subject:(TNF )

1. 藤原, 範雄. 腫瘍壊死因子産生阻害剤の合成と構造活性相関および薬理作用に関する研究 : Synthesis, pharmacological evaluation and SAR study of novel tumor necrosis factor-alpha inhibitors; シュヨウエシインシサンセイソガイザイノゴウセイトコウゾウカッセイソウカンオヨビヤクリサヨウニカンスルケンキュウ.

Degree: Nara Institute of Science and Technology / 奈良先端科学技術大学院大学

URL: http://hdl.handle.net/10061/5235

Subjects/Keywords: TNF

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

APA (6^th Edition):

藤原, �. (n.d.). 腫瘍壊死因子産生阻害剤の合成と構造活性相関および薬理作用に関する研究 : Synthesis, pharmacological evaluation and SAR study of novel tumor necrosis factor-alpha inhibitors; シュヨウエシインシサンセイソガイザイノゴウセイトコウゾウカッセイソウカンオヨビヤクリサヨウニカンスルケンキュウ. (Thesis). Nara Institute of Science and Technology / 奈良先端科学技術大学院大学. Retrieved from http://hdl.handle.net/10061/5235

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):

藤原, 範雄. “腫瘍壊死因子産生阻害剤の合成と構造活性相関および薬理作用に関する研究 : Synthesis, pharmacological evaluation and SAR study of novel tumor necrosis factor-alpha inhibitors; シュヨウエシインシサンセイソガイザイノゴウセイトコウゾウカッセイソウカンオヨビヤクリサヨウニカンスルケンキュウ.” Thesis, Nara Institute of Science and Technology / 奈良先端科学技術大学院大学. Accessed January 26, 2021. http://hdl.handle.net/10061/5235.

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):

藤原, 範雄. “腫瘍壊死因子産生阻害剤の合成と構造活性相関および薬理作用に関する研究 : Synthesis, pharmacological evaluation and SAR study of novel tumor necrosis factor-alpha inhibitors; シュヨウエシインシサンセイソガイザイノゴウセイトコウゾウカッセイソウカンオヨビヤクリサヨウニカンスルケンキュウ.” Web. 26 Jan 2021.

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

Vancouver:

藤原 �. 腫瘍壊死因子産生阻害剤の合成と構造活性相関および薬理作用に関する研究 : Synthesis, pharmacological evaluation and SAR study of novel tumor necrosis factor-alpha inhibitors; シュヨウエシインシサンセイソガイザイノゴウセイトコウゾウカッセイソウカンオヨビヤクリサヨウニカンスルケンキュウ. [Internet] [Thesis]. Nara Institute of Science and Technology / 奈良先端科学技術大学院大学; [cited 2021 Jan 26]. Available from: http://hdl.handle.net/10061/5235.

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:

藤原 �. 腫瘍壊死因子産生阻害剤の合成と構造活性相関および薬理作用に関する研究 : Synthesis, pharmacological evaluation and SAR study of novel tumor necrosis factor-alpha inhibitors; シュヨウエシインシサンセイソガイザイノゴウセイトコウゾウカッセイソウカンオヨビヤクリサヨウニカンスルケンキュウ. [Thesis]. Nara Institute of Science and Technology / 奈良先端科学技術大学院大学; Available from: http://hdl.handle.net/10061/5235

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

2. Sousa, Cláudia Emanuele Carvalho de. Caracterização do eixo imune-pineal: mecanismo de ação do controle da função pineal pela citocina pró-inflamatória TNF.

Degree: Mestrado, Fisiologia Geral, 2011, University of São Paulo

URL: http://www.teses.usp.br/teses/disponiveis/41/41135/tde-27042011-131503/ ;

►

O TNF atua diretamente sobre a pineal inibindo a via biossintética da melatonina. De forma semelhante o LPS, potente ativador da resposta imune inata, tem… (more)

▼

O TNF atua diretamente sobre a pineal inibindo a via biossintética da melatonina. De forma semelhante o LPS, potente ativador da resposta imune inata, tem efeito inibitório sobre a produção de melatonina e seu precursor. A supressão da síntese noturna de melatonina é admitida de forma a permitir a montagem da resposta inflamatória, tanto durante o dia como à noite. Dados do grupo tem demonstrado que o NFKB é um fator constitutivamente expresso na glândula pineal e que o ritmo diário de translocação pode ser determinante para o início da síntese de melatonina. A inibição de sua ativação potencia a síntese de melatonina enquanto que fatores que classicamente promovem a sua ativação inibem esta produção. Nesta dissertação, verificamos as moléculas envolvidas no reconhecimento e na de sinalização desta citocina na pineal. Demonstramos que a pineal está apta a responder ao TNF, células gliais da pineal e as células secretoras, os pinealócitos, expressam constitutivamente o receptor TNF-R1. O TNF promove a translocação nuclear dos dímeros p50/p50 e p50/RelA do NFKB em glândulas pineais em cultura. Confirmamos a ativação desta via em pinealócitos pela análise da proteína inibitória IKB. Vimos que a ativação desse fator é essencial para expressão da iNOS e a produção de NO induzida por TNF em pinealócitos isolados. Além disso, mostramos que o TNF promove a redução da expressão do receptor TNF-R1 na membrana de pinealócitos. Em resumo, mostramos neste trabalho que a pineal está instrumentalizada a responder ao TNF, e que os pinealócitos são alvos diretos para o seu reconhecimento. Confirmamos a relevância do fator NFKB na resposta da pineal em situações de injúria, ampliando o conceito de que a pineal está apta a detectar moléculas do processo inflamatório.

