoids; Exercise; Mice; Transgenic mice; Inhibitors

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

APA (6^th Edition):

Κατσιμπούλας, . �. (2013). Ο ρόλος των ενδοκανναβινοειδών στην αθηροσκλήρωση: πειραματική μελέτη. (Thesis). National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ). Retrieved from http://hdl.handle.net/10442/hedi/38033

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):

Κατσιμπούλας, Μιχαήλ. “Ο ρόλος των ενδοκανναβινοειδών στην αθηροσκλήρωση: πειραματική μελέτη.” 2013. Thesis, National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ). Accessed January 18, 2021. http://hdl.handle.net/10442/hedi/38033.

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

MLA Handbook (7^th Edition):

Κατσιμπούλας, Μιχαήλ. “Ο ρόλος των ενδοκανναβινοειδών στην αθηροσκλήρωση: πειραματική μελέτη.” 2013. Web. 18 Jan 2021.

Vancouver:

Κατσιμπούλας �. Ο ρόλος των ενδοκανναβινοειδών στην αθηροσκλήρωση: πειραματική μελέτη. [Internet] [Thesis]. National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ); 2013. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/10442/hedi/38033.

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

Council of Science Editors:

Κατσιμπούλας �. Ο ρόλος των ενδοκανναβινοειδών στην αθηροσκλήρωση: πειραματική μελέτη. [Thesis]. National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ); 2013. Available from: http://hdl.handle.net/10442/hedi/38033

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

Dalhousie University

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

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 January 18, 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. 18 Jan 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 Jan 18]. 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 of Hong Kong

20. Siu, Kwan-yin. The development and characterization of a knockout model for secretin.

Degree: 2008, University of Hong Kong

URL: http://hdl.handle.net/10722/55588

Subjects/Keywords: Secretin.; Transgenic mice - Physiology.

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

APA (6^th Edition):

Siu, K. (2008). The development and characterization of a knockout model for secretin. (Thesis). University of Hong Kong. Retrieved from http://hdl.handle.net/10722/55588

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):

Siu, Kwan-yin. “The development and characterization of a knockout model for secretin.” 2008. Thesis, University of Hong Kong. Accessed January 18, 2021. http://hdl.handle.net/10722/55588.

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

MLA Handbook (7^th Edition):

Siu, Kwan-yin. “The development and characterization of a knockout model for secretin.” 2008. Web. 18 Jan 2021.

Vancouver:

Siu K. The development and characterization of a knockout model for secretin. [Internet] [Thesis]. University of Hong Kong; 2008. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/10722/55588.

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

Council of Science Editors:

Siu K. The development and characterization of a knockout model for secretin. [Thesis]. University of Hong Kong; 2008. Available from: http://hdl.handle.net/10722/55588

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

University of Hong Kong

21. 鍾志堅. The development and characterization of a gene-knockout mouse model for secretin receptor.

Degree: 2005, University of Hong Kong

URL: http://hdl.handle.net/10722/134065

Subjects/Keywords: Transgenic mice - Physiology.; Secretin - Receptors.

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APA (6^th Edition):

鍾志堅.. (2005). The development and characterization of a gene-knockout mouse model for secretin receptor. (Thesis). University of Hong Kong. Retrieved from http://hdl.handle.net/10722/134065

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

Chicago Manual of Style (16^th Edition):

鍾志堅.. “The development and characterization of a gene-knockout mouse model for secretin receptor.” 2005. Thesis, University of Hong Kong. Accessed January 18, 2021. http://hdl.handle.net/10722/134065.

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

MLA Handbook (7^th Edition):

鍾志堅.. “The development and characterization of a gene-knockout mouse model for secretin receptor.” 2005. Web. 18 Jan 2021.

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

Vancouver:

鍾志堅.. The development and characterization of a gene-knockout mouse model for secretin receptor. [Internet] [Thesis]. University of Hong Kong; 2005. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/10722/134065.

