subject:(Mice Inbred C57BL)

1. Navarro, Claudia Daniele Carvalho, 1987-. Desequilíbrio redox devido à perda da transidrogenase-NAD(P) mitocondrial agrava doença hepática gordurosa induzida por dieta hiperlipídica em camundongos = Redox imbalance due to the loss of mitochondrial NAD(P)-transhydrogenase aggravates high fat diet-induced fatty liver disease in mice: Redox imbalance due to the loss of mitochondrial NAD(P)-transhydrogenase aggravates high fat diet-induced fatty liver disease in mice.

Degree: 2017, Universidade Estadual de Campinas

URL: http://repositorio.unicamp.br/jspui/handle/REPOSIP/331764

► Abstract: The mechanisms by which a high fat diet (HFD) promotes nonalcoholic fatty liver disease (NAFLD) appear to involve liver mitochondrial dysfunctions and redox imbalance.… (more)

▼ Abstract: The mechanisms by which a high fat diet (HFD) promotes nonalcoholic fatty liver disease (NAFLD) appear to involve liver mitochondrial dysfunctions and redox imbalance. We hypothesized that a HFD would increase mitochondrial reliance on NAD(P)-transhydrogenase (NNT) as the source of NADPH for antioxidant systems that counteract NAFLD development. Therefore, we studied HFD-induced liver mitochondrial dysfunctions and NAFLD in C57Unib.B6 congenic mice with (Nnt+/+) or without (Nnt-/-) NNT activity; the spontaneously mutated allele (Nnt-/-) was inherited from the C57BL/6J mouse substrain. After 20 weeks on a HFD, Nnt-/- mice exhibited a higher prevalence of steatohepatitis and content of liver triglycerides compared to Nnt+/+ mice on an identical diet. Under a HFD, the aggravated NAFLD phenotype in the Nnt-/- mice was accompanied by an increased H2O2 release rate from mitochondria, decreased aconitase activity (a redox-sensitive mitochondrial enzyme) and higher susceptibility to Ca2+-induced mitochondrial permeability transition. In addition, HFD led to the phosphorylation (inhibition) of pyruvate dehydrogenase (PDH) and markedly reduced the ability of liver mitochondria to remove peroxide in Nnt-/- mice. Reactivation of PDH in the presence of ADP or dichloroacetate (pharmacological activation) restored the peroxide removal capability of mitochondria from Nnt-/- mice on a HFD. Noteworthy, compared to mice that were chow-fed, the HFD did not impair peroxide removal nor elicit redox imbalance in mitochondria from Nnt+/+ mice. Therefore, HFD interacted with Nnt mutation to generate PDH inhibition and further suppression of peroxide removal. We conclude that NNT plays a critical role in counteracting mitochondrial redox imbalance, PDH inhibition and advancement of NAFLD in mice fed a HFD. The present study provide seminal experimental evidence that redox imbalance in liver mitochondria potentiates the progression from simple steatosis to steatohepatitis following a HFD Advisors/Committee Members: UNIVERSIDADE ESTADUAL DE CAMPINAS (CRUESP), Vercesi, Anibal Eugenio, 1946- (advisor), Castilho, Roger Frigério, 1972- (coadvisor), Universidade Estadual de Campinas. Faculdade de Ciências Médicas (institution), Programa de Pós-Graduação em Fisiopatologia Médica (nameofprogram), Sposito, Andrei Carvalho (committee member), Mori, Marcelo Alves (committee member), Filho, Antonio Galina (committee member), Cunha, Fernanda Marques da (committee member).

Subjects/Keywords: Fígado gorduroso; Camundongos endogâmicos C57BL; Fatty liver; Mice, Inbred C57BL

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APA (6^th Edition):

Navarro, Claudia Daniele Carvalho, 1. (2017). Desequilíbrio redox devido à perda da transidrogenase-NAD(P) mitocondrial agrava doença hepática gordurosa induzida por dieta hiperlipídica em camundongos = Redox imbalance due to the loss of mitochondrial NAD(P)-transhydrogenase aggravates high fat diet-induced fatty liver disease in mice: Redox imbalance due to the loss of mitochondrial NAD(P)-transhydrogenase aggravates high fat diet-induced fatty liver disease in mice. (Thesis). Universidade Estadual de Campinas. Retrieved from http://repositorio.unicamp.br/jspui/handle/REPOSIP/331764

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):

Navarro, Claudia Daniele Carvalho, 1987-. “Desequilíbrio redox devido à perda da transidrogenase-NAD(P) mitocondrial agrava doença hepática gordurosa induzida por dieta hiperlipídica em camundongos = Redox imbalance due to the loss of mitochondrial NAD(P)-transhydrogenase aggravates high fat diet-induced fatty liver disease in mice: Redox imbalance due to the loss of mitochondrial NAD(P)-transhydrogenase aggravates high fat diet-induced fatty liver disease in mice.” 2017. Thesis, Universidade Estadual de Campinas. Accessed March 07, 2021. http://repositorio.unicamp.br/jspui/handle/REPOSIP/331764.

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

MLA Handbook (7^th Edition):

Navarro, Claudia Daniele Carvalho, 1987-. “Desequilíbrio redox devido à perda da transidrogenase-NAD(P) mitocondrial agrava doença hepática gordurosa induzida por dieta hiperlipídica em camundongos = Redox imbalance due to the loss of mitochondrial NAD(P)-transhydrogenase aggravates high fat diet-induced fatty liver disease in mice: Redox imbalance due to the loss of mitochondrial NAD(P)-transhydrogenase aggravates high fat diet-induced fatty liver disease in mice.” 2017. Web. 07 Mar 2021.

Vancouver:

Navarro, Claudia Daniele Carvalho 1. Desequilíbrio redox devido à perda da transidrogenase-NAD(P) mitocondrial agrava doença hepática gordurosa induzida por dieta hiperlipídica em camundongos = Redox imbalance due to the loss of mitochondrial NAD(P)-transhydrogenase aggravates high fat diet-induced fatty liver disease in mice: Redox imbalance due to the loss of mitochondrial NAD(P)-transhydrogenase aggravates high fat diet-induced fatty liver disease in mice. [Internet] [Thesis]. Universidade Estadual de Campinas; 2017. [cited 2021 Mar 07]. Available from: http://repositorio.unicamp.br/jspui/handle/REPOSIP/331764.

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

Council of Science Editors:

Navarro, Claudia Daniele Carvalho 1. Desequilíbrio redox devido à perda da transidrogenase-NAD(P) mitocondrial agrava doença hepática gordurosa induzida por dieta hiperlipídica em camundongos = Redox imbalance due to the loss of mitochondrial NAD(P)-transhydrogenase aggravates high fat diet-induced fatty liver disease in mice: Redox imbalance due to the loss of mitochondrial NAD(P)-transhydrogenase aggravates high fat diet-induced fatty liver disease in mice. [Thesis]. Universidade Estadual de Campinas; 2017. Available from: http://repositorio.unicamp.br/jspui/handle/REPOSIP/331764

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

Florida Atlantic University

2. Cinalli Jr., David A. INVESTIGATING THE NEURAL CIRCUITRY SUPPORTING OBJECT RECOGNITION MEMORY IN C57BL/6J MICE.

Degree: 2020, Florida Atlantic University

URL: http://fau.digital.flvc.org/islandora/object/fau:44404

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The hippocampus, a brain region that is part of the limbic system in the medial temporal lobe, is critical to episodic memory, or the memory… (more)

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The hippocampus, a brain region that is part of the limbic system in the medial temporal lobe, is critical to episodic memory, or the memory of autobiographical events. The hippocampus plays an important role in the consolidation of information from short-term memory into more permanent long-term memory and spatial memory which enables navigation. Hippocampal damage in humans has been linked to memory loss, such as in Alzheimer’s disease and other dementias, as well as in amnesia such as in the case of patient H.M. The role of the hippocampus has been well characterized in humans but is less understood in rodents due to contradictory findings. While rodents have served well as model organisms in developing our understanding of the cognitive map that is critical for spatial navigation, there has been substantial contention over the degree to which the rodent hippocampus supports non-spatial memory, specifically the memory for items or objects previously encountered. The overall objective of this research is to gain a better understanding of how neuronal circuits involving the hippocampus and perirhinal cortex function to support object memory in the brain. Chemogenetic technologies such as DREADDs (designer receptor exclusively activated by designer drugs) have proven to be effective tools in remote manipulation of neuronal activity. First, a series of behavioral tasks was used to validate the effects of DREADD inactivation in the CA1 region of dorsal hippocampus in C57BL/6J male mice. DREADD inhibition resulted in significant impairment in the spontaneous object recognition (SOR) task and of spatial memory in the Morris water maze. In conjunction, mice were implanted with bilateral perirhinal cortex guide cannulae to allow for temporary muscimol inactivation during distinct time points in the SOR task to further investigate the nature of its relationship with the hippocampus. The results reveal an unexpected role for the perirhinal cortex in the retrieval of strong object memory. Finally, Arc mRNA expression was quantified in CA1 of dorsal hippocampus and perirhinal cortex following both weak and strong object memory formation. The results indicate that the perirhinal cortex and hippocampus have distinct, yet complementary roles in object recognition memory and that distinction is gated by memory strength. Understanding the neural mechanisms supporting the weak-strong object memory distinction in mice is an important step not only in validating mice as a suitable model system to study episodic memory in humans, but also in developing treatments and understanding the underlying causes of diseases affecting long-term memory such as Alzheimer’s disease.

2020

Degree granted: Dissertation (Ph.D.) – Florida Atlantic University, 2020.

Collection: FAU

Advisors/Committee Members: Stackman, Jr., Robert W. (Thesis advisor), Florida Atlantic University (Degree grantor), Department of Psychology, Charles E. Schmidt College of Science.

Subjects/Keywords: Neural circuitry; Hippocampus; Perirhinal Cortex; Memory; Mice, Inbred C57BL

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

APA (6^th Edition):

Cinalli Jr., D. A. (2020). INVESTIGATING THE NEURAL CIRCUITRY SUPPORTING OBJECT RECOGNITION MEMORY IN C57BL/6J MICE. (Thesis). Florida Atlantic University. Retrieved from http://fau.digital.flvc.org/islandora/object/fau:44404

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):

Cinalli Jr., David A. “INVESTIGATING THE NEURAL CIRCUITRY SUPPORTING OBJECT RECOGNITION MEMORY IN C57BL/6J MICE.” 2020. Thesis, Florida Atlantic University. Accessed March 07, 2021. http://fau.digital.flvc.org/islandora/object/fau:44404.

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

MLA Handbook (7^th Edition):

Cinalli Jr., David A. “INVESTIGATING THE NEURAL CIRCUITRY SUPPORTING OBJECT RECOGNITION MEMORY IN C57BL/6J MICE.” 2020. Web. 07 Mar 2021.

Vancouver:

Cinalli Jr. DA. INVESTIGATING THE NEURAL CIRCUITRY SUPPORTING OBJECT RECOGNITION MEMORY IN C57BL/6J MICE. [Internet] [Thesis]. Florida Atlantic University; 2020. [cited 2021 Mar 07]. Available from: http://fau.digital.flvc.org/islandora/object/fau:44404.

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

Council of Science Editors:

Cinalli Jr. DA. INVESTIGATING THE NEURAL CIRCUITRY SUPPORTING OBJECT RECOGNITION MEMORY IN C57BL/6J MICE. [Thesis]. Florida Atlantic University; 2020. Available from: http://fau.digital.flvc.org/islandora/object/fau:44404

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

3. Kelly, Michele A. Characterization of the dopamine D2 receptor deficient mouse and the effects of background strain.

Degree: PhD, 1997, Oregon Health Sciences University

URL: doi:10.6083/M4HQ3X58 ; http://digitalcommons.ohsu.edu/etd/2612

Subjects/Keywords: Receptors, Dopamine D2; Mice, Inbred Strains; Mice, Inbred C57BL; Prolactin; Locomotion

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

APA (6^th Edition):

Kelly, M. A. (1997). Characterization of the dopamine D2 receptor deficient mouse and the effects of background strain. (Doctoral Dissertation). Oregon Health Sciences University. Retrieved from doi:10.6083/M4HQ3X58 ; http://digitalcommons.ohsu.edu/etd/2612

Chicago Manual of Style (16^th Edition):

Kelly, Michele A. “Characterization of the dopamine D2 receptor deficient mouse and the effects of background strain.” 1997. Doctoral Dissertation, Oregon Health Sciences University. Accessed March 07, 2021. doi:10.6083/M4HQ3X58 ; http://digitalcommons.ohsu.edu/etd/2612.

MLA Handbook (7^th Edition):

Kelly, Michele A. “Characterization of the dopamine D2 receptor deficient mouse and the effects of background strain.” 1997. Web. 07 Mar 2021.

Vancouver:

Kelly MA. Characterization of the dopamine D2 receptor deficient mouse and the effects of background strain. [Internet] [Doctoral dissertation]. Oregon Health Sciences University; 1997. [cited 2021 Mar 07]. Available from: doi:10.6083/M4HQ3X58 ; http://digitalcommons.ohsu.edu/etd/2612.

Council of Science Editors:

Kelly MA. Characterization of the dopamine D2 receptor deficient mouse and the effects of background strain. [Doctoral Dissertation]. Oregon Health Sciences University; 1997. Available from: doi:10.6083/M4HQ3X58 ; http://digitalcommons.ohsu.edu/etd/2612

4. Finnell, Richard H. The fetal hydantoin syndrome : an animal model :.

Degree: PhD, 1980, Oregon Health Sciences University

URL: doi:10.6083/M48W3BH8 ; http://digitalcommons.ohsu.edu/etd/2281

Subjects/Keywords: Disease Models, Animal; Epilepsy – embryology; Epilepsy – genetics; Hydantoins – adverse effects; Mice, Inbred C3H; Mice, Inbred C57BL; Mice, Quaking; Phenytoin – adverse effects

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

APA (6^th Edition):

Finnell, R. H. (1980). The fetal hydantoin syndrome : an animal model :. (Doctoral Dissertation). Oregon Health Sciences University. Retrieved from doi:10.6083/M48W3BH8 ; http://digitalcommons.ohsu.edu/etd/2281

Chicago Manual of Style (16^th Edition):

Finnell, Richard H. “The fetal hydantoin syndrome : an animal model :.” 1980. Doctoral Dissertation, Oregon Health Sciences University. Accessed March 07, 2021. doi:10.6083/M48W3BH8 ; http://digitalcommons.ohsu.edu/etd/2281.