TNF acts directly on the pineal gland by inhibiting the biosynthesis of melatonin. Similarly, LPS, a potent activator of the innate immune response has an inhibitory effect on the production of melatonin and its precursor. The suppression of nocturnal melatonin synthesis is admitted to allow the full mounting of the inflammatory response both during the day and night. Data from our laboratory have shown that the NFKB is constitutively expressed in the pineal gland and that the daily rate of translocation can be determinant for the onset of melatonin synthesis. Inhibition of their activation potentiates melatonin synthesis whereas factors that promote its activation classically inhibit this production. In this dissertation we find the molecules involved in recognition and signaling of this cytokine in the pineal. We demonstrated that the pineal is responsive to TNF, the pineal glial cells and secretory cells, the pinealocytes, constitutively express the TNF-R1. TNF promotes nuclear translocation of p50/RelA and p50/p50 NFKB dimers in the pineal glands in culture. We confirmed the activation of this pathway in pinealocytes by analyzing the inhibitory protein IKB. We have seen that the activation of this factor is essential for iNOS expression and NO production induced by…

Advisors/Committee Members: Markus, Regina Pekelmann.

Subjects/Keywords: Glândula pineal; NFKB; NFKB; Pineal gland; TNF; TNF; TNF-R1; TNF-R1

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

APA (6^th Edition):

Sousa, C. E. C. d. (2011). Caracterização do eixo imune-pineal: mecanismo de ação do controle da função pineal pela citocina pró-inflamatória TNF. (Masters Thesis). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/41/41135/tde-27042011-131503/ ;

Chicago Manual of Style (16^th Edition):

Sousa, Cláudia Emanuele Carvalho de. “Caracterização do eixo imune-pineal: mecanismo de ação do controle da função pineal pela citocina pró-inflamatória TNF.” 2011. Masters Thesis, University of São Paulo. Accessed January 26, 2021. http://www.teses.usp.br/teses/disponiveis/41/41135/tde-27042011-131503/ ;.

MLA Handbook (7^th Edition):

Sousa, Cláudia Emanuele Carvalho de. “Caracterização do eixo imune-pineal: mecanismo de ação do controle da função pineal pela citocina pró-inflamatória TNF.” 2011. Web. 26 Jan 2021.

Vancouver:

Sousa CECd. Caracterização do eixo imune-pineal: mecanismo de ação do controle da função pineal pela citocina pró-inflamatória TNF. [Internet] [Masters thesis]. University of São Paulo; 2011. [cited 2021 Jan 26]. Available from: http://www.teses.usp.br/teses/disponiveis/41/41135/tde-27042011-131503/ ;.

Council of Science Editors:

Sousa CECd. Caracterização do eixo imune-pineal: mecanismo de ação do controle da função pineal pela citocina pró-inflamatória TNF. [Masters Thesis]. University of São Paulo; 2011. Available from: http://www.teses.usp.br/teses/disponiveis/41/41135/tde-27042011-131503/ ;

University of Illinois – Chicago

3. Lee, Wan-Ju. Utilization and Risk of Serious Infection Associated with TNF-α Inhibitors in Children and Young Adults.

Degree: 2016, University of Illinois – Chicago

URL: http://hdl.handle.net/10027/21614

► This dissertation examined use of tumor necrosis factor-alpha inhibitors (TNFI) and risk of TNFI-associated serious infection compared to oral immunosuppressants in children and young adults… (more)