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

Council of Science Editors:

鍾志堅.. The development and characterization of a gene-knockout mouse model for secretin receptor. [Thesis]. University of Hong Kong; 2005. Available from: http://hdl.handle.net/10722/134065

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

University of Rochester

22. Moshkani, Safiehkhatoon. B Cells in Inflamed Lymph Nodes: A Link between Inflammation and Autoimmunity.

Degree: PhD, 2012, University of Rochester

URL: http://hdl.handle.net/1802/25517

► TNF- transgenic (TNFtg) mice develop a spontaneous inflammatory joint disease resembling rheumatoid arthritis (RA) in patients. Bin cells phenotypically defined as CD23+CD21highCD1dhigh B cells have… (more)

▼ TNF- transgenic (TNFtg) mice develop a spontaneous inflammatory joint disease resembling rheumatoid arthritis (RA) in patients. Bin cells phenotypically defined as CD23+CD21highCD1dhigh B cells have been shown to accumulate in the lymph nodes (LNs) that drain inflamed tissues of TNFtg mice and are involved in the significant histological and functional LN alterations that accompany disease exacerbation. Work presented in this thesis characterizes the origin and potential function of Bin cells. Via adoptive transfer of sorted GFP+ follicular B (FoB) cells we show that Bin cells can be generated from circulating FoB that preferentially home to the inflamed LNs of TNFtg mice and rapidly change their phenotype in the node proinflammatory environment. Remarkably, we found the Bin phenotype in WT lymph nodes after challenge with a T-dependent antigen (Ag) in adjuvant. Interestingly Bin cells display a germinal center phenotype at higher rates compared to FoB cells. Moreover, Ag-free adjuvant can induce Bin phenotype in draining LN of wild type mice, indicating that Bin induction is not dependent on exogenous Ag. Furthermore, we show that Bin cells can capture and process Ag-immune complexes in a CD21 –dependent manner more efficiently than FoB cells, and express higher levels of MHC-II, CD80 and CD86. In addition, we show that Bin cells are more potent than FoB cells in providing co-stimulation to antigen-specific CD4+T cells and eliciting cytokine production. Collectively, we propose that Bin cells: i) are a polyclonal population of B cells which derive from circulating FoB cells early in inflammation, and ii) play a role in facilitating T cell response during acute infections by promiscuous Ag presentation to T cells, thus increasing the chance of Ag-specific T cells meeting their cognate Ag before development of Ag-specific B cell clones. In cases of chronic inflammation such as in inflamed LNs of TNFtg mice, continuous presence of factor(s) responsible for induction of Bin phenotype results in persistence of Bin cells and their accumulation in inflamed LNs. The unusual accumulation of these cells may contribute to disruption of lymph node structure and further draining malfunction, as well as tolerance breakdown, leading to exacerbation of the disease. The work presented here provides new insights into pathogenesis of the autoimmune diseases and the development of new preventive and therapeutic strategies.

Subjects/Keywords: Autoimmunity; B Cells; Inflammation; Lymph Node; Rheumatoid Arthritis; TNF-Transgenic Mice

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

APA (6^th Edition):

Moshkani, S. (2012). B Cells in Inflamed Lymph Nodes: A Link between Inflammation and Autoimmunity. (Doctoral Dissertation). University of Rochester. Retrieved from http://hdl.handle.net/1802/25517

Chicago Manual of Style (16^th Edition):

Moshkani, Safiehkhatoon. “B Cells in Inflamed Lymph Nodes: A Link between Inflammation and Autoimmunity.” 2012. Doctoral Dissertation, University of Rochester. Accessed January 18, 2021. http://hdl.handle.net/1802/25517.

MLA Handbook (7^th Edition):

Moshkani, Safiehkhatoon. “B Cells in Inflamed Lymph Nodes: A Link between Inflammation and Autoimmunity.” 2012. Web. 18 Jan 2021.

Vancouver:

Moshkani S. B Cells in Inflamed Lymph Nodes: A Link between Inflammation and Autoimmunity. [Internet] [Doctoral dissertation]. University of Rochester; 2012. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/1802/25517.