MLA Handbook (7^th Edition):

Finnell, Richard H. “The fetal hydantoin syndrome : an animal model :.” 1980. Web. 07 Mar 2021.

Vancouver:

Finnell RH. The fetal hydantoin syndrome : an animal model :. [Internet] [Doctoral dissertation]. Oregon Health Sciences University; 1980. [cited 2021 Mar 07]. Available from: doi:10.6083/M48W3BH8 ; http://digitalcommons.ohsu.edu/etd/2281.

Council of Science Editors:

Finnell RH. The fetal hydantoin syndrome : an animal model :. [Doctoral Dissertation]. Oregon Health Sciences University; 1980. Available from: doi:10.6083/M48W3BH8 ; http://digitalcommons.ohsu.edu/etd/2281

5. Hefeneider, Steven Henry. Cytofluorometric evaluation of the antigen binding cell response to tumor associated antigens in the mouse.

Degree: PhD, 1981, Oregon Health Sciences University

URL: doi:10.6083/M4XK8CQ2 ; http://digitalcommons.ohsu.edu/etd/2276

Subjects/Keywords: Antigens, Neoplasm; B-Lymphocytes; T-Lymphocytes; Macrophages; Melanoma; Mice, Inbred C57BL; Receptors, Antigen

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

APA (6^th Edition):

Hefeneider, S. H. (1981). Cytofluorometric evaluation of the antigen binding cell response to tumor associated antigens in the mouse. (Doctoral Dissertation). Oregon Health Sciences University. Retrieved from doi:10.6083/M4XK8CQ2 ; http://digitalcommons.ohsu.edu/etd/2276

Chicago Manual of Style (16^th Edition):

Hefeneider, Steven Henry. “Cytofluorometric evaluation of the antigen binding cell response to tumor associated antigens in the mouse.” 1981. Doctoral Dissertation, Oregon Health Sciences University. Accessed March 07, 2021. doi:10.6083/M4XK8CQ2 ; http://digitalcommons.ohsu.edu/etd/2276.

MLA Handbook (7^th Edition):

Hefeneider, Steven Henry. “Cytofluorometric evaluation of the antigen binding cell response to tumor associated antigens in the mouse.” 1981. Web. 07 Mar 2021.

Vancouver:

Hefeneider SH. Cytofluorometric evaluation of the antigen binding cell response to tumor associated antigens in the mouse. [Internet] [Doctoral dissertation]. Oregon Health Sciences University; 1981. [cited 2021 Mar 07]. Available from: doi:10.6083/M4XK8CQ2 ; http://digitalcommons.ohsu.edu/etd/2276.

Council of Science Editors:

Hefeneider SH. Cytofluorometric evaluation of the antigen binding cell response to tumor associated antigens in the mouse. [Doctoral Dissertation]. Oregon Health Sciences University; 1981. Available from: doi:10.6083/M4XK8CQ2 ; http://digitalcommons.ohsu.edu/etd/2276

6. Lessov, Christina Nikolov. Behavioral assessment of common determinants of drug and ethanol-induced sensitization and the role of ethanol-induced sensitization in voluntary ethanol drinking and ethanol-induced conditioned taste aversion.

Degree: PhD, 2000, Oregon Health Sciences University

URL: doi:10.6083/M4X928MF ; http://digitalcommons.ohsu.edu/etd/3322

Subjects/Keywords: Alcohol Drinking; Behavior, Animal; Drug Tolerance; Receptors, Dopamine D2; Mice, Inbred C57BL

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

APA (6^th Edition):

Lessov, C. N. (2000). Behavioral assessment of common determinants of drug and ethanol-induced sensitization and the role of ethanol-induced sensitization in voluntary ethanol drinking and ethanol-induced conditioned taste aversion. (Doctoral Dissertation). Oregon Health Sciences University. Retrieved from doi:10.6083/M4X928MF ; http://digitalcommons.ohsu.edu/etd/3322

Chicago Manual of Style (16^th Edition):

Lessov, Christina Nikolov. “Behavioral assessment of common determinants of drug and ethanol-induced sensitization and the role of ethanol-induced sensitization in voluntary ethanol drinking and ethanol-induced conditioned taste aversion.” 2000. Doctoral Dissertation, Oregon Health Sciences University. Accessed March 07, 2021. doi:10.6083/M4X928MF ; http://digitalcommons.ohsu.edu/etd/3322.

MLA Handbook (7^th Edition):

Lessov, Christina Nikolov. “Behavioral assessment of common determinants of drug and ethanol-induced sensitization and the role of ethanol-induced sensitization in voluntary ethanol drinking and ethanol-induced conditioned taste aversion.” 2000. Web. 07 Mar 2021.

Vancouver:

Lessov CN. Behavioral assessment of common determinants of drug and ethanol-induced sensitization and the role of ethanol-induced sensitization in voluntary ethanol drinking and ethanol-induced conditioned taste aversion. [Internet] [Doctoral dissertation]. Oregon Health Sciences University; 2000. [cited 2021 Mar 07]. Available from: doi:10.6083/M4X928MF ; http://digitalcommons.ohsu.edu/etd/3322.

Council of Science Editors:

Lessov CN. Behavioral assessment of common determinants of drug and ethanol-induced sensitization and the role of ethanol-induced sensitization in voluntary ethanol drinking and ethanol-induced conditioned taste aversion. [Doctoral Dissertation]. Oregon Health Sciences University; 2000. Available from: doi:10.6083/M4X928MF ; http://digitalcommons.ohsu.edu/etd/3322

Universidade do Estado do Rio de Janeiro

7. Leonardo de Souza Mendonça. Alteração do tecido adiposo e fígado em modelo experimental de síndrome metabólica: ação de agonista PPAR-gama e bloqueador de receptor AT1 da angiotensina 2.

Degree: PhD, 2013, Universidade do Estado do Rio de Janeiro

URL: http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=5116 ;

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Este trabalho teve como objetivo investigar os efeitos da telmisartana (agonista PPAR-gama parcial), losartana (puro bloqueador do receptor AT1 da angiotensina II) e rosiglitazona (agonista… (more)

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Este trabalho teve como objetivo investigar os efeitos da telmisartana (agonista PPAR-gama parcial), losartana (puro bloqueador do receptor AT1 da angiotensina II) e rosiglitazona (agonista PPAR-gama) em modelo experimental de síndrome metabólica. Os alvos do estudo foram a pressão arterial, metabolismo de carboidratos, resistência insulínica, inflamação, tecido adiposo e fígado. Camundongos C57BL/6 (a partir de 3 meses de idade) foram alimentados com dieta padrão (SC, n = 10) ou dieta hiperlipídica rica em sal (HFHS, n = 40) por 12 semanas. Após esse tempo, os animais do grupo HFHS foram subdivididos em 4 grupos (n = 10): HFHS (sem tratamento), ROSI (HFHS tratado com rosiglitazona), TELM (HFHS tratado com telmisartana) e LOS (HFHS tratado com losartana) por 5 semanas. O grupo HFHS apresentou um significante ganho de peso e aumento da pressão arterial sistólica, hiperinsulinemia com resistência insulínica, hiperleptinemia, hipertrofia de adipócitos bem como um quadro de esteatose hepática e níveis aumentados da citocina inflamatória interleucina-6 (IL-6). Os animais tratados com telmisartana chegou ao final do experimento com massa corporal similar ao grupo SC, com reversão do quadro de resistência insulínica, com pressão arterial normal, adipócitos de tamanho normal e sem apresentar esteatose hepática. Além disso, o tratamento com telmisartana aumentou a expressão de PPARγ e adiponectina no tecido adiposo epididimal. A expressão da proteína desacopladora-1 (UCP-1) no tecido adiposo branco (TAB) também foi aumentada. O tratamento com losartana diminuiu a pressão arterial para valores normais, porém com menores efeitos nos parâmetros metabólicos dos animais. O presente modelo experimental de ganho de peso e hipertensão induzidos por dieta mimetiza a síndrome metabólica humana. Neste modelo, a telmisartana aumentou a expressão de UCP-1 no TAB, preveniu o ganho de peso e melhorou a sensibilidade à insulina e a esteatose hepática dos camundongos C57BL/6, provavelmente devido à ativação PPAR-gama.

The study aimed to investigate the effects of telmisartan (a partial PPAR gamma agonist), losartan (a pure angiotensin II receptor blocker) and rosiglitazone (PPAR gamma agonist) in a mice model of metabolic syndrome (MetS). The targets of this study were blood pressure (BP), carbohydrate metabolism, insulin resistance, inflammation, white adipose tissue (WAT) and liver. Male C57BL/6 mice were studied over 17 weeks after being separated into two major groups according to diet: standard chow (SC, 10% fat, n = 10) or high-fat high-salt chow (HFHS, 60% fat, 7% salt, n = 40). In the last 5 weeks of the experiment, the HFHS group was divided into four groups (n = 10): untreated HFHS, ROSI (HFHS plus rosiglitazone), TELM (HFHS plus telmisartan), and LOS (HFHS plus losartan). The HFHS group had significantly greater body mass and BP, in addition to hyperinsulinemia with insulin resistance, hyperleptinemia, adipocyte hypertrophy and hepatic steatosis as well as increased inflammatory cytokine levels. Animals treated with…

Advisors/Committee Members: Eliete Bouskela, Egberto Gaspar de Moura, Claudio Buarque Benchimol, Eduardo Vera Tibiriçá, Carlos Alberto Mandarim-de-Lacerda.

Subjects/Keywords: Síndrome metabólica; PPAR-gama; C57BL/6; Tecido adiposo; Fígado; Síndrome metabólica Teses; Tecido adiposo Teses; Fígado Teses; PPAR-gama Agonistas; Camundongos Endogâmicos C57BL.; Metabolic syndrome; PPAR-gamma; C57BL/6; Adipose tissue; Liver; Metabolic syndrome - Theses; Adipose tissue - Theses; Liver - Theses; PPAR-gamma - Agonists; Mice, Inbred C57BL; CITOLOGIA E BIOLOGIA CELULAR

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

APA (6^th Edition):

Mendonça, L. d. S. (2013). Alteração do tecido adiposo e fígado em modelo experimental de síndrome metabólica: ação de agonista PPAR-gama e bloqueador de receptor AT1 da angiotensina 2. (Doctoral Dissertation). Universidade do Estado do Rio de Janeiro. Retrieved from http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=5116 ;

Chicago Manual of Style (16^th Edition):

Mendonça, Leonardo de Souza. “Alteração do tecido adiposo e fígado em modelo experimental de síndrome metabólica: ação de agonista PPAR-gama e bloqueador de receptor AT1 da angiotensina 2.” 2013. Doctoral Dissertation, Universidade do Estado do Rio de Janeiro. Accessed March 07, 2021. http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=5116 ;.

MLA Handbook (7^th Edition):

Mendonça, Leonardo de Souza. “Alteração do tecido adiposo e fígado em modelo experimental de síndrome metabólica: ação de agonista PPAR-gama e bloqueador de receptor AT1 da angiotensina 2.” 2013. Web. 07 Mar 2021.

Vancouver:

Mendonça LdS. Alteração do tecido adiposo e fígado em modelo experimental de síndrome metabólica: ação de agonista PPAR-gama e bloqueador de receptor AT1 da angiotensina 2. [Internet] [Doctoral dissertation]. Universidade do Estado do Rio de Janeiro; 2013. [cited 2021 Mar 07]. Available from: http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=5116 ;.

Council of Science Editors:

Mendonça LdS. Alteração do tecido adiposo e fígado em modelo experimental de síndrome metabólica: ação de agonista PPAR-gama e bloqueador de receptor AT1 da angiotensina 2. [Doctoral Dissertation]. Universidade do Estado do Rio de Janeiro; 2013. Available from: http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=5116 ;

8. Junqueira, Mara de Souza. Caracterização das vias de transformação maligna de uma nova linhagem estabelecida de melanoma murino.

Degree: Mestrado, Oncologia, 2006, University of São Paulo

URL: http://www.teses.usp.br/teses/disponiveis/5/5155/tde-20092010-183837/ ;

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Ao longo dos processos de imortalização e transformação maligna, as células adquirem inúmeras alterações genéticas, que são causadas por fatores endógenos e exógenos como agentes… (more)

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Ao longo dos processos de imortalização e transformação maligna, as células adquirem inúmeras alterações genéticas, que são causadas por fatores endógenos e exógenos como agentes biológicos e a geração de espécies reativas de oxigênio. Neste trabalho, uma linhagem celular espontaneamente transformada foi clonada a partir de explantes de embriões de camundongos C57bl/6. Esta linhagem mostrou-se produtora de pigmento escuro; a análise citoquímica e ultraestrutural permitiu caracterizar a linhagem como tendo origem melanocítica. A linhagem, denominada Mgal3, mostrou-se tumorigênica quando implantada no tecido subcutâneo de animais singenéicos, apresentando capacidade de disseminação linfática, dando origem a metástases em linfonodos, o que permitiu caracteriza-la como uma linhagem de melanoma murino. O processo de transformação deste melanoma caracterizou-se pela expressão de genes retrovirais endógenos, com expressão do antígeno associado a melanoma (MAA), reconhecido pelo anticorpo monoclonal MM2-9B6; ausência de mutações nos exons 5 a 8 do gene supressor de tumor TP53; e, silenciamento do gene CDKN2a, que codifica duas proteínas que atuam em redes de supressão de tumores, p16INK4a e p19ARF. A perda de expressão de pelo menos um destes produtos gênicos parece associada a mecanismos epigenéticos, uma vez que o tratamento de Mgal3 com o inibidor de DNA metiltransferase 5-Aza-2-deoxicitidina, restaurou a transcrição de pelo menos um dos transcritos do gene CDKN2a. Da mesma forma, observamos que o gene LGALS3, que codifica a lectina animal galectina-3 também é silenciado nesta linhagem, mostrando que esta molécula não está associada à manutenção desta célula transformada em condições de cultivo.

A novel murine melanoma cell line named Mgal3 was generated from embryo explants. This cell line gave rise to metastatic tumors when injected subcutaneously in C57bl/6 mice. Tumor histogenesis was determined at the cytochemical (Fontana Masson staining), immunohistochemical (staining with anti-HMB45 and anti-S100) and ultrastructural levels. Mgal3 produces high amounts of retroviral C particles and was recognized by the mAb MM2-9B6, which reacts with a melanoma associated antigen derived from the envelope of the ecotropic retrovirus MelArv. No mutations were found in TP53 exons 5-8, however loss of CDKN2a expression was observed. Treatment of Mgal3 with the demethylating agent azadeoxycytidine indicated that at least one of the genes encoded at the CDKN2a locus was silenced by promoter hypermethylation. Furthermore, this cell line did not express the animal lectin, galectin-3. The galectin-3 gene promoter seemed to be hypermethylated, since treatment of Mgal3 with azadeoxycytidine led to the de novo expression of the lectin.

Advisors/Committee Members: Chammas, Roger.

Subjects/Keywords: Camundongos endogâmicos C57BL; Endogenous retroviruses; Inbred C57BL mice; Melanoma; Melanoma; p14ARF protein; Protein p16; Proteína P14ARF; Proteína P16 5; Retrovírus endógenos

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

APA (6^th Edition):

Junqueira, M. d. S. (2006). Caracterização das vias de transformação maligna de uma nova linhagem estabelecida de melanoma murino. (Masters Thesis). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/5/5155/tde-20092010-183837/ ;

Chicago Manual of Style (16^th Edition):

Junqueira, Mara de Souza. “Caracterização das vias de transformação maligna de uma nova linhagem estabelecida de melanoma murino.” 2006. Masters Thesis, University of São Paulo. Accessed March 07, 2021. http://www.teses.usp.br/teses/disponiveis/5/5155/tde-20092010-183837/ ;.

MLA Handbook (7^th Edition):

Junqueira, Mara de Souza. “Caracterização das vias de transformação maligna de uma nova linhagem estabelecida de melanoma murino.” 2006. Web. 07 Mar 2021.

Vancouver:

Junqueira MdS. Caracterização das vias de transformação maligna de uma nova linhagem estabelecida de melanoma murino. [Internet] [Masters thesis]. University of São Paulo; 2006. [cited 2021 Mar 07]. Available from: http://www.teses.usp.br/teses/disponiveis/5/5155/tde-20092010-183837/ ;.

Council of Science Editors:

Junqueira MdS. Caracterização das vias de transformação maligna de uma nova linhagem estabelecida de melanoma murino. [Masters Thesis]. University of São Paulo; 2006. Available from: http://www.teses.usp.br/teses/disponiveis/5/5155/tde-20092010-183837/ ;

9. Catani, João Paulo Portela. Terapia gênica do câncer associando reparo da via p53 à imunoestimulação por IFNbeta.

Degree: PhD, Oncologia, 2014, University of São Paulo

URL: http://www.teses.usp.br/teses/disponiveis/5/5155/tde-26112014-100519/ ;

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Os avanços científicos das últimas décadas permitiram que a compreensão do câncer evoluísse de uma visão simplista, na qual o principal motor seria uma atividade… (more)

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Os avanços científicos das últimas décadas permitiram que a compreensão do câncer evoluísse de uma visão simplista, na qual o principal motor seria uma atividade celular hiperploriferativa, para uma visão mais complexa onde o estado fisiológico geral permite a gênese e progressão tumoral. Essa evolução permite o desenvolvimento de novas abordagens terapêuticas e traz novas esperanças para o tratamento de muitos tipos de cânceres ainda extremamente deletérios. Dentro desse novo panorama, terapias que estimulem a imunidade antitumoral têm se mostrado extremamente promissoras. Nesse trabalho, procuramos investigar os efeitos antitumorais desencadeados pela combinação da indução de morte celular e imunoestimulação. Para tanto, visamos à recuperação da via de p53 (pela transferência gênica do próprio p53 ou p19) associada à transferência gênica de IFNbeta. A transferência gênica foi mediada por vetores adenovirais do sorotipo 5. Nossas observações, em um modelo murino de carcinoma pulmonar, permitem concluir que esta linhagem é sensível a morte induzida pela transferência gênica de p19 e não p53. Porém, a transferência gênica intratumoral de IFNbeta se mostrou chave no controle do crescimento do tumor primário. Destacamos, entretanto, que a associação de IFNbeta com p19 produziu efeitos imunoprotetores superiores à transferência de IFNbeta ou p19 sozinhos. Tal efeito parece ser dependente da indução de fatores quimiotáxicos e conseqüente recrutamento de neutrófilos para o sítio tumoral. O efeito da transferência gênica combinada de ambos os genes IFNbeta e p19 se mostrou ainda mais promissor quando associado à cisplatina, induzindo uma notável redução no crescimento tumoral

Scientific advances from the last decades enabled the evolution of our knowledge of cancer from a simplistic vision, in which the main motor was an excessive cell proliferation, to a more complex one, where the general physiologic state enables tumorigenesis and tumor progression. This evolution enabled the development of new therapies and brings new hopes for the treatment of several types of cancers. In this context, therapies that induce an antitumor immunity are very promising. In this work, we are investigating the antitumor effects triggered by the combination of cell death induction and immunostimulation. To this end, we aimed to restore p53 pathway (by p53 or p19 gene transfer) associated with immunostimulation by IFNbeta gene transfer. The gene transfer was mediated by Adenovectors Serotype 5. Our observations in a murine model of lung cancer showed that this cell line is sensitive to cell death induced by p19 gene transfer, but not p53. Nevertheless, intratumoral gene transfer of IFNbeta, was crucial in controlling tumor growth. Moreover, p19 and IFNbeta association induced higher immunoprotecting effects than p19 or IFNbeta alone. This effect seems to be depending on the induction of chemotactic factors, and the recruitment of neutrophils to the tumor site. The effect of combined gene transfer of p19 and IFNbeta was even more promising…

Advisors/Committee Members: Strauss, Bryan Eric.

Subjects/Keywords: Camundongos endogâmicos C57BL; Gene therapy; Immunotherapy; Imunoterapia; Inhibitor p16 quinase ciclin-dependent; Inibidor p16 quinase ciclinadependente; Inteferon beta; Interferon beta 3; Mice inbred C57BL; Neoplasias pulmonares; Proteína supressora de tumor p53; Pulmonary neoplasms; Terapia genética; Tumor suppressor protein p53

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

APA (6^th Edition):

Catani, J. P. P. (2014). Terapia gênica do câncer associando reparo da via p53 à imunoestimulação por IFNbeta. (Doctoral Dissertation). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/5/5155/tde-26112014-100519/ ;

Chicago Manual of Style (16^th Edition):

Catani, João Paulo Portela. “Terapia gênica do câncer associando reparo da via p53 à imunoestimulação por IFNbeta.” 2014. Doctoral Dissertation, University of São Paulo. Accessed March 07, 2021. http://www.teses.usp.br/teses/disponiveis/5/5155/tde-26112014-100519/ ;.

MLA Handbook (7^th Edition):

Catani, João Paulo Portela. “Terapia gênica do câncer associando reparo da via p53 à imunoestimulação por IFNbeta.” 2014. Web. 07 Mar 2021.

Vancouver:

Catani JPP. Terapia gênica do câncer associando reparo da via p53 à imunoestimulação por IFNbeta. [Internet] [Doctoral dissertation]. University of São Paulo; 2014. [cited 2021 Mar 07]. Available from: http://www.teses.usp.br/teses/disponiveis/5/5155/tde-26112014-100519/ ;.

Council of Science Editors:

Catani JPP. Terapia gênica do câncer associando reparo da via p53 à imunoestimulação por IFNbeta. [Doctoral Dissertation]. University of São Paulo; 2014. Available from: http://www.teses.usp.br/teses/disponiveis/5/5155/tde-26112014-100519/ ;

10. Medrano, Ruan Felipe Vieira. Investigação da resposta imunológica antitumoral induzida por células B16F10 tratadas pela combinação p19Arf e interferon-beta em um modelo de vacinação profilático para melanoma murino.

Degree: Mestrado, Oncologia, 2013, University of São Paulo

URL: http://www.teses.usp.br/teses/disponiveis/5/5155/tde-28052013-110728/ ;

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Dados recentes do nosso laboratório demonstram que somente a co-transdução, não a tradução individual, com vetores adenovirais portadores de Interferon-beta (IFN?) (citocina imuno modulatória) e… (more)

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Dados recentes do nosso laboratório demonstram que somente a co-transdução, não a tradução individual, com vetores adenovirais portadores de Interferon-beta (IFN?) (citocina imuno modulatória) e p19Arf (parceira funcional da proteína supressora de tumor p53) resulta na morte celular massiva do melanoma murino B16F10. A capacidade desse tratamento combinado de induzir uma resposta imune antitumoral ainda não foi avaliada. Dessa maneira, o objetivo do presente trabalho foi investigar se células B16F0 tratadas por essa combinação são capazes de induzir uma resposta imune antitumoral em um modelo de vacinação profilático de melanoma. Para isso, essas células foram co-transduzidas com os vetores AdPGp19 e AdPGIFN? e 48 horas depois, inoculadas como agente vacinal no flanco esquerdo (sítio da vacina) de camundongos C57BL/6 imunocompetentes. Sete dias após a última vacinação, esses animais foram desafiados com células B16F10 naïve no flanco direito (sítio do desafio). A progressão tumoral do desafio foi significativamente reduzida, mesmo quando o desafio tumoral foi feito 73 dias após da vacinação. Porém, como os animais imunizados desenvolveram tumores no sítio da vacina, condições para o uso dessas células tratadas foram avaliadas, revelando que: o número de células e de aplicações usadas durante a vacinação tem influência no aparecimento desse tumores, e que apenas com o tratamento combinado os camundongos permanecem livres de tumor. A influência do sistema imune para este resultado foi revelada após protocolo de imunussupressão. Em seguida, o papel da p19Arf e do IFN? na proteção antitumoral da combinação foi estudado. In vitro, os efeitos antitumorais da combinação parecem ser mais influentes da reposição de p19Arf do que da expressão de IFN?, mas já in vivo, na presença do sistema imune, foram mais dependentes do IFN?. Com a combinação estes efeitos mostraram-se mais pronunciados, induzindo uma proteção antitumoral e maior sobrevida aos animais vacinados. Estes resultados indicam que a combinação p19Arf e IFN? pode ser aplicada como um agente imunoterápico e sugerem que a associação entre morte celular e imuno estimulação pode beneficiar o tratamento contra o câncer

Previously, we have shown in a mouse melanoma model of in situ gene therapy that co-transduction, but not individual application, with adenovirus vectors expressing the Interferon-beta (IFN?) (immune modulatory cytokine) and p19Arf (functional partner of the p53 tumor suppressor) transgenes results in massive cell death and reduced tumor progression. However, the capability of this combined treatment to stimulate an antitumor immune response has not been evaluated. Therefore, the aim of this work was to investigate, trough a prophylactic vaccine model, if B16F10 cells treated by the p19Arf and IFN? combination could induce such immune response. To do so, these cells were co-transduced by the AdPGp19 e AdPGIFN? adenoviral vectors and 48 hours after, inoculated as a vaccine agent in the left flank (vaccine site) of immune competent C57BL/6 mice. Seven…

Advisors/Committee Members: Strauss, Bryan Eric.

Subjects/Keywords: Camundongos endogâmicos C57BL; Cancer vaccines; Cell death; Experimental melanoma; Interferon tipo I; Interferon type I; Melanoma experimental; Mice inbred C57BL; Morte celular; Neoplasias; Neoplasms; Proteína supressora de tumor p53; Tumor supressor protein p53; Vacinas anticâncer

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

APA (6^th Edition):

Medrano, R. F. V. (2013). Investigação da resposta imunológica antitumoral induzida por células B16F10 tratadas pela combinação p19Arf e interferon-beta em um modelo de vacinação profilático para melanoma murino. (Masters Thesis). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/5/5155/tde-28052013-110728/ ;

Chicago Manual of Style (16^th Edition):

Medrano, Ruan Felipe Vieira. “Investigação da resposta imunológica antitumoral induzida por células B16F10 tratadas pela combinação p19Arf e interferon-beta em um modelo de vacinação profilático para melanoma murino.” 2013. Masters Thesis, University of São Paulo. Accessed March 07, 2021. http://www.teses.usp.br/teses/disponiveis/5/5155/tde-28052013-110728/ ;.

MLA Handbook (7^th Edition):

Medrano, Ruan Felipe Vieira. “Investigação da resposta imunológica antitumoral induzida por células B16F10 tratadas pela combinação p19Arf e interferon-beta em um modelo de vacinação profilático para melanoma murino.” 2013. Web. 07 Mar 2021.

Vancouver:

Medrano RFV. Investigação da resposta imunológica antitumoral induzida por células B16F10 tratadas pela combinação p19Arf e interferon-beta em um modelo de vacinação profilático para melanoma murino. [Internet] [Masters thesis]. University of São Paulo; 2013. [cited 2021 Mar 07]. Available from: http://www.teses.usp.br/teses/disponiveis/5/5155/tde-28052013-110728/ ;.

Council of Science Editors:

Medrano RFV. Investigação da resposta imunológica antitumoral induzida por células B16F10 tratadas pela combinação p19Arf e interferon-beta em um modelo de vacinação profilático para melanoma murino. [Masters Thesis]. University of São Paulo; 2013. Available from: http://www.teses.usp.br/teses/disponiveis/5/5155/tde-28052013-110728/ ;

11. Braux, Julien. Influence d'un phosphate de calcium substitué en strontium sur la physiologie de l'ostéoblaste humain en culture et évaluation de son potentiel de réparation osseusse chez la souris : Strontium substituted calcium phosphate influence on human osteoblasts physiology and evaluation of his potential bone healing capability on a mouse model.

Degree: Docteur es, Sciences biologiques, 2011, Reims

URL: http://www.theses.fr/2011REIM0201

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Les phosphates de calcium sont des biomatériaux couramment utilisés dans de nombreuses spécialités médicales. L'amélioration de ces biomatériaux vise à augmenter leur ostéointégration et leur… (more)

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Les phosphates de calcium sont des biomatériaux couramment utilisés dans de nombreuses spécialités médicales. L'amélioration de ces biomatériaux vise à augmenter leur ostéointégration et leur bioactivité. Le strontium possédant d'intéressantes capacités de modification de la physiologie osseuse, l'incorporation de ce dernier au sein de phosphates de calcium par substitution ionique pourrait permettre un déplacement de la balance osseuse vers la formation osseuse.Notre travail a permis de démontrer la capacité des particules de phosphates de calcium substitués en strontium à augmenter la prolifération des ostéoblastes en culture et à modifier l'expression et la synthèse des principales protéines impliquées dans la physiologie osseuse (Collagène de type I, Serpine H1, métalloprotéinases matricielles 1 et 2, inhibiteurs tissulaires des MMPs). Par ailleurs, la poudre de phosphates de calcium ne contenant pas de strontium a entrainé une sécrétion accrue de chimiokines pro-inflammatoires (MCP-1 et GRO-?) qui n'a pas été observée pour la poudre substituée. Enfin, des études in-vivo réalisées dans un modèle de défaut osseux murin a permis de démontrer une plus grande résorbabilité de la poudre contenant du strontium et sa plus grande capacité à stimuler la réparation osseuse.