Council of Science Editors:

Moshkani S. B Cells in Inflamed Lymph Nodes: A Link between Inflammation and Autoimmunity. [Doctoral Dissertation]. University of Rochester; 2012. Available from: http://hdl.handle.net/1802/25517

University of Alberta

23. Hsi Dickie, Belinda. Advancing the Alb-uPA/SCID/Bg Chimeric Mouse.

Degree: PhD, Department of Surgery, 2009, University of Alberta

URL: https://era.library.ualberta.ca/files/rr171x54d

► The feasibility of the Alb-uPA/SCID/Bg chimeric mouse as a model for Hepatitis C Virus (HCV) infection was assessed experimentally by (1) the infection and treatment… (more)

Subjects/Keywords: Hepatitis C; Mouse Model; Transgenic mice; Alb-uPA/SCID/Beige mouse

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APA (6^th Edition):

Hsi Dickie, B. (2009). Advancing the Alb-uPA/SCID/Bg Chimeric Mouse. (Doctoral Dissertation). University of Alberta. Retrieved from https://era.library.ualberta.ca/files/rr171x54d

Chicago Manual of Style (16^th Edition):

Hsi Dickie, Belinda. “Advancing the Alb-uPA/SCID/Bg Chimeric Mouse.” 2009. Doctoral Dissertation, University of Alberta. Accessed January 18, 2021. https://era.library.ualberta.ca/files/rr171x54d.

MLA Handbook (7^th Edition):

Hsi Dickie, Belinda. “Advancing the Alb-uPA/SCID/Bg Chimeric Mouse.” 2009. Web. 18 Jan 2021.

Vancouver:

Hsi Dickie B. Advancing the Alb-uPA/SCID/Bg Chimeric Mouse. [Internet] [Doctoral dissertation]. University of Alberta; 2009. [cited 2021 Jan 18]. Available from: https://era.library.ualberta.ca/files/rr171x54d.

Council of Science Editors:

Hsi Dickie B. Advancing the Alb-uPA/SCID/Bg Chimeric Mouse. [Doctoral Dissertation]. University of Alberta; 2009. Available from: https://era.library.ualberta.ca/files/rr171x54d

University of Oulu

24. Chen, Z. (Zhijun). Characterization of the 2-enoyl thioester reductase of mitochondrial fatty acid synthesis type II in mammals.

Degree: 2008, University of Oulu

URL: http://urn.fi/urn:isbn:9789514289804

► Abstract A data base search using the amino acid sequence of Saccharomyces cerevisiae Etr1p, the last enzyme of mitochondrial fatty acid synthesis type II (FAS… (more)

Subjects/Keywords: MECR/ETR1; biochemistry; lipid; mitochondria; structural enzymology; transgenic mice

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

APA (6^th Edition):

Chen, Z. (. (2008). Characterization of the 2-enoyl thioester reductase of mitochondrial fatty acid synthesis type II in mammals. (Doctoral Dissertation). University of Oulu. Retrieved from http://urn.fi/urn:isbn:9789514289804

Chicago Manual of Style (16^th Edition):

Chen, Z (Zhijun). “Characterization of the 2-enoyl thioester reductase of mitochondrial fatty acid synthesis type II in mammals.” 2008. Doctoral Dissertation, University of Oulu. Accessed January 18, 2021. http://urn.fi/urn:isbn:9789514289804.

MLA Handbook (7^th Edition):

Chen, Z (Zhijun). “Characterization of the 2-enoyl thioester reductase of mitochondrial fatty acid synthesis type II in mammals.” 2008. Web. 18 Jan 2021.

Vancouver:

Chen Z(. Characterization of the 2-enoyl thioester reductase of mitochondrial fatty acid synthesis type II in mammals. [Internet] [Doctoral dissertation]. University of Oulu; 2008. [cited 2021 Jan 18]. Available from: http://urn.fi/urn:isbn:9789514289804.