Calcium phosphate are widely used in medicine. Their upgrade tend to enhance their biocompatibility and their bioactivity. Strontium has interesting capability to modify the bone physiologie. Its incorporation in calcium phosphates could lead to modify the bone balance toward osteogenesis.The present work reveal the capacities of such biomaterials to enhance the replication of osteoblasts ant to modify the expression and the synthesis of proteins implicated in the bone balance (type I collagen, serpinH1, Matrix metalloproteinases 1 and 2, tissular inhibitors of MMPs). Moreover, non substituted calcium phosphate powders enhance the expression and synthesis of inflammatory cytokines (MCP-1 and Gro-a). This fact was not observed with the non substituted powder. In-vivo studies on a mouse model permit us to demonstrate the higher resorbability and the higher bone healing capability of the substituted powder.

Advisors/Committee Members: Laurent-Maquin, Dominique (thesis director), Laquerriere, Patrice (thesis director).

Subjects/Keywords: Os et tissu osseux; Metalloproteases; Souris de lignée C57BL; Collagène de type1; Strontium; Ostéoblastes; Phosphate de sodium; Matrix metalloproteinases; Test ELISA; Chimiokine CXCL1; Bone and bones; Metalloproteases; Mice, inbred c57bl; Collagen type I; Strontium; Osteoblasts; Sodium phosphate; Matrix metalloproteinases; Enzyme-Linked immunosorbent assay; Chemokine cxcl1

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

APA (6^th Edition):

Braux, J. (2011). Influence d'un phosphate de calcium substitué en strontium sur la physiologie de l'ostéoblaste humain en culture et évaluation de son potentiel de réparation osseusse chez la souris : Strontium substituted calcium phosphate influence on human osteoblasts physiology and evaluation of his potential bone healing capability on a mouse model. (Doctoral Dissertation). Reims. Retrieved from http://www.theses.fr/2011REIM0201

Chicago Manual of Style (16^th Edition):

Braux, Julien. “Influence d'un phosphate de calcium substitué en strontium sur la physiologie de l'ostéoblaste humain en culture et évaluation de son potentiel de réparation osseusse chez la souris : Strontium substituted calcium phosphate influence on human osteoblasts physiology and evaluation of his potential bone healing capability on a mouse model.” 2011. Doctoral Dissertation, Reims. Accessed March 07, 2021. http://www.theses.fr/2011REIM0201.

MLA Handbook (7^th Edition):

Braux, Julien. “Influence d'un phosphate de calcium substitué en strontium sur la physiologie de l'ostéoblaste humain en culture et évaluation de son potentiel de réparation osseusse chez la souris : Strontium substituted calcium phosphate influence on human osteoblasts physiology and evaluation of his potential bone healing capability on a mouse model.” 2011. Web. 07 Mar 2021.

Vancouver:

Braux J. Influence d'un phosphate de calcium substitué en strontium sur la physiologie de l'ostéoblaste humain en culture et évaluation de son potentiel de réparation osseusse chez la souris : Strontium substituted calcium phosphate influence on human osteoblasts physiology and evaluation of his potential bone healing capability on a mouse model. [Internet] [Doctoral dissertation]. Reims; 2011. [cited 2021 Mar 07]. Available from: http://www.theses.fr/2011REIM0201.

Council of Science Editors:

Braux J. Influence d'un phosphate de calcium substitué en strontium sur la physiologie de l'ostéoblaste humain en culture et évaluation de son potentiel de réparation osseusse chez la souris : Strontium substituted calcium phosphate influence on human osteoblasts physiology and evaluation of his potential bone healing capability on a mouse model. [Doctoral Dissertation]. Reims; 2011. Available from: http://www.theses.fr/2011REIM0201

12. Eom, Tae-Yeon. Regulation of neural precursor cell apoptosis and proliferation by glycogen synthase kinase-3.

Degree: PhD, 2009, University of Alabama – Birmingham

URL: http://contentdm.mhsl.uab.edu/u?/etd,390

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Neurogenesis is a crucial process for development, plasticity, and regenerative capacity of the developing and adult brain. Impairment of neurogenesis has been implicated in the… (more)

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Neurogenesis is a crucial process for development, plasticity, and regenerative capacity of the developing and adult brain. Impairment of neurogenesis has been implicated in the etiology of psychiatric disorders. Although substantial studies have shown that therapeutic interventions enhance neurogenesis, much less is known about what factors impair neurogenesis. Thus, the present work examined if glycogen synthase kinase-3 (GSK3) has a role in impaired neurogenesis, focusing on apoptosis and proliferation of neural precursor cells (NPCs). This investigation found that GSK3 promotes apoptotic signaling in cultured NPCs subjected to two insults, trophic factor withdrawal and genotoxic stress. Both stimuli activated GSK3, Bax, and caspase-3. Pharmacological inhibition of GSK3 activity reduced Bax and caspase-3 activation in both bax+/+ and bax-/- NPCs. GSK3[beta] interacted with p53 after DNA damage in NPCs. This study also investigated the role of hyperactive GSK3 on NPC proliferation in the adult hippocampus using homozygous S21A/S9A-GSK3[alpha]/[beta] knockin mice. In vivo measurements of BrdU positive cells showed a drastic 40 % impairment of proliferation in GSK3 knockin mice. Impaired neurogenesis observed in vivo was not due to direct effects of hyperactive GSK3 in NPCs because proliferation in vitro was equivalent in NPCs from both GSK3 knockin and wild-type mice, suggesting in vivo deficiency in GSK3 knockin mice of an external promoter of NPC proliferation. Measurements of two neurotrophins demonstrated less vascular endothelial growth factor, but not brain-derived neurotrophic factor, in the hippocampus of GSK3 knockin mice than wild-type mice, suggesting insufficient support molecules in vivo in GSK3 knockin mice impairs neurogenesis. Chronic administration of lithium and fluoxetine, which increase inhibitory serine-phosphorylation of wild-type GSK3, increased NPC proliferation in wild-type, but not GSK3 knockin, mice. Overall, this study reveals that GSK3 may be a crucial modulator of apoptosis and proliferation of NPCs. NPCs are sensitive to loss of trophic factors and genotoxic stress, and GSK3 inhibitors are capable of enhancing NPC survival. Blocked inhibitory control of GSK3 impairs NPC proliferation in the adult hippocampus and the capacity of therapeutic drugs to stimulate neurogenesis, likely through deficient environmental factors that support neurogenesis, which may contribute to psychiatric diseases and responses to therapeutic drugs.

vii, 126 p. : ill., digital, PDF file

Cell Biology

Joint Health Sciences

GSK3 Neural Precursor Cell Apoptosis Proliferation Neurogenesis P53

UNRESTRICTED

Advisors/Committee Members: Jope, Richard S., Bijur, Gautam Johnson, Gail V.W. Roth, Kevin A. Serra, Rosa.

Subjects/Keywords: Apoptosis<; br>; Glycogen Synthase Kinase 3 – metabolism<; br>; Mice, Inbred C57BL<; br>; Mice, Knockout<; br>; Mice, Transgenic<; br>; Neurons – cytology<; br>; Phosphorylation

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

APA (6^th Edition):

Eom, T. (2009). Regulation of neural precursor cell apoptosis and proliferation by glycogen synthase kinase-3. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,390

Chicago Manual of Style (16^th Edition):

Eom, Tae-Yeon. “Regulation of neural precursor cell apoptosis and proliferation by glycogen synthase kinase-3.” 2009. Doctoral Dissertation, University of Alabama – Birmingham. Accessed March 07, 2021. http://contentdm.mhsl.uab.edu/u?/etd,390.

MLA Handbook (7^th Edition):

Eom, Tae-Yeon. “Regulation of neural precursor cell apoptosis and proliferation by glycogen synthase kinase-3.” 2009. Web. 07 Mar 2021.

Vancouver:

Eom T. Regulation of neural precursor cell apoptosis and proliferation by glycogen synthase kinase-3. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2009. [cited 2021 Mar 07]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,390.

Council of Science Editors:

Eom T. Regulation of neural precursor cell apoptosis and proliferation by glycogen synthase kinase-3. [Doctoral Dissertation]. University of Alabama – Birmingham; 2009. Available from: http://contentdm.mhsl.uab.edu/u?/etd,390

13. Takara, Kenyo; Maruo, Naoki; Oka, Kyoko; Kaji, Chiaki; Hatakeyama, Yuji; Sawa, Naruhiko; Kato, Yukinari; Yamashita, Junro; Kojima, Hiroshi. Morphological study of tooth development in podoplanin-deficient mice. : Morphological study of tooth development in podoplanin-deficient mice.

Degree: 博士（歯学）, 2018, Fukuoka Dental College / 福岡歯科大学

URL: http://id.nii.ac.jp/1167/00000066/

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Podoplanin is a mucin-type highly O-glycosylated glycoprotein identified in several somatyic cells: podocytes, alveolar epithelial cells, lymphatic endothelial cells, lymph node stromal fibroblastic reticular cells,… (more)

Subjects/Keywords: ポドプラニン; 川本法; コンディショナルノックアウトマウス; Wnt1; 歯; Animals; Bone and Bones; Cells, Cultured; Dentin; Gene Knockout Techniques; Genes, Reporter; Kidney; Membrane Glycoproteins; Mice; Mice, Inbred C57BL; Mice, Knockout; Mice, Transgenic; Neural Crest; Odontogenesis; Organ Specificity; Podocytes; Respiratory System; Stress, Mechanical; Tooth Germ; Transgenes; podoplanin; Kawamoto's film method; conditional knockout mice; Wnt1; tooth

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

APA (6^th Edition):

Takara, Kenyo; Maruo, Naoki; Oka, Kyoko; Kaji, Chiaki; Hatakeyama, Yuji; Sawa, Naruhiko; Kato, Yukinari; Yamashita, Junro; Kojima, H. (2018). Morphological study of tooth development in podoplanin-deficient mice. : Morphological study of tooth development in podoplanin-deficient mice. (Thesis). Fukuoka Dental College / 福岡歯科大学. Retrieved from http://id.nii.ac.jp/1167/00000066/

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):

Takara, Kenyo; Maruo, Naoki; Oka, Kyoko; Kaji, Chiaki; Hatakeyama, Yuji; Sawa, Naruhiko; Kato, Yukinari; Yamashita, Junro; Kojima, Hiroshi. “Morphological study of tooth development in podoplanin-deficient mice. : Morphological study of tooth development in podoplanin-deficient mice.” 2018. Thesis, Fukuoka Dental College / 福岡歯科大学. Accessed March 07, 2021. http://id.nii.ac.jp/1167/00000066/.

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

MLA Handbook (7^th Edition):

Takara, Kenyo; Maruo, Naoki; Oka, Kyoko; Kaji, Chiaki; Hatakeyama, Yuji; Sawa, Naruhiko; Kato, Yukinari; Yamashita, Junro; Kojima, Hiroshi. “Morphological study of tooth development in podoplanin-deficient mice. : Morphological study of tooth development in podoplanin-deficient mice.” 2018. Web. 07 Mar 2021.

Vancouver:

Takara, Kenyo; Maruo, Naoki; Oka, Kyoko; Kaji, Chiaki; Hatakeyama, Yuji; Sawa, Naruhiko; Kato, Yukinari; Yamashita, Junro; Kojima H. Morphological study of tooth development in podoplanin-deficient mice. : Morphological study of tooth development in podoplanin-deficient mice. [Internet] [Thesis]. Fukuoka Dental College / 福岡歯科大学; 2018. [cited 2021 Mar 07]. Available from: http://id.nii.ac.jp/1167/00000066/.

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

Council of Science Editors:

Takara, Kenyo; Maruo, Naoki; Oka, Kyoko; Kaji, Chiaki; Hatakeyama, Yuji; Sawa, Naruhiko; Kato, Yukinari; Yamashita, Junro; Kojima H. Morphological study of tooth development in podoplanin-deficient mice. : Morphological study of tooth development in podoplanin-deficient mice. [Thesis]. Fukuoka Dental College / 福岡歯科大学; 2018. Available from: http://id.nii.ac.jp/1167/00000066/

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

14. Dhaher, Ronnie. Determining the role of the extended amygdala in regulating alcohol consumption in C57BL/6J mice.

Degree: PhD, 2007, Oregon Health Sciences University

URL: doi:10.6083/M44747TN ; http://digitalcommons.ohsu.edu/etd/324

Subjects/Keywords: Extended amygdala; C57BL/6J mice; Ethanol consumption; Ethanol dependence; Amygdala; Mice, Inbred Strains; Alcohol Drinking; Alcoholism; Medicine

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

APA (6^th Edition):

Dhaher, R. (2007). Determining the role of the extended amygdala in regulating alcohol consumption in C57BL/6J mice. (Doctoral Dissertation). Oregon Health Sciences University. Retrieved from doi:10.6083/M44747TN ; http://digitalcommons.ohsu.edu/etd/324

Chicago Manual of Style (16^th Edition):

Dhaher, Ronnie. “Determining the role of the extended amygdala in regulating alcohol consumption in C57BL/6J mice.” 2007. Doctoral Dissertation, Oregon Health Sciences University. Accessed March 07, 2021. doi:10.6083/M44747TN ; http://digitalcommons.ohsu.edu/etd/324.

MLA Handbook (7^th Edition):

Dhaher, Ronnie. “Determining the role of the extended amygdala in regulating alcohol consumption in C57BL/6J mice.” 2007. Web. 07 Mar 2021.

Vancouver:

Dhaher R. Determining the role of the extended amygdala in regulating alcohol consumption in C57BL/6J mice. [Internet] [Doctoral dissertation]. Oregon Health Sciences University; 2007. [cited 2021 Mar 07]. Available from: doi:10.6083/M44747TN ; http://digitalcommons.ohsu.edu/etd/324.

Council of Science Editors:

Dhaher R. Determining the role of the extended amygdala in regulating alcohol consumption in C57BL/6J mice. [Doctoral Dissertation]. Oregon Health Sciences University; 2007. Available from: doi:10.6083/M44747TN ; http://digitalcommons.ohsu.edu/etd/324

15. Luz, Carolina Portela. Preparação, caracterização e utilização dos radiofármacos (18F)FAZA e [[99mc] (O)HL91] para detecção de hipóxia em cultura de células e em tumores em modelo animal.

Degree: Mestrado, Oncologia, 2013, University of São Paulo

URL: http://www.teses.usp.br/teses/disponiveis/5/5155/tde-22012014-144309/ ;

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Hipóxia é definida como a baixa teor de oxigênio. Nos tumores a principal causa da hipóxia é a isquemia, que ocorre em função do rápido… (more)

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Hipóxia é definida como a baixa teor de oxigênio. Nos tumores a principal causa da hipóxia é a isquemia, que ocorre em função do rápido crescimento da massa tumoral e diminuição ou obstrução dos vasos sanguíneos que irrigam o interior dos tumores. Como a hipóxia é uma das causas do aumento da resistência à radioterapia de radiação e algumas formas de quimioterapia, a identificação de tumores com regiões de hipóxia é de elevada relevância e a utilização de radiofármacos tem sido muito promissora, por ser um método não invasivo e que podem mapear diferentes alterações fisiológicas associadas à hipóxia. Neste trabalho sintetizamos o ligante [[99mTc](O)2HL91], com rendimento final de síntese de 82,6% e preparamos o respectivo complexo de tecnécio, com eficiência de marcação maior que 97 %; também foi preparado o radiofármaco (18F)FAZA, com eficiência de marcação de 17,9% e pureza radioquímica, após purificação, maior que 86 %. Estudos de captação em células de melanoma murino B16F10, apresentaram taxa de captação de 0,73%, em condições de normóxia e de 8,5 % em condições de hipóxia para o [[99mTc](O)2HL91] , sobe as mesmas condições, de 0,73% e 0,98%, para o (18F)FAZA, respectivamente. Estudos de biodistribuição ex vivo mostraram taxa de captação em tumores da ordem de 4,3% para o [[99mTc](O)2HL91] e de 0,56% para o (18F)FAZA, a relação tumor/sangue foi de 2,6% e 2,5%, respectivamente. Para ambos os rins são a principal via de excreção. Análise, por autorradiografia, de cortes dos tumores mostraram claramente a concentração do [[99mTc](O)2HL91] em regiões de hipóxia/necrose. Imagem da distribuição dos radiofármacos em camundongos C57/Bl6, com tumores de células B16F10, utilizando sistema hibrido PET/SPECT/CT dedicado a pequenos animais, mostraram que a concentração do [[99mTc](O)2HL91] permitiu visualizar captação difusa em regiões do tumor, o mesmo foi observado para o (18F)FAZA, mas em uma taxa menor. Em conclusão, os resultados obtidos apresentam as possibilidades de preparação e utilização de dois radiofármacos, o [[99mTc](O)2HL91] e o (18F)FAZA, como agentes marcadores para hipóxia, utilizando as técnicas de SPECT e PET para imagem. Todavia, novos estudos deverão ser realizados para determinação da especificidade desses radiofármacos em diferentes linhagens tumorais

Hypoxia is a deficiency of oxygen in the cell. In tumors the primary cause of hypoxia is ischemia, which occurs due to the rapid growth of the tumor mass and reduction or blockage of the blood vessels decreasing nutrients and oxygen supply in more internal regions of the tumors. Once hypoxia is one cause of the increased resistance to radiation therapy and some forms of chemotherapy, their identification in tumors is highly relevant and use of radiopharmaceuticals has been very promising, because it is a noninvasive and can map different physiological changes associated with hypoxia. In this work, we synthesized the ligand [[99mTc](O)2HL91] given a final synthesis yield of 82.6% and prepared their technetium complex with the labeling efficiency…

Advisors/Committee Members: Buchpiguel, Carlos Alberto.

Subjects/Keywords: Anoxia/diagnosis; Anóxia/diagnóstico; Camundongos endogâmicos C57BL; Compostos radiofarmacêuticos; Fluorine radioisotops; Melanoma experimental; Melanoma experimental; Mice inbred C57BL; Neoplasias; Neoplasms; Positron-emission tomography and computed tomography; Radioisótopos de flúor; Radiopharcaceuticals; Technetium/diagnostic use; Tecnécio/uso diagnóstico; Tomografia computadorizada de emissão de fóton único; Tomografia por emissão de pósitrons e tomografia computadorizada; Tomography emission computed single photon

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

APA (6^th Edition):

Luz, C. P. (2013). Preparação, caracterização e utilização dos radiofármacos (18F)FAZA e [[99mc] (O)HL91] para detecção de hipóxia em cultura de células e em tumores em modelo animal. (Masters Thesis). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/5/5155/tde-22012014-144309/ ;

Chicago Manual of Style (16^th Edition):

Luz, Carolina Portela. “Preparação, caracterização e utilização dos radiofármacos (18F)FAZA e [[99mc] (O)HL91] para detecção de hipóxia em cultura de células e em tumores em modelo animal.” 2013. Masters Thesis, University of São Paulo. Accessed March 07, 2021. http://www.teses.usp.br/teses/disponiveis/5/5155/tde-22012014-144309/ ;.

MLA Handbook (7^th Edition):

Luz, Carolina Portela. “Preparação, caracterização e utilização dos radiofármacos (18F)FAZA e [[99mc] (O)HL91] para detecção de hipóxia em cultura de células e em tumores em modelo animal.” 2013. Web. 07 Mar 2021.

Vancouver:

Luz CP. Preparação, caracterização e utilização dos radiofármacos (18F)FAZA e [[99mc] (O)HL91] para detecção de hipóxia em cultura de células e em tumores em modelo animal. [Internet] [Masters thesis]. University of São Paulo; 2013. [cited 2021 Mar 07]. Available from: http://www.teses.usp.br/teses/disponiveis/5/5155/tde-22012014-144309/ ;.

Council of Science Editors:

Luz CP. Preparação, caracterização e utilização dos radiofármacos (18F)FAZA e [[99mc] (O)HL91] para detecção de hipóxia em cultura de células e em tumores em modelo animal. [Masters Thesis]. University of São Paulo; 2013. Available from: http://www.teses.usp.br/teses/disponiveis/5/5155/tde-22012014-144309/ ;

16. Evangelista, Monick Junho do Amaral. Avaliação de radiofármacos com [[99mTc]glucarato] e (18F)FAZA na determinação de hipóxia em células e tumores de melanoma murino B16F10.

Degree: Mestrado, Oncologia, 2013, University of São Paulo

URL: http://www.teses.usp.br/teses/disponiveis/5/5155/tde-05022014-115549/ ;

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A baixa oxigenação (hipóxia) altera drasticamente o metabolismo celular e a forma de produção de ATP, que em tumores pode estimular e permitir que as… (more)

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A baixa oxigenação (hipóxia) altera drasticamente o metabolismo celular e a forma de produção de ATP, que em tumores pode estimular e permitir que as células desenvolvam mecanismos de escape, adaptação e resistência, contribuindo não só para um comportamento maligno e agressivo, mas também lhes conferindo resistência a tratamentos quimioterapêuticos e radioterapêuticos. A detecção de regiões de hipóxia em tumores pode ser realizada com diferentes radiofármacos. Neste trabalho preparamos e avaliamos o comportamento dos radiofármacos (18F)FAZA e [[99mTc]glucarato]- em células de melanoma murino B16F10, correlacionando dados bioquímicos e histopatológicos com a captação celular dos radiofármacos in vitro e com imagens em equipamento PET/SPECT/CT obtidas de camundongos C57Bl6 implantados com tumores. O (18F)FAZA foi obtido em rendimento de 17,9 % e pureza radioquímica de 86,72 %, enquanto que o rendimento e pureza radioquímica do [[99mTc]glucarato]- foi superior a 95 %, sendo que este complexo se liga à proteínas plasmáticas com taxa de aproximadamente 40 % e o complexo é desestabilizados pela mesmas, após 4 horas de incubação a 37 °C. O complexo também não é estável na presença de cisteína e histidina. A captação in vitro do [[99mTc]glucarato]- nas células foi da ordem de 0,1 % independente da condição e do tempo, enquanto que a captação de (18F)FAZA atingiu 0,9 % sob hipóxia e 0,2 % sob normóxia, nos primeiros 15 minutos de estudo. A biodistribuição ex vivo em camundongos apresentou taxa de captação por grama de tumor e razão tumor/sangue da ordem de 0,04 % e 1,49 para o [[99mTc]glucarato]- e de 0,34 % e 1,39 para o (18F)FAZA, em tempo de 1 hora. Imagem obtidas de camundongos, mostraram intensa captação da (18F)FDG no tumor, e tanto (18F)FAZA quanto [[99mTc]glucarato]- foram capazes de evidenciar regiões de hipóxia ou necrose, respectivamente, nos tumores, ainda que com baixa taxa de captação. Imagens autorradiográficas do [[99mTc]glucarato]- nos tumores excisados dos animais apresentaram distribuição homogênea no tumor, com algumas áreas de captação sugeridas como necróticas; tomando a autorradiografia como referência, o [[99mTc]glucarato]- não se concentrou na córtex renal, região reconhecidamente hipóxica. Assim, (18F)FAZA e [[99mTc]glucarato]- puderam ser preparados em nosso laboratório com qualidade suficiente para uso em pesquisa e demonstram potencial para utilização em novos estudos visando a detecção de regiões de hipóxia ou necrose, respectivamente

The low oxygen concentration, also named hypoxia, drastically alters cellular metabolism and the production form of ATP which, in tumors, can stimulate and allow cells to develop mechanisms for escape, adaptation and resistance, contributing not only to malignant and aggressive behavior, but also their conferring resistance to chemotherapeutic and radiotherapeutic treatments. The detection of regions of hypoxia in tumors can be performed using different radiopharmaceuticals. In this work we prepared and evaluated the behavior of radiopharmaceuticals (18F)FAZA…

Advisors/Committee Members: Buchpiguel, Carlos Alberto.

Subjects/Keywords: Ácido glucárico; B16 melanoma; Camundongos endogâmicos C57BL; Cell hypoxia; Compostos radiofarmacêuticos; Fluorine radioisotopes; Glucaric acid; Hipóxia celular; Melanoma B16; Mice inbred C57BL; Neoplasias; Neoplasms; Positron-emission tomography and computed tomography; Radioisotopos de flúor; Radiopharcaceuticals; Technetium 99m; Tecnécio/uso diagnóstico; Tomografia computadorizada de emissão de fóton único; Tomografia por emissão de pósitrons e tomografia computadorizada; Tomography emission-computed single-photon

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

APA (6^th Edition):

Evangelista, M. J. d. A. (2013). Avaliação de radiofármacos com [[99mTc]glucarato] e (18F)FAZA na determinação de hipóxia em células e tumores de melanoma murino B16F10. (Masters Thesis). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/5/5155/tde-05022014-115549/ ;

Chicago Manual of Style (16^th Edition):

Evangelista, Monick Junho do Amaral. “Avaliação de radiofármacos com [[99mTc]glucarato] e (18F)FAZA na determinação de hipóxia em células e tumores de melanoma murino B16F10.” 2013. Masters Thesis, University of São Paulo. Accessed March 07, 2021. http://www.teses.usp.br/teses/disponiveis/5/5155/tde-05022014-115549/ ;.

MLA Handbook (7^th Edition):

Evangelista, Monick Junho do Amaral. “Avaliação de radiofármacos com [[99mTc]glucarato] e (18F)FAZA na determinação de hipóxia em células e tumores de melanoma murino B16F10.” 2013. Web. 07 Mar 2021.

Vancouver:

Evangelista MJdA. Avaliação de radiofármacos com [[99mTc]glucarato] e (18F)FAZA na determinação de hipóxia em células e tumores de melanoma murino B16F10. [Internet] [Masters thesis]. University of São Paulo; 2013. [cited 2021 Mar 07]. Available from: http://www.teses.usp.br/teses/disponiveis/5/5155/tde-05022014-115549/ ;.

Council of Science Editors:

Evangelista MJdA. Avaliação de radiofármacos com [[99mTc]glucarato] e (18F)FAZA na determinação de hipóxia em células e tumores de melanoma murino B16F10. [Masters Thesis]. University of São Paulo; 2013. Available from: http://www.teses.usp.br/teses/disponiveis/5/5155/tde-05022014-115549/ ;

17. Tsutsumi, Takashi; Kajiya, Hiroshi; Goto, Kazuko; Takahashi, Yutaka. Hyperocclusion up-regulates CCL3 expression in CCL2- and CCR2-deficient mice. : Hyperocclusion up-regulates CCL3 expression in CCL2- and CCR2-deficient mice.

Degree: 博士（歯学）, 2014, Fukuoka Dental College / 福岡歯科大学

URL: http://id.nii.ac.jp/1167/00000016/

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Excessive mechanical stress (MS) during hyperocclusion is known to result in disappearance of the alveolar hard line, enlargement of the periodontal ligament (PDL) space, and… (more)

Subjects/Keywords: traumatic dental occlusion; mechanical stress; bone resorption; Acid Phosphatase; Alveolar Bone Loss; Alveolar Process; Animals; Biomechanical Phenomena; Cell Culture Techniques; Chemokine CCL2; Chemokine CCL3; Chemokine CCL5; Dental Occlusion, Traumatic; Isoenzymes; Malocclusion; Mice; Mice, Inbred C57BL; Mice, Knockout; Osteoclasts; Periodontal Ligament; Receptors, CCR1; Receptors, CCR2; Signal Transduction; Stress, Mechanical; Time Factors; Up-Regulation

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

APA (6^th Edition):

Tsutsumi, Takashi; Kajiya, Hiroshi; Goto, Kazuko; Takahashi, Y. (2014). Hyperocclusion up-regulates CCL3 expression in CCL2- and CCR2-deficient mice. : Hyperocclusion up-regulates CCL3 expression in CCL2- and CCR2-deficient mice. (Thesis). Fukuoka Dental College / 福岡歯科大学. Retrieved from http://id.nii.ac.jp/1167/00000016/

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):

Tsutsumi, Takashi; Kajiya, Hiroshi; Goto, Kazuko; Takahashi, Yutaka. “Hyperocclusion up-regulates CCL3 expression in CCL2- and CCR2-deficient mice. : Hyperocclusion up-regulates CCL3 expression in CCL2- and CCR2-deficient mice.” 2014. Thesis, Fukuoka Dental College / 福岡歯科大学. Accessed March 07, 2021. http://id.nii.ac.jp/1167/00000016/.