Council of Science Editors:

Chen Z(. Characterization of the 2-enoyl thioester reductase of mitochondrial fatty acid synthesis type II in mammals. [Doctoral Dissertation]. University of Oulu; 2008. Available from: http://urn.fi/urn:isbn:9789514289804

University of Michigan

25. Osborn, Laurelee. Expression Of Amylase Genes In Transgenic Mice.

Degree: PhD, Molecular biology, 1987, University of Michigan

URL: http://hdl.handle.net/2027.42/128119

► The amylase multigene family is a useful model system for the study of evolution and regulation of gene expression. I have characterized two nonallelic murine… (more)

Subjects/Keywords: Amylase; Expression; Genes; Mice; Transgenic

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APA (6^th Edition):

Osborn, L. (1987). Expression Of Amylase Genes In Transgenic Mice. (Doctoral Dissertation). University of Michigan. Retrieved from http://hdl.handle.net/2027.42/128119

Chicago Manual of Style (16^th Edition):

Osborn, Laurelee. “Expression Of Amylase Genes In Transgenic Mice.” 1987. Doctoral Dissertation, University of Michigan. Accessed January 18, 2021. http://hdl.handle.net/2027.42/128119.

MLA Handbook (7^th Edition):

Osborn, Laurelee. “Expression Of Amylase Genes In Transgenic Mice.” 1987. Web. 18 Jan 2021.

Vancouver:

Osborn L. Expression Of Amylase Genes In Transgenic Mice. [Internet] [Doctoral dissertation]. University of Michigan; 1987. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/2027.42/128119.

Council of Science Editors:

Osborn L. Expression Of Amylase Genes In Transgenic Mice. [Doctoral Dissertation]. University of Michigan; 1987. Available from: http://hdl.handle.net/2027.42/128119

Penn State University

26. Shi, Chenxu. INVESTIGATIONS OF POLYAMINE FUNCTION USING TRANSGENIC MOUSE MODELS WITH SPERMIDINE SYNTHASE AND S-ADENOSYLMETHIONINE DECARBOXYLASE OVEREXPRESSION .

Degree: 2011, Penn State University

URL: https://submit-etda.libraries.psu.edu/catalog/12128

► Polyamines, including putrescine, spermidine, and spermine, are ubiquitous polycationic compounds that are essential for cell growth and differentiation. To better understand cellular function of polyamines,… (more)

▼ Polyamines, including putrescine, spermidine, and spermine, are ubiquitous polycationic compounds that are essential for cell growth and differentiation. To better understand cellular function of polyamines, two transgenic mouse models with either widespread constitutive overexpression of spermidine synthase (SpdS) or regulated expression of S-adenosylmethionine decarboxylase (AdoMetDC) in the skin were created and characterized. SpdS is a polyamine biosynthetic enzyme, and it transfers an aminopropyl group from decarboxylated S-adenosylmethionine (dcAdoMet) to putrescine to produce spermidine. We generated a transgenic mouse line that overexpresses human spermidine synthase from a composite cytomegalovirus- immediate early gene enhancer/chicken β-actin promoter (CAG) in order to determine the impact of elevated SpdS activity on murine development and physiology, and to enable simultaneous overexpression of SpdS and other polyamine biosynthetic enzymes by combining transgenic models. CAG-SpdS mice were viable and fertile and exhibited a reduced tissue spermine:spermidine ratio that correlated with the level of SpdS activity. We also demonstrated that the combined overexpression of both SpdS and spermine synthase (SpmS) in CAG-SpdS/CAG-SpmS bitransgenic mice did not impair murine viability or lead to overt developmental abnormalities but instead normalizes the elevated tissue spermine:spermidine ratios of CAG-SpmS mice. Finally, upon breeding of CAG-SpdS mice to MHC (α-myosin heavy chain)-AdoMetDC mice with a >100-fold increase in cardiac AdoMetDC activity, CAG-SpdS/MHC-AdoMetDC bitransgenic animals were produced at the expected frequency and exhibited cardiac polyamine levels comparable to MHC-AdoMetDC littermates. Taken together these results indicate that SpdS levels are unlikely to exert significant regulatory effects on cellular polyamine content and function. Previous studies suggest that the increased levels of polyamines, especially putrescine, play a critical role in skin tumor development. AdoMetDC is a rate-limiting enzyme in the polyamine biosynthetic pathway. It catalyzes the decarboxylation of S-adenosylmethionine (AdoMet) to generate dcAdoMet that serves as the aminopropyl donor for the production of spermidine and spermine from the precursor putrescine. We utilized the Tet-off system to generate transgenic mice with regulated expression of AdoMetDC in skin basal keratinocytes directed by the Keratin 5 promoter to enhance our understanding of the role played by AdoMetDC in controlling polyamine levels and of polyamine function in epithelial carcinogenesis. We found that untreated transgenic mice displayed a 7 to 8-fold increase in epidermal and dermal AdoMetDC activity at 7 weeks of age, and a corresponding increase in the enzymatic product dcAdoMet levels. These mice also exhibited a thin fur phenotype that could be eliminated by doxycycline treatment. A skin chemical carcinogenesis experiment on these mice demonstrated that AdoMetDC overexpression resulted in a 46% reduction in tumor… Advisors/Committee Members: David J Feith, Ph D, Dissertation Advisor/Co-Advisor, David J Feith, Committee Chair/Co-Chair, Anthony Edward Pegg, Committee Member, Lisa M Shantz, Committee Member, Edward Joseph Gunther, Committee Member, Scot R Kimball, Committee Member, Barbara Ann Miller, Committee Member.