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

MLA Handbook (7^th Edition):

Tsutsumi, Takashi; Kajiya, Hiroshi; Goto, Kazuko; Takahashi, Yutaka. “Hyperocclusion up-regulates CCL3 expression in CCL2- and CCR2-deficient mice. : Hyperocclusion up-regulates CCL3 expression in CCL2- and CCR2-deficient mice.” 2014. Web. 07 Mar 2021.

Vancouver:

Tsutsumi, Takashi; Kajiya, Hiroshi; Goto, Kazuko; Takahashi Y. Hyperocclusion up-regulates CCL3 expression in CCL2- and CCR2-deficient mice. : Hyperocclusion up-regulates CCL3 expression in CCL2- and CCR2-deficient mice. [Internet] [Thesis]. Fukuoka Dental College / 福岡歯科大学; 2014. [cited 2021 Mar 07]. Available from: http://id.nii.ac.jp/1167/00000016/.

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

Council of Science Editors:

Tsutsumi, Takashi; Kajiya, Hiroshi; Goto, Kazuko; Takahashi Y. Hyperocclusion up-regulates CCL3 expression in CCL2- and CCR2-deficient mice. : Hyperocclusion up-regulates CCL3 expression in CCL2- and CCR2-deficient mice. [Thesis]. Fukuoka Dental College / 福岡歯科大学; 2014. Available from: http://id.nii.ac.jp/1167/00000016/

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

18. Wadsworth, Teri L. The effects of plant derived antioxidants on LPS-induced production of tumor necrosis factor alpha and nitric oxide.

Degree: PhD, 2001, Oregon Health Sciences University

URL: doi:10.6083/M4542KW6 ; http://digitalcommons.ohsu.edu/etd/3266

Subjects/Keywords: Antioxidants; Nitric Oxide Synthase; Tumor Necrosis Factor-alpha; Lipopolysaccharides; Mice, Inbred C57BL; Ginkgo biloba

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

APA (6^th Edition):

Wadsworth, T. L. (2001). The effects of plant derived antioxidants on LPS-induced production of tumor necrosis factor alpha and nitric oxide. (Doctoral Dissertation). Oregon Health Sciences University. Retrieved from doi:10.6083/M4542KW6 ; http://digitalcommons.ohsu.edu/etd/3266

Chicago Manual of Style (16^th Edition):

Wadsworth, Teri L. “The effects of plant derived antioxidants on LPS-induced production of tumor necrosis factor alpha and nitric oxide.” 2001. Doctoral Dissertation, Oregon Health Sciences University. Accessed March 07, 2021. doi:10.6083/M4542KW6 ; http://digitalcommons.ohsu.edu/etd/3266.

MLA Handbook (7^th Edition):

Wadsworth, Teri L. “The effects of plant derived antioxidants on LPS-induced production of tumor necrosis factor alpha and nitric oxide.” 2001. Web. 07 Mar 2021.

Vancouver:

Wadsworth TL. The effects of plant derived antioxidants on LPS-induced production of tumor necrosis factor alpha and nitric oxide. [Internet] [Doctoral dissertation]. Oregon Health Sciences University; 2001. [cited 2021 Mar 07]. Available from: doi:10.6083/M4542KW6 ; http://digitalcommons.ohsu.edu/etd/3266.

Council of Science Editors:

Wadsworth TL. The effects of plant derived antioxidants on LPS-induced production of tumor necrosis factor alpha and nitric oxide. [Doctoral Dissertation]. Oregon Health Sciences University; 2001. Available from: doi:10.6083/M4542KW6 ; http://digitalcommons.ohsu.edu/etd/3266

19. Dinulescu, Daniela M. Role of mahogany in melanocortin signaling.

Degree: PhD, 2000, Oregon Health Sciences University

URL: doi:10.6083/M4Z60MCZ ; http://digitalcommons.ohsu.edu/etd/3314

Subjects/Keywords: Receptors, Corticotropin; Obesity – genetics; Hyperphagia – genetics; Basal Metabolism; Motor Activity; Mice, Inbred C57BL; Proteins

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

APA (6^th Edition):

Dinulescu, D. M. (2000). Role of mahogany in melanocortin signaling. (Doctoral Dissertation). Oregon Health Sciences University. Retrieved from doi:10.6083/M4Z60MCZ ; http://digitalcommons.ohsu.edu/etd/3314

Chicago Manual of Style (16^th Edition):

Dinulescu, Daniela M. “Role of mahogany in melanocortin signaling.” 2000. Doctoral Dissertation, Oregon Health Sciences University. Accessed March 07, 2021. doi:10.6083/M4Z60MCZ ; http://digitalcommons.ohsu.edu/etd/3314.

MLA Handbook (7^th Edition):

Dinulescu, Daniela M. “Role of mahogany in melanocortin signaling.” 2000. Web. 07 Mar 2021.

Vancouver:

Dinulescu DM. Role of mahogany in melanocortin signaling. [Internet] [Doctoral dissertation]. Oregon Health Sciences University; 2000. [cited 2021 Mar 07]. Available from: doi:10.6083/M4Z60MCZ ; http://digitalcommons.ohsu.edu/etd/3314.

Council of Science Editors:

Dinulescu DM. Role of mahogany in melanocortin signaling. [Doctoral Dissertation]. Oregon Health Sciences University; 2000. Available from: doi:10.6083/M4Z60MCZ ; http://digitalcommons.ohsu.edu/etd/3314

20. Heldwein, Kurt A. Molecular characterization of the type 2 corticotropin-releasing hormone receptor.

Degree: PhD, 2000, Oregon Health Sciences University

URL: doi:10.6083/M4154FB7 ; http://digitalcommons.ohsu.edu/etd/3298

Subjects/Keywords: Receptors, Corticotropin-Releasing Hormone; Gene Expression Regulation; Mice, Inbred C57BL; Muscle, Skeletal – physiology; Heart – physiology; Cytokines

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

APA (6^th Edition):

Heldwein, K. A. (2000). Molecular characterization of the type 2 corticotropin-releasing hormone receptor. (Doctoral Dissertation). Oregon Health Sciences University. Retrieved from doi:10.6083/M4154FB7 ; http://digitalcommons.ohsu.edu/etd/3298

Chicago Manual of Style (16^th Edition):

Heldwein, Kurt A. “Molecular characterization of the type 2 corticotropin-releasing hormone receptor.” 2000. Doctoral Dissertation, Oregon Health Sciences University. Accessed March 07, 2021. doi:10.6083/M4154FB7 ; http://digitalcommons.ohsu.edu/etd/3298.

MLA Handbook (7^th Edition):

Heldwein, Kurt A. “Molecular characterization of the type 2 corticotropin-releasing hormone receptor.” 2000. Web. 07 Mar 2021.

Vancouver:

Heldwein KA. Molecular characterization of the type 2 corticotropin-releasing hormone receptor. [Internet] [Doctoral dissertation]. Oregon Health Sciences University; 2000. [cited 2021 Mar 07]. Available from: doi:10.6083/M4154FB7 ; http://digitalcommons.ohsu.edu/etd/3298.

Council of Science Editors:

Heldwein KA. Molecular characterization of the type 2 corticotropin-releasing hormone receptor. [Doctoral Dissertation]. Oregon Health Sciences University; 2000. Available from: doi:10.6083/M4154FB7 ; http://digitalcommons.ohsu.edu/etd/3298

21. Chuang, Gin C. The effects of environmental ozone exposure on vascular function, oxidative stress, and atherosclerosis.

Degree: PhD, 2010, University of Alabama – Birmingham

URL: http://contentdm.mhsl.uab.edu/u?/etd,809

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Exposure to air pollutants are known to induce airway inflammation, decrease lung function, and worsen existing pulmonary conditions such as asthma. Additionally, air pollutant exposure… (more)

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Exposure to air pollutants are known to induce airway inflammation, decrease lung function, and worsen existing pulmonary conditions such as asthma. Additionally, air pollutant exposure has also been shown to impact cardiovascular health. Although these pollutant-induced cardiovascular effects were considered to be mediated by the direct action of pollutants upon the cardiovascular tissue and/or the indirect release of pro-inflammatory factors into the circulation, the relative contribution of the two pathways remained equivocal. Recently, several epidemiology studies associated ozone exposure with cardiovascular mortalities. However, relatively few studies to date have examined ozone in this context. In order to address our hypothesis that ozone exposure can indeed influence cardiovascular function, we modeled acute and chronic ozone exposure in C57Bl/6J and apoE-/- mice, respectively. Acutely, animals exposed to 5 days of ozone displayed increased heart rate and diastolic blood pressure. Also, their aortas exhibited impaired endothelium-dependent vascular relaxation and increased mitochondrial oxidative stress; both mechanisms are known to be involved in atherosclerosis development. In the chronic exposure models, aortas from animals exposed to 40 ozone days exhibited increased atherosclerosis lesion area, while those from animals exposed for 10 or 20 days did not. Interestingly, newborn mice exposed to 15 ozone days exhibited increased lesion area when their aortas were assessed in adulthood, suggesting that ozone exposure during childhood increases one’s atherogenic risk. Finally, aortas from animals exposed to 20 ozone days exhibited increased mitochondrial oxidative stress, although it was attenuated versus animals in the acute exposure model. Since these animals did not exhibit a significant increase in atherogenesis, further studies are needed to determine whether these mitochondrial oxidative stress alterations are indicative of either a pre-atherogenic or an atheroprotective phenotype. Taken together, these findings demonstrate that both acute and chronic ozone exposures can alter functional and oxidative stress endpoints in the aorta, with age and exposure regimen acting to influence one’s susceptibility. Importantly, because ozone’s reactivity precludes it from entering the circulation, these findings imply that other inducers of pulmonary inflammation, such as asthma, may also affect cardiovascular health through a common pathway or mediator.

1 online resource (ix, 124 p. : ill., digital, PDF file).

Pathology

Joint Health Sciences;

oxone atherosclerosis oxidative stress cardiovascular mitochondria mice

UNRESTRICTED

Advisors/Committee Members: Ballinger, Scott W., Darley-Usmar, Victor M. , Dickinson, Dale A. , Postlethwait, Edward M. , White, C. Roger.

Subjects/Keywords: Air Pollutants – adverse effects<; br>; Atherosclerosis – etiology<; br>; Mice, Inbred C57BL<; br>; Mitochondrial Diseases – etiology<; br>; Oxidative Stress – physiology<; br>; Ozone – adverse effects

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

APA (6^th Edition):

Chuang, G. C. (2010). The effects of environmental ozone exposure on vascular function, oxidative stress, and atherosclerosis. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,809

Chicago Manual of Style (16^th Edition):

Chuang, Gin C. “The effects of environmental ozone exposure on vascular function, oxidative stress, and atherosclerosis.” 2010. Doctoral Dissertation, University of Alabama – Birmingham. Accessed March 07, 2021. http://contentdm.mhsl.uab.edu/u?/etd,809.

MLA Handbook (7^th Edition):

Chuang, Gin C. “The effects of environmental ozone exposure on vascular function, oxidative stress, and atherosclerosis.” 2010. Web. 07 Mar 2021.

Vancouver:

Chuang GC. The effects of environmental ozone exposure on vascular function, oxidative stress, and atherosclerosis. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2010. [cited 2021 Mar 07]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,809.

Council of Science Editors:

Chuang GC. The effects of environmental ozone exposure on vascular function, oxidative stress, and atherosclerosis. [Doctoral Dissertation]. University of Alabama – Birmingham; 2010. Available from: http://contentdm.mhsl.uab.edu/u?/etd,809

Duke University

22. Chen, Yu-Hsun Jason. An entirely cell-based system to generate single-chain antibodies against cell surface receptors.

Degree: 2008, Duke University

URL: http://hdl.handle.net/10161/903

► The generation of recombinant antibodies (Abs) using phage display is a proven method to obtain a large variety of Abs that bind with high affinity… (more)

▼ The generation of recombinant antibodies (Abs) using phage display is a proven method to obtain a large variety of Abs that bind with high affinity to a given antigen (Ag). Traditionally, the generation of single chain Abs depends on the use of recombinant proteins in several stages of the procedure. This can be a problem, especially in the case of cell surface receptors, because Abs generated and selected against recombinant proteins may not bind the same protein expressed on a cell surface in its native form and because the expression of some receptors as recombinant proteins is problematic. To overcome these difficulties, we developed a strategy to generate single chain Abs that does not require the use of purified protein at any stage of the procedure. In this strategy, stably transfected cells are used for the immunization of mice, measuring Ab responses to immunization, panning the phage library, high throughputs creening of arrayed phage clones, and characterization of recombinant single chain variable regions(scFvs). This strategy was used to generate a panel of single chain Abs specific for the innate immunity receptor Toll‐like receptor2 (TLR2). Once generated, individual scFvs were subcloned into an expression vector allowing the production of recombinant antibodies in insect cells, thus avoiding the contamination of recombinant Abs with microbial products. This cell‐based system efficiently generates Abs that bind native molecules displayed on cell surfaces, bypasses the requirement of recombinant protein production, and avoids risks of microbial component contamination. However, an inconvenience of this strategy is that it requires construction of a new library for each target TLR. This problem might be solved by using non‐immune antibody libraries to obtain antibodies against multiple TLRs. Non‐immune libraries contain a wide variety of antibodies but these are often low affinity, while immune libraries, derived from immunized animals, containa high frequency of high affinity antibodies, but are typically limited to a single antigen. In addition, it can be difficult to produce non‐immune libraries with sufficient complexity to select Abs against multiple Ags. Because the re‐assortment of VH and VL regions that occurs during antibody library construction greatly increases library complexity, we hypothesized that an immune antibody library produced against one member of a protein family would contain antibodies specific for other members of the same protein family. Here, we tested this hypothesis by mining an existing anti‐hTLR2 antibody library for antibodies specific for other members of the TLR family. This procedure, which we refer to as homolog mining, proved to be effective. Using a cell‐based system to pan and screen our anti‐hTLR2 library, we identified single chain antibodies specific for three of the four hTLR2 homologs we targeted. The antibodies identified, anti‐murine TLR2, anti‐hTLR5, and anti‐hTLR6, bind specifically to their target, with no cross‐reactivity to hTLR2 or other TLRs tested.… Advisors/Committee Members: Gunn, Michael Dee (advisor), Dawson, Jeffrey (advisor), Kelsoe, Garnett (advisor), He, You-Wen (advisor), Staats, Herman (advisor).