Subjects/Keywords: Polyamines; S-adenosylmethionine decarboxylase; Spermidine synthase; Transgenic mice; Nonmelanoma skin cancer

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

APA (6^th Edition):

Shi, C. (2011). INVESTIGATIONS OF POLYAMINE FUNCTION USING TRANSGENIC MOUSE MODELS WITH SPERMIDINE SYNTHASE AND S-ADENOSYLMETHIONINE DECARBOXYLASE OVEREXPRESSION . (Thesis). Penn State University. Retrieved from https://submit-etda.libraries.psu.edu/catalog/12128

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):

Shi, Chenxu. “INVESTIGATIONS OF POLYAMINE FUNCTION USING TRANSGENIC MOUSE MODELS WITH SPERMIDINE SYNTHASE AND S-ADENOSYLMETHIONINE DECARBOXYLASE OVEREXPRESSION .” 2011. Thesis, Penn State University. Accessed January 18, 2021. https://submit-etda.libraries.psu.edu/catalog/12128.

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

MLA Handbook (7^th Edition):

Shi, Chenxu. “INVESTIGATIONS OF POLYAMINE FUNCTION USING TRANSGENIC MOUSE MODELS WITH SPERMIDINE SYNTHASE AND S-ADENOSYLMETHIONINE DECARBOXYLASE OVEREXPRESSION .” 2011. Web. 18 Jan 2021.

Vancouver:

Shi C. INVESTIGATIONS OF POLYAMINE FUNCTION USING TRANSGENIC MOUSE MODELS WITH SPERMIDINE SYNTHASE AND S-ADENOSYLMETHIONINE DECARBOXYLASE OVEREXPRESSION . [Internet] [Thesis]. Penn State University; 2011. [cited 2021 Jan 18]. Available from: https://submit-etda.libraries.psu.edu/catalog/12128.

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

Council of Science Editors:

Shi C. INVESTIGATIONS OF POLYAMINE FUNCTION USING TRANSGENIC MOUSE MODELS WITH SPERMIDINE SYNTHASE AND S-ADENOSYLMETHIONINE DECARBOXYLASE OVEREXPRESSION . [Thesis]. Penn State University; 2011. Available from: https://submit-etda.libraries.psu.edu/catalog/12128

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

Boston University

27. Lee, Rebecca Arwyn. L2PB1 cell depletion with diphtheria toxin in PD-L2 KIKO mice.

Degree: MS, Medical Sciences, 2015, Boston University

URL: http://hdl.handle.net/2144/16050

► As we learn more about immune cell subpopulations, we find an increasingly complex system of cells with diverse functions. L2pB1 cells are a PD-L2 positive… (more)

Subjects/Keywords: Immunology; B1a cells; B cells; Depletion; Diabetes; Diphtheria toxin; Transgenic mice

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

APA (6^th Edition):

Lee, R. A. (2015). L2PB1 cell depletion with diphtheria toxin in PD-L2 KIKO mice. (Masters Thesis). Boston University. Retrieved from http://hdl.handle.net/2144/16050

Chicago Manual of Style (16^th Edition):

Lee, Rebecca Arwyn. “L2PB1 cell depletion with diphtheria toxin in PD-L2 KIKO mice.” 2015. Masters Thesis, Boston University. Accessed January 18, 2021. http://hdl.handle.net/2144/16050.

MLA Handbook (7^th Edition):

Lee, Rebecca Arwyn. “L2PB1 cell depletion with diphtheria toxin in PD-L2 KIKO mice.” 2015. Web. 18 Jan 2021.

Vancouver:

Lee RA. L2PB1 cell depletion with diphtheria toxin in PD-L2 KIKO mice. [Internet] [Masters thesis]. Boston University; 2015. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/2144/16050.

Council of Science Editors:

Lee RA. L2PB1 cell depletion with diphtheria toxin in PD-L2 KIKO mice. [Masters Thesis]. Boston University; 2015. Available from: http://hdl.handle.net/2144/16050

Brigham Young University

28. Jimenez Rondan, Felix Ruben. The Biology of Claudin 6 (Cldn6) in the Developing Mouse Lung.

Degree: PhD, 2015, Brigham Young University

URL: https://scholarsarchive.byu.edu/cgi/viewcontent.cgi?article=5413&context=etd

► The tight junctions (TJ), which are located in the apical region between epithelial and endothelial cells, regulate the paracellular diffusion of ions and small molecules… (more)

▼ The tight junctions (TJ), which are located in the apical region between epithelial and endothelial cells, regulate the paracellular diffusion of ions and small molecules and play an important role in maintaining cell polarity, cell-cell integrity, and permeability. In the lung, epithelial cells are attached by TJ structures. They provide a permeable barrier and cell communication. The loss of barrier integrity, which is maintained by the expression of claudins (Cldn), results in cellular permibilization and leads to paracellular diffusion of solutes and harmful molecules. There are 27 known Cldn homologous members in mice and human. Cldn6 is mostly expressed in embryonic stem cells and associated with the programing of epithelial cells during embryo development and lung morphogenesis. In order to test the hypothesis that Cldn6 expression affects lung morphogenesis, we analyzed the expression pattern of Cldn6 during lung ontogenesis to examine cell-specific expression pattern of Cldn6 during each embryonic period in the mouse lung. Also, we assessed transcriptional regulators and control mechanisms that precisely influence Cldn6 expression in pulmonary cells. We discovered that Cldn6 is an important tight junctional component expressed by pulmonary epithelium during lung organogenesis. We found that normal down-regulation of Cldn6 as development proceeds influences differentiation associated with the transition between the embryonic to the alveolar stage. Conditional gain-of-function and loss-of-function experiments in animal models prove to be the most beneficial tool in deciphering the impact of Cldn in organ formation and maintenance. We generated a conditional transgenic mouse that provides the opportunity to genetically up-regulate Cldn6 in distal lung. Our transgenic mouse showed a delay in lung development and down-regulation of transcriptional factors. Cldn6 is both temporally and spatially controlled in the developing lung and its regulation is maintained by critical transcriptional control networks managed by TTF-1. In lung diseases, altered Cldn expression leads to diseases such as COPD, asthma, and ARDS. The tight junctional proteins are differentially regulated by tobacco smoke exposure and Cldn6 is potentially involved as neighboring epithelial cells respond to tobacco smoke. We exposed adult mice to controlled doses of second hand smoke during four days and A-549 cells to 10% CSE for 6 hours. We discovered that mice lungs respond by down-regulating Cldn6 basal levels and impair barrier function. These results reveal that midgestational up-regulation of Cldn6 and its marked down-regulation as development proceeds illustrate the notion that Cldn6 function is important during early programming stages of lung morphogenesis.