Subjects/Keywords: Animals; Antibody Affinity; Antibody Specificity; Biological Assay; Cell Line; Drosophila melanogaster; Humans; Immunoglobulin Fragments; Immunoglobulin Variable Region; Mice; Mice, Inbred BALB C; Mice, Inbred C57BL; Peptide Library; Receptors, Cell Surface; Recombinant Proteins; Toll-Like Receptor 2

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

APA (6^th Edition):

Chen, Y. J. (2008). An entirely cell-based system to generate single-chain antibodies against cell surface receptors. (Thesis). Duke University. Retrieved from http://hdl.handle.net/10161/903

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):

Chen, Yu-Hsun Jason. “An entirely cell-based system to generate single-chain antibodies against cell surface receptors. ” 2008. Thesis, Duke University. Accessed March 07, 2021. http://hdl.handle.net/10161/903.

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

MLA Handbook (7^th Edition):

Chen, Yu-Hsun Jason. “An entirely cell-based system to generate single-chain antibodies against cell surface receptors. ” 2008. Web. 07 Mar 2021.

Vancouver:

Chen YJ. An entirely cell-based system to generate single-chain antibodies against cell surface receptors. [Internet] [Thesis]. Duke University; 2008. [cited 2021 Mar 07]. Available from: http://hdl.handle.net/10161/903.

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

Council of Science Editors:

Chen YJ. An entirely cell-based system to generate single-chain antibodies against cell surface receptors. [Thesis]. Duke University; 2008. Available from: http://hdl.handle.net/10161/903

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

23. 山本, 梓司. Protective and therapeutic role of 2-carba-cyclic phosphatidic acid in demyelinating disease. : 脱髄性疾患における環状ホスファチジン酸誘導体の脱髄抑制及び治療効果.

Degree: 博士(医学), 2018, Saitama Medical University / 埼玉医科大学

URL: http://id.nii.ac.jp/1386/00000615/

►

Multiple sclerosis is a neuroinflammatory demyelinating and neurodegenerative disease of the central nervous system characterized by recurrent and progressive demyelination/remyelination cycles, neuroinflammation, oligodendrocyte loss, demyelination,… (more)

▼

Multiple sclerosis is a neuroinflammatory demyelinating and neurodegenerative disease of the central nervous system characterized by recurrent and progressive demyelination/remyelination cycles, neuroinflammation, oligodendrocyte loss, demyelination, and axonal degeneration. Cyclic phosphatidic acid (cPA) is a natural phospholipid mediator with a unique cyclic phosphate ring structure at the sn-2 and sn-3 positions of the glycerol backbone. We reported earlier that cPA elicits a neurotrophin-like action and protects hippocampal neurons from ischemia-induced delayed neuronal death. We designed, chemically synthesized, and metabolically stabilized derivatives of cPA: 2-carba-cPA (2ccPA), a synthesized compound in which one of the phosphate oxygen molecules is replaced with a methylene group at the sn-2 position. In the present study, we investigated whether 2ccPA exerts protective effects in oligodendrocytes and suppresses pathology in the two most common mouse models of multiple sclerosis.

To evaluate whether 2ccPA has potential beneficial effects on the pathology of multiple sclerosis, we investigated the effects of 2ccPA on oligodendrocyte cell death in vitro and administrated 2ccPA to mouse models of experimental autoimmune encephalomyelitis (EAE) and cuprizone-induced demyelination.

We demonstrated that 2ccPA suppressed the CoCl

-induced increase in the Bax/Bcl-2 protein expression ratio and phosphorylation levels of p38MAPK and JNK protein. 2ccPA treatment reduced cuprizone-induced demyelination, microglial activation, NLRP3 inflammasome, and motor dysfunction. Furthermore, 2ccPA treatment reduced autoreactive T cells and macrophages, spinal cord injury, and pathological scores in EAE, the autoimmune multiple sclerosis mouse model.

We demonstrated that 2ccPA protected oligodendrocytes via suppression of the mitochondrial apoptosis pathway. Also, we found beneficial effects of 2ccPA in the multiperiod of cuprizone-induced demyelination and the pathology of EAE. These data indicate that 2ccPA may be a promising compound for the development of new drugs to treat demyelinating disease and ameliorate the symptoms of multiple sclerosis.

平成29年度

Subjects/Keywords: Animals; Anti-Inflammatory Agents; Apoptosis; Cell Differentiation; Cell Line, Transformed; Cuprizone; Demyelinating Diseases; Disease Models, Animal; Female; Gene Expression Regulation; Humans; MAP Kinase Signaling System; Male; Mice; Mice, Inbred C57BL; Monoamine Oxidase Inhibitors; Myelin Sheath; NLR Family, Pyrin Domain-Containing 3 Protein; Phosphatidic Acids; Proto-Oncogene Proteins c-bcl-2; p38 Mitogen-Activated Protein Kinases

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

APA (6^th Edition):

山本, �. (2018). Protective and therapeutic role of 2-carba-cyclic phosphatidic acid in demyelinating disease. : 脱髄性疾患における環状ホスファチジン酸誘導体の脱髄抑制及び治療効果. (Thesis). Saitama Medical University / 埼玉医科大学. Retrieved from http://id.nii.ac.jp/1386/00000615/

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):

山本, 梓司. “Protective and therapeutic role of 2-carba-cyclic phosphatidic acid in demyelinating disease. : 脱髄性疾患における環状ホスファチジン酸誘導体の脱髄抑制及び治療効果.” 2018. Thesis, Saitama Medical University / 埼玉医科大学. Accessed March 07, 2021. http://id.nii.ac.jp/1386/00000615/.

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

MLA Handbook (7^th Edition):

山本, 梓司. “Protective and therapeutic role of 2-carba-cyclic phosphatidic acid in demyelinating disease. : 脱髄性疾患における環状ホスファチジン酸誘導体の脱髄抑制及び治療効果.” 2018. Web. 07 Mar 2021.

Vancouver:

山本 �. Protective and therapeutic role of 2-carba-cyclic phosphatidic acid in demyelinating disease. : 脱髄性疾患における環状ホスファチジン酸誘導体の脱髄抑制及び治療効果. [Internet] [Thesis]. Saitama Medical University / 埼玉医科大学; 2018. [cited 2021 Mar 07]. Available from: http://id.nii.ac.jp/1386/00000615/.

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

Council of Science Editors:

山本 �. Protective and therapeutic role of 2-carba-cyclic phosphatidic acid in demyelinating disease. : 脱髄性疾患における環状ホスファチジン酸誘導体の脱髄抑制及び治療効果. [Thesis]. Saitama Medical University / 埼玉医科大学; 2018. Available from: http://id.nii.ac.jp/1386/00000615/

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

University of Missouri – Columbia

24. Moore, Alex W. Effects of adrenoreceptor activation and aging on skeletal muscle arterioles at rest and during rapid onset vasodilation.

Degree: 2010, University of Missouri – Columbia

URL: http://hdl.handle.net/10355/12012

► Sympathetic nerve activity (SNA) induces arteriolar vasoconstriction via [alpha]-adrenoreceptor ([alpha]AR) activation. Whether [alpha]AR activation affects the spread of rapid onset vasodilation (ROV) in contracting muscle… (more)

Subjects/Keywords: Alpha adrenoreceptors; Blood vessles – Dilation; Muscle contraction – Regulation; Aging; Mice as laboratory animals; Receptors, Adrenergic, alpha-1 – metabolism; Receptors, Adrenergic, alpha-2 – metabolism; Vasodilation – physiology; Muscle Contraction – physiology; Aging – physiology; Mice, Inbred C57BL

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

APA (6^th Edition):

Moore, A. W. (2010). Effects of adrenoreceptor activation and aging on skeletal muscle arterioles at rest and during rapid onset vasodilation. (Thesis). University of Missouri – Columbia. Retrieved from http://hdl.handle.net/10355/12012

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):

Moore, Alex W. “Effects of adrenoreceptor activation and aging on skeletal muscle arterioles at rest and during rapid onset vasodilation.” 2010. Thesis, University of Missouri – Columbia. Accessed March 07, 2021. http://hdl.handle.net/10355/12012.

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

MLA Handbook (7^th Edition):

Moore, Alex W. “Effects of adrenoreceptor activation and aging on skeletal muscle arterioles at rest and during rapid onset vasodilation.” 2010. Web. 07 Mar 2021.

Vancouver:

Moore AW. Effects of adrenoreceptor activation and aging on skeletal muscle arterioles at rest and during rapid onset vasodilation. [Internet] [Thesis]. University of Missouri – Columbia; 2010. [cited 2021 Mar 07]. Available from: http://hdl.handle.net/10355/12012.

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

Council of Science Editors:

Moore AW. Effects of adrenoreceptor activation and aging on skeletal muscle arterioles at rest and during rapid onset vasodilation. [Thesis]. University of Missouri – Columbia; 2010. Available from: http://hdl.handle.net/10355/12012

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

25. Pearson, Todd. The Genetic Basis of Resistance to Transplantation Tolerance Induced by Costimulation Blockade in NOD Mice: a Dissertation.

Degree: Immunology and Microbiology, Program in Molecular Medicine, 2003, U of Massachusetts : Med

URL: https://escholarship.umassmed.edu/gsbs_diss/16

► The NOD mouse is a widely studied model of type 1 diabetes. The loss of self-tolerance leading to autoimmune diabetes in NOD mice involves… (more)

▼ The NOD mouse is a widely studied model of type 1 diabetes. The loss of self-tolerance leading to autoimmune diabetes in NOD mice involves at least 27 genetic loci. Curing type I diabetes in mice and humans by islet transplantation requires overcoming both allorejection and recurrent autoimmunity. This has been achieved with systemic immunosuppression, but tolerance induction would be preferable. In addition to their genetic defects in self-tolerance, NOD mice resist peripheral transplantation tolerance induced by costimulation blockade using donor-specific transfusion and anti-CDl54 antibody. Failure has been attributed to the underlying autoimmunity, assuming that autoimmunity and resistance to transplantation tolerance have a common basis. Hypothesizing that these two abnormalities might be related, we investigated whether they had a common genetic basis. Diabetes-resistant NOD and C57BL/6 stocks congenic for various reciprocally introduced Idd loci were assessed for their ability to be tolerized. Surprisingly, in NOD congenic mice that are almost completely protected from diabetes, costimulation blockade failed to prolong skin allograft survival. In reciprocal C57BL/6 congenic mice with NOD-derived Idd loci, skin allograft survival was readily prolonged by costimulation blockade. Unexpectedly, we observed that (NOD x C57BL/6)F1 mice, which have no diabetes, nonetheless resist induction of tolerance to skin allografts. Further analyses revealed that the F1 mice shared the dendritic cell maturation defects and abnormal CD4⁺ T cell responses of the NOD but had lost its defects in macrophage maturation and NK cell activity. Finally, using a genome wide scan approach, we have identified four suggestive markers in the mouse genome that control the survival of skin allografts following DST and anti-CD154 mAb therapy. We suggest that mechanisms controlling autoimmunity and transplantation tolerance in NOD mice are not completely overlapping and are potentially distinct, or that the genetic threshold for normalizing the transplantation tolerance defect is higher than that for preventing autoimmune diabetes. We conclude that resistance to allograft tolerance induction in the NOD mouse is not a direct consequence of overt autoimmunity and that autoimmunity and resistance to costimulation blockade-induced transplantation tolerance phenotypes in NOD mice are not under identical genetic control. Advisors/Committee Members: Dr. Dale Greiner.

Subjects/Keywords: Islets of Langerhans Transplantation; Transplantation Tolerance; Immunosuppression; Autoimmunity; Graft Rejection; Antigens; CD40; Mice; Inbred NOD; Mice; Inbred C57BL; Animal Experimentation and Research; Endocrine System Diseases; Genetic Phenomena; Immune System Diseases; Nutritional and Metabolic Diseases; Surgical Procedures, Operative; Therapeutics

Record Details Similar Records Cite « Share

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

APA (6^th Edition):

Pearson, T. (2003). The Genetic Basis of Resistance to Transplantation Tolerance Induced by Costimulation Blockade in NOD Mice: a Dissertation. (Doctoral Dissertation). U of Massachusetts : Med. Retrieved from https://escholarship.umassmed.edu/gsbs_diss/16

Chicago Manual of Style (16^th Edition):

Pearson, Todd. “The Genetic Basis of Resistance to Transplantation Tolerance Induced by Costimulation Blockade in NOD Mice: a Dissertation.” 2003. Doctoral Dissertation, U of Massachusetts : Med. Accessed March 07, 2021. https://escholarship.umassmed.edu/gsbs_diss/16.

MLA Handbook (7^th Edition):

Pearson, Todd. “The Genetic Basis of Resistance to Transplantation Tolerance Induced by Costimulation Blockade in NOD Mice: a Dissertation.” 2003. Web. 07 Mar 2021.

Vancouver:

Pearson T. The Genetic Basis of Resistance to Transplantation Tolerance Induced by Costimulation Blockade in NOD Mice: a Dissertation. [Internet] [Doctoral dissertation]. U of Massachusetts : Med; 2003. [cited 2021 Mar 07]. Available from: https://escholarship.umassmed.edu/gsbs_diss/16.

Council of Science Editors:

Pearson T. The Genetic Basis of Resistance to Transplantation Tolerance Induced by Costimulation Blockade in NOD Mice: a Dissertation. [Doctoral Dissertation]. U of Massachusetts : Med; 2003. Available from: https://escholarship.umassmed.edu/gsbs_diss/16

University of Florida

26. Kubanis, Patricia Joan, 1955-. Age-related memory loss and neurobiological changes in the C57BL/6 mouse.

Degree: 1981, University of Florida

URL: https://ufdc.ufl.edu/AA00028789

Subjects/Keywords: Academic achievement; Age groups; Cerebral cortex; Cholinergics; Hippocampus; Memory; Memory disorders; Rats; Receptors; Statistical significance; Memory – physiology ( mesh ); Mice, Inbred C57BL – physiology ( mesh ); Neuroanatomy ( mesh ); Neuroscience thesis Ph.D ( mesh )

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

APA (6^th Edition):

Kubanis, Patricia Joan, 1. (1981). Age-related memory loss and neurobiological changes in the C57BL/6 mouse. (Thesis). University of Florida. Retrieved from https://ufdc.ufl.edu/AA00028789

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):

Kubanis, Patricia Joan, 1955-. “Age-related memory loss and neurobiological changes in the C57BL/6 mouse.” 1981. Thesis, University of Florida. Accessed March 07, 2021. https://ufdc.ufl.edu/AA00028789.