Subjects/Keywords: claudin 6; mice; transgenic; murine; lung; Cell and Developmental Biology; Physiology

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

APA (6^th Edition):

Jimenez Rondan, F. R. (2015). The Biology of Claudin 6 (Cldn6) in the Developing Mouse Lung. (Doctoral Dissertation). Brigham Young University. Retrieved from https://scholarsarchive.byu.edu/cgi/viewcontent.cgi?article=5413&context=etd

Chicago Manual of Style (16^th Edition):

Jimenez Rondan, Felix Ruben. “The Biology of Claudin 6 (Cldn6) in the Developing Mouse Lung.” 2015. Doctoral Dissertation, Brigham Young University. Accessed January 18, 2021. https://scholarsarchive.byu.edu/cgi/viewcontent.cgi?article=5413&context=etd.

MLA Handbook (7^th Edition):

Jimenez Rondan, Felix Ruben. “The Biology of Claudin 6 (Cldn6) in the Developing Mouse Lung.” 2015. Web. 18 Jan 2021.

Vancouver:

Jimenez Rondan FR. The Biology of Claudin 6 (Cldn6) in the Developing Mouse Lung. [Internet] [Doctoral dissertation]. Brigham Young University; 2015. [cited 2021 Jan 18]. Available from: https://scholarsarchive.byu.edu/cgi/viewcontent.cgi?article=5413&context=etd.

Council of Science Editors:

Jimenez Rondan FR. The Biology of Claudin 6 (Cldn6) in the Developing Mouse Lung. [Doctoral Dissertation]. Brigham Young University; 2015. Available from: https://scholarsarchive.byu.edu/cgi/viewcontent.cgi?article=5413&context=etd

NSYSU

29. Huang, Chi-Yuan. Inhibition of GDNF Signaling Reduces Tumorigenic Potential and Metastasis in Glioblastoma Multiforme.

Degree: Master, Institute of Biomedical Sciences, 2018, NSYSU

URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0710118-094036

► Glioblastoma multiforme (GBM) is the most common, deadly and aggressive brain tumor arising from glial cells. In contrast to other solid cancers, clinical trials in… (more)

Subjects/Keywords: high recurrence; Malignant tumor; transgenic mice; Glioblastoma multiforme; knockdown

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

APA (6^th Edition):

Huang, C. (2018). Inhibition of GDNF Signaling Reduces Tumorigenic Potential and Metastasis in Glioblastoma Multiforme. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0710118-094036

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):

Huang, Chi-Yuan. “Inhibition of GDNF Signaling Reduces Tumorigenic Potential and Metastasis in Glioblastoma Multiforme.” 2018. Thesis, NSYSU. Accessed January 18, 2021. http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0710118-094036.

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

MLA Handbook (7^th Edition):

Huang, Chi-Yuan. “Inhibition of GDNF Signaling Reduces Tumorigenic Potential and Metastasis in Glioblastoma Multiforme.” 2018. Web. 18 Jan 2021.

Vancouver:

Huang C. Inhibition of GDNF Signaling Reduces Tumorigenic Potential and Metastasis in Glioblastoma Multiforme. [Internet] [Thesis]. NSYSU; 2018. [cited 2021 Jan 18]. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0710118-094036.

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

Council of Science Editors:

Huang C. Inhibition of GDNF Signaling Reduces Tumorigenic Potential and Metastasis in Glioblastoma Multiforme. [Thesis]. NSYSU; 2018. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0710118-094036

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

University of Texas Southwestern Medical Center

30. Chang, Alexander S. Analysis of Circadian Rhythm Using a Novel SCN-Specific Cre Transgenic Mouse Line.

Degree: 2010, University of Texas Southwestern Medical Center

URL: http://hdl.handle.net/2152.5/247

► The neurons that make up the suprachiasmatic nucleus (SCN) temporally organize behavior into circadian cycles of activity and rest. When dissociated, these neurons individually oscillate… (more)

▼ The neurons that make up the suprachiasmatic nucleus (SCN) temporally organize behavior into circadian cycles of activity and rest. When dissociated, these neurons individually oscillate with various period, phase, and amplitude. These conflicting results can be reconciled if inter-neuronal networking in the SCN is required for a consolidated behavioral circadian rhythm. To test this hypothesis, a novel SCN-specific Cre transgenic mouse line, named NMS-Cre, was developed by inserting a bicistronic Cre expression cassette at the 3’-untranslated region of the Neuromedin S (NMS) gene. By crossing NMS-Cre line to a lox-STOP-lox diphtheria toxin receptor line, behavioral circadian rhythm was disrupted upon intraperitoneal injection of diphtheria toxin. A histological examination showed that diphtheria toxin injection eliminated ~85% of NMS-Cre containing neurons at the SCN. Next, I generated NMS-Cre mediated Bmal1 conditional knockout animals to study behavioral rhythm output when most of the SCN neurons are without a molecular oscillator. The NMS-Cre(+);Bmal1flox/flox animals have essentially normal circadian rhythm of locomotor activity. Then, I generated NMS-Cre mediated Vesicular GABA Transporter (VGAT) conditional knockout animals because GABA has long been suspected to play a role in behavioral circadian rhythm. The NMS-Cre;VGATflox/flox animals performed normally in behavioral circadian rhythm parameter such as free-running period, robustness, and phase response curve. These in vivo data demonstrated a model that intra-SCN neuronal network is required for behavioral circadian rhythm, and can be a conduit that mediates molecular clock outputs from a small number of SCN neurons. Despite the fact that virtually all SCN neurons are GABAergic, GABA is an unlikely transmitter for this intra-SCN networking. Finally, NMS knockout animals have a well-consolidated behavioral circadian rhythm. However, when subjected to photic phase advancement, NMS knockout animals shifted their activity onset time quicker than wild type control animals. In situ hybridization results ruled out that an altered response to light stimuli or dampened molecular clock oscillation in the SCN as the cause for the rapid phase shift. NMS knockout animals switching from constant illumination to constant dark environment are unable to return to the typical less than twenty-four hour free-running period. Therefore, NMS is involved in a circadian pacemaker function. Advisors/Committee Members: Yanagisawa, Masashi.

Subjects/Keywords: Circadian Rhythm; Neuropeptides; Mice, Transgenic

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

APA (6^th Edition):

Chang, A. S. (2010). Analysis of Circadian Rhythm Using a Novel SCN-Specific Cre Transgenic Mouse Line. (Thesis). University of Texas Southwestern Medical Center. Retrieved from http://hdl.handle.net/2152.5/247

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):

Chang, Alexander S. “Analysis of Circadian Rhythm Using a Novel SCN-Specific Cre Transgenic Mouse Line.” 2010. Thesis, University of Texas Southwestern Medical Center. Accessed January 18, 2021. http://hdl.handle.net/2152.5/247.

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

MLA Handbook (7^th Edition):

Chang, Alexander S. “Analysis of Circadian Rhythm Using a Novel SCN-Specific Cre Transgenic Mouse Line.” 2010. Web. 18 Jan 2021.

Vancouver:

Chang AS. Analysis of Circadian Rhythm Using a Novel SCN-Specific Cre Transgenic Mouse Line. [Internet] [Thesis]. University of Texas Southwestern Medical Center; 2010. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/2152.5/247.

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

Council of Science Editors:

Chang AS. Analysis of Circadian Rhythm Using a Novel SCN-Specific Cre Transgenic Mouse Line. [Thesis]. University of Texas Southwestern Medical Center; 2010. Available from: http://hdl.handle.net/2152.5/247

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

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Open Access Theses and Dissertations