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

MLA Handbook (7^th Edition):

Kubanis, Patricia Joan, 1955-. “Age-related memory loss and neurobiological changes in the C57BL/6 mouse.” 1981. Web. 07 Mar 2021.

Vancouver:

Kubanis, Patricia Joan 1. Age-related memory loss and neurobiological changes in the C57BL/6 mouse. [Internet] [Thesis]. University of Florida; 1981. [cited 2021 Mar 07]. Available from: https://ufdc.ufl.edu/AA00028789.

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

Council of Science Editors:

Kubanis, Patricia Joan 1. Age-related memory loss and neurobiological changes in the C57BL/6 mouse. [Thesis]. University of Florida; 1981. Available from: https://ufdc.ufl.edu/AA00028789

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

27. Nagaoka, Yoshiyuki; Kajiya, Hiroshi; Ozeki, Satoru; Ikebe, Tetsuro. Mevalonates restore zoledronic acid-induced osteoclastogenesis inhibition. : Mevalonates restore zoledronic acid-induced osteoclastogenesis inhibition.

Degree: 博士（歯学）, 2015, Fukuoka Dental College / 福岡歯科大学

URL: http://id.nii.ac.jp/1167/00000038/

►

Bisphosphonate-related osteonecrosis of the jaw (BRONJ) is likely to be caused by continuous imperfection of bone healing after surgical treatments in patients with long-term administration… (more)

▼

Bisphosphonate-related osteonecrosis of the jaw (BRONJ) is likely to be caused by continuous imperfection of bone healing after surgical treatments in patients with long-term administration of nitrogen-containing bisphosphonates (NBPs). NBPs inhibit osteoclastic bone resorption by impairing the mevalonic acid sterol pathway in osteoclasts. Thus, we hypothesized that exogenous mevalonic acid metabolites restore the inhibitory effects of NBPs on osteoclastogenesis and bone remodeling. To clarify the effects of mevalonic acid metabolites, especially geranylgeranyl pyrophosphate (GGPP) and geranylgeranyl transferase substrate geranylgeranyl acid (GGOH), we examined the effects of zoledronic acid with or without GGOH or GGPP on osteoclast differentiation, multinucleation, and bone mineral deposition in tooth-extracted sockets. Zoledronic acid decreased the number of tartrate-resistant acid phosphatase (TRAP)-positive multinuclear cells derived from mouse osteoclast precursors treated with receptor activator of nuclear factor-κB ligand and macrophage colony-stimulating factor. Zoledronic acid simultaneously suppressed not only the expressions of osteoclastic differentiation-related molecules such as TRAP, cathepsin K, calcitonin receptor, and vacuolar H-ATPase but also those of multinucleation-related molecules such as dendrocyte-expressed 7 transmembrane proteins and osteoclast stimulatory transmembrane protein. Treatment with GGOH or GGPP, but not farnesyl acid, restored the zoledronic acid-inhibited number of TRAP-positive multinuclear cells together with the expressions of these molecules. Although intraperitoneal administration of zoledronic acid and lipopolysaccharide into mice appeared to induce BRONJ-like lesions with empty bone lacunae and decreased mineral deposition in tooth-extracted socket, both GGOH and GGPP partially restored the inhibitory effects on zoledronic acid-related mineral deposition. These results suggest the potential of mevalonic acid metabolites as therapeutic agents for BRONJ.

2014年度

Subjects/Keywords: 顎骨壊死; 破骨細胞; 骨代謝; 口腔外科; ゲラニルゲラニルピロリン酸; 細胞融合; osteonecrosis; osteoclasts; oral surgery; geranylgeranyl pyrophosphate; DC-STAMP; Acid Phosphatase; Adaptor Proteins, Signal Transducing; Animals; Bisphosphonate-Associated Osteonecrosis of the Jaw; Bone Density Conservation Agents; Bone Remodeling; Calcification, Physiologic; Cathepsin K; Cell Differentiation; Cells, Cultured; Diphosphonates; Diterpenes; Farnesol; Imidazoles; Isoenzymes; Lipopolysaccharides; Macrophages; Male; Maxilla; Membrane Proteins; Mevalonic Acid; Mice; Mice, Inbred C57BL; Osteoclasts; Polyisoprenyl Phosphates; Receptors, Calcitonin; Salmonella; Tooth Socket; Vacuolar Proton-Translocating ATPases

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

APA (6^th Edition):

Nagaoka, Yoshiyuki; Kajiya, Hiroshi; Ozeki, Satoru; Ikebe, T. (2015). Mevalonates restore zoledronic acid-induced osteoclastogenesis inhibition. : Mevalonates restore zoledronic acid-induced osteoclastogenesis inhibition. (Thesis). Fukuoka Dental College / 福岡歯科大学. Retrieved from http://id.nii.ac.jp/1167/00000038/

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):

Nagaoka, Yoshiyuki; Kajiya, Hiroshi; Ozeki, Satoru; Ikebe, Tetsuro. “Mevalonates restore zoledronic acid-induced osteoclastogenesis inhibition. : Mevalonates restore zoledronic acid-induced osteoclastogenesis inhibition.” 2015. Thesis, Fukuoka Dental College / 福岡歯科大学. Accessed March 07, 2021. http://id.nii.ac.jp/1167/00000038/.

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

MLA Handbook (7^th Edition):

Nagaoka, Yoshiyuki; Kajiya, Hiroshi; Ozeki, Satoru; Ikebe, Tetsuro. “Mevalonates restore zoledronic acid-induced osteoclastogenesis inhibition. : Mevalonates restore zoledronic acid-induced osteoclastogenesis inhibition.” 2015. Web. 07 Mar 2021.

Vancouver:

Nagaoka, Yoshiyuki; Kajiya, Hiroshi; Ozeki, Satoru; Ikebe T. Mevalonates restore zoledronic acid-induced osteoclastogenesis inhibition. : Mevalonates restore zoledronic acid-induced osteoclastogenesis inhibition. [Internet] [Thesis]. Fukuoka Dental College / 福岡歯科大学; 2015. [cited 2021 Mar 07]. Available from: http://id.nii.ac.jp/1167/00000038/.

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

Council of Science Editors:

Nagaoka, Yoshiyuki; Kajiya, Hiroshi; Ozeki, Satoru; Ikebe T. Mevalonates restore zoledronic acid-induced osteoclastogenesis inhibition. : Mevalonates restore zoledronic acid-induced osteoclastogenesis inhibition. [Thesis]. Fukuoka Dental College / 福岡歯科大学; 2015. Available from: http://id.nii.ac.jp/1167/00000038/

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

28. Jin, Cong. Particulate allergens potentiate allergic asthma in mice through sustained IgE-mediated mast cell activation.

Degree: 2010, Duke University

URL: http://hdl.handle.net/10161/2358

► In recent years, the incidence of allergic asthma as well as the severity of disease has rapidly increased worldwide. Numerous epidemiological studies have related the… (more)

Subjects/Keywords: Air Pollutants; Allergens; Animals; Antigens, CD; Antigens, CD63; Asthma; Bronchial Hyperreactivity; Disease Models, Animal; Endocytosis; Gene Expression Regulation; Hypersensitivity; Immunoglobulin E; Inflammation; Lipids; Male; Mast Cells; Membrane Microdomains; Mice; Mice, Inbred C57BL; Platelet Membrane Glycoproteins

…sAg in sensitized mice… …65 Figure 6: MCs mediate differential AHR responses to sAg and pAg in sensitized mice. 69… …Figure 7: MCs mediate differential BAL eosinophil responses to sAg and pAg in sensitized mice… …mice… …cavity of sensitized mice…

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

APA (6^th Edition):

Jin, C. (2010). Particulate allergens potentiate allergic asthma in mice through sustained IgE-mediated mast cell activation. (Thesis). Duke University. Retrieved from http://hdl.handle.net/10161/2358

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):

Jin, Cong. “Particulate allergens potentiate allergic asthma in mice through sustained IgE-mediated mast cell activation. ” 2010. Thesis, Duke University. Accessed March 07, 2021. http://hdl.handle.net/10161/2358.

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

MLA Handbook (7^th Edition):

Jin, Cong. “Particulate allergens potentiate allergic asthma in mice through sustained IgE-mediated mast cell activation. ” 2010. Web. 07 Mar 2021.

Vancouver:

Jin C. Particulate allergens potentiate allergic asthma in mice through sustained IgE-mediated mast cell activation. [Internet] [Thesis]. Duke University; 2010. [cited 2021 Mar 07]. Available from: http://hdl.handle.net/10161/2358.

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

Council of Science Editors:

Jin C. Particulate allergens potentiate allergic asthma in mice through sustained IgE-mediated mast cell activation. [Thesis]. Duke University; 2010. Available from: http://hdl.handle.net/10161/2358

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

Queens University

29. Ong, Edmund. Investigating the Effects of Prolonged Mu Opioid Receptor Activation Upon Opioid Receptor Heteromerization .

Degree: Pharmacology and Toxicology, Queens University

URL: http://hdl.handle.net/1974/15437

► Opioid receptors are the sites of action for morphine and most other clinically-used opioid drugs. Abundant evidence now demonstrates that different opioid receptor types can… (more)

▼ Opioid receptors are the sites of action for morphine and most other clinically-used opioid drugs. Abundant evidence now demonstrates that different opioid receptor types can physically associate to form heteromers. Owing to their constituent monomers’ involvement in analgesia, mu/delta opioid receptor (M/DOR) heteromers have been a particular focus of attention. Understandings of the physiological relevance of M/DOR formation remain limited in large part due to the reliance of existing M/DOR findings upon contrived heterologous systems. This thesis investigated the physiological relevance of M/DOR generation following prolonged MOR activation. To address M/DOR in endogenous tissues, suitable model systems and experimental tools were established. This included a viable dorsal root ganglion (DRG) neuron primary culture model, antisera specifically directed against M/DOR, a quantitative immunofluorescence colocalizational analysis method, and a floxed-Stop, FLAG-tagged DOR conditional knock-in mouse model. The development and implementation of such techniques make it possible to conduct experiments addressing the nature of M/DOR heteromers in systems with compelling physiological relevance. Seeking to both reinforce and extend existing findings from heterologous systems, it was first necessary to demonstrate the existence of M/DOR heteromers. Using antibodies directed against M/DOR itself as well as constituent monomers, M/DOR heteromers were identified in endogenous tissues and demonstrated to increase in abundance following prolonged mu opioid receptor (MOR) activation by morphine. The next experiments addressed an aspect of the functional consequences of M/DOR formation in endogenous tissues by investigating the post-internalization trafficking of delta opioid receptor (DOR) in conditions of augmented M/DOR formation. These experiments identified perturbations to DOR trafficking consistent with incorporation into a M/DOR species with probabilistic post-internalisation trafficking behaviour intermediate to that of either constituent and responsive to both MOR and DOR agonists in a manner subject to blockade by DOR antagonist. These studies provide concurrent evidence of the existence and functionality of physiologically-relevant M/DOR heteromers in endogenous tissues.

Subjects/Keywords: Delta Opioid Receptor ; Mu Opioid Receptor ; Trafficking ; Internalization ; Dorsal Root Ganglia ; Morphine ; DAMGO ; Deltorphin II ; SNC80 ; SDM-25N ; Adenylate Cyclase ; Adenylate Cyclase: Metabolism ; Animals ; Antibodies ; Antibodies: Metabolism ; Blotting ; Brain ; Brain: Metabolism ; CHO Cells ; Cricetinae ; Cricetulus ; Enzyme-Linked Immunosorbent Assay ; Gene Expression Regulation ; Gene Expression Regulation: Physiology ; Immunohistochemistry ; Immunocytochemistry ; Immunoprecipitation ; Inbred c57bl ; Knockout ; Mice ; Morphine: Administration & Dosage ; Morphine: Pharmacology ; Multiprotein Complexes ; Multiprotein Complexes: Metabolism ; Neurons ; Neurons: Metabolism ; Opioid ; Rats ; Receptors ; Signal Transduction ; Signal Transduction: Physiology ; Western ; Delta ; Delta: Genetics ; Delta: Metabolism ; Mu ; Mu: Metabolism ; Colocalization ; Colocalizational Analysis ; Degradation ; G-Protein Coupled Receptor ; Microscopy ; Molecular Biology ; Receptor Post-Internalization Trafficking ; Recycling ; Oligomerization ; Receptor Signaling

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Ong, E. (n.d.). Investigating the Effects of Prolonged Mu Opioid Receptor Activation Upon Opioid Receptor Heteromerization . (Thesis). Queens University. Retrieved from http://hdl.handle.net/1974/15437

Note: this citation may be lacking information needed for this citation format:
No year of publication.
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Ong, Edmund. “Investigating the Effects of Prolonged Mu Opioid Receptor Activation Upon Opioid Receptor Heteromerization .” Thesis, Queens University. Accessed March 07, 2021. http://hdl.handle.net/1974/15437.

Note: this citation may be lacking information needed for this citation format:
No year of publication.
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Ong, Edmund. “Investigating the Effects of Prolonged Mu Opioid Receptor Activation Upon Opioid Receptor Heteromerization .” Web. 07 Mar 2021.

Note: this citation may be lacking information needed for this citation format:
No year of publication.

Vancouver:

Ong E. Investigating the Effects of Prolonged Mu Opioid Receptor Activation Upon Opioid Receptor Heteromerization . [Internet] [Thesis]. Queens University; [cited 2021 Mar 07]. Available from: http://hdl.handle.net/1974/15437.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
No year of publication.

Council of Science Editors:

Ong E. Investigating the Effects of Prolonged Mu Opioid Receptor Activation Upon Opioid Receptor Heteromerization . [Thesis]. Queens University; Available from: http://hdl.handle.net/1974/15437

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
No year of publication.

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