▼ This dissertation examined use of tumor necrosis factor-alpha inhibitors (TNFI) and risk of TNFI-associated serious infection compared to oral immunosuppressants in children and young adults with juvenile idiopathic arthritis (JIA)/rheumatoid arthritis (RA) and inflammatory bowel disease (IBD). Four retrospective cohort studies were conducted using the Truven Health MarketScan Research Database (2009-2013). TNFI treatment patterns, early TNFI therapy rates, and time to TNFI initiation were examined in incident JIA/RA and IBD cohorts. Serious infections were defined as those requiring hospitalization. Cox proportional hazard models were used to estimate the risk of serious infection associated with TNFIs in JIA and IBD cohorts. High-dimensional propensity score models were used to control for potential confounding. In two studies examining treatment patterns, 18.6% of the incident JIA/RA cohort initiated TNFIs, and etanercept was most commonly used, while in the incident IBD cohort, 27.6% initiated TNFIs, and infliximab was most commonly used. In both cohorts, time from new diagnosis to first TNFI prescription was shorter in more recent years. Specifically, early TNFI therapy increased over time in the IBD cohort. In a third study, 2,495 JIA patients were followed for 1,810 person-years. Serious infection rates were 2.7/100 person-years for TNFIs and 1.28/100 person-years for disease-modifying antirheumatic drugs (DMARD). TNFI monotherapy posed a 2.7-fold increase in risk of serious infection compared to DMARDs alone. In the fourth study, 10,838 IBD patients were followed for 9,849 person-years. Serious infection rates were 5.25/100 person-years for TNFIs and 3.59/100 person-years for immunomodulators (methotrexate and thiopurines). New use of TNFI monotherapy was associated with a 1.36-fold higher risk of serious infection compared to immunomodulator initiation. The risk of serious infection differed by individual TNFIs and route of administration. This dissertation characterized the utilization of TNFIs and indicated that a more aggressive treatment approach has emerged for children and young adults with JIA/RA and IBD despite an FDA warning about TNFI-associated serious infections. However, study findings support the warning for children with JIA and IBD. This dissertation provides insights into how TNFIs are being used and informs decision-making about use of these drugs–particularly regarding balancing the benefits and risks of TNFIs. Advisors/Committee Members: Schumock, Glen T (advisor), Lee, Todd A (committee member), Calip, Gregory S (committee member), Suda, Katie J (committee member), Briars, Leslie (committee member), Schumock, Glen T (chair).

Subjects/Keywords: TNF inhibitors; infections

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

APA (6^th Edition):

Lee, W. (2016). Utilization and Risk of Serious Infection Associated with TNF-α Inhibitors in Children and Young Adults. (Thesis). University of Illinois – Chicago. Retrieved from http://hdl.handle.net/10027/21614

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):

Lee, Wan-Ju. “Utilization and Risk of Serious Infection Associated with TNF-α Inhibitors in Children and Young Adults.” 2016. Thesis, University of Illinois – Chicago. Accessed January 26, 2021. http://hdl.handle.net/10027/21614.

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

MLA Handbook (7^th Edition):

Lee, Wan-Ju. “Utilization and Risk of Serious Infection Associated with TNF-α Inhibitors in Children and Young Adults.” 2016. Web. 26 Jan 2021.

Vancouver:

Lee W. Utilization and Risk of Serious Infection Associated with TNF-α Inhibitors in Children and Young Adults. [Internet] [Thesis]. University of Illinois – Chicago; 2016. [cited 2021 Jan 26]. Available from: http://hdl.handle.net/10027/21614.

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

Council of Science Editors:

Lee W. Utilization and Risk of Serious Infection Associated with TNF-α Inhibitors in Children and Young Adults. [Thesis]. University of Illinois – Chicago; 2016. Available from: http://hdl.handle.net/10027/21614

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

University of Rochester

4. Chen, Tony (1981 - ). The Role of interstitial fluid flow as a mediator of matrix anisotropy and as a protective mechanism against inflammation in cartilage tissue engineering.

Degree: PhD, 2011, University of Rochester

URL: http://hdl.handle.net/1802/14143

► Injuries to articular cartilage are debilitating and typically require surgical intervention due to the tissue’s inability to self-repair. Current surgical options for focal cartilage defects… (more)

▼ Injuries to articular cartilage are debilitating and typically require surgical intervention due to the tissue’s inability to self-repair. Current surgical options for focal cartilage defects are successful only in treating the associated symptoms, but produce inconsistent clinical outcomes in the long term, and are implicated in degenerative joint changes years later. As an alternative, functional tissue engineering may soon offer translational approaches for cartilage repair by producing implantable artificial tissues that recapitulate the composition, structure, and function of the native tissue. While current tissue engineering bioreactors that introduce various physiologically inspired mechanical stimuli are able to reproduce the mechanical properties of native cartilage, recreating the tissue’s structural and compositional anisotropy, which might influence the integration of the implanted tissue with the surrounding cartilage, has to date remained elusive. Furthermore, the fate of the engineered construct during the inflammatory phase that ensues upon implantation in the joint has been less studied, as most of the literature focuses on developing engineered cartilage in idealized culture conditions in vitro, and for the most part neglects the interplay between inflammation and repair mechanobiology. This dissertation sets to recreate aspects of the characteristic zonal anisotropy of articular cartilage using custom-designed bioreactors based on Couette and Poiseuille flow with the hypothesis that interstitial fluid flow can influence matrix synthesis and the alignment of collagen fibers. Using in situ hybridization and immunohistochemistry, tissue engineered cartilage (TEC) hydrogels that were cultured in a novel bioreactor that simulates rotational Couette flow demonstrated an increase in aggrecan and type II collagen mRNA expression and protein synthesis near the surface of the hydrogel exposed to the flow, compared to deeper regions within the hydrogel and control hydrogels not stimulated by Couette flow. Furthermore, the alignment of the collagen fibers in the superficial layer of the bioreactor-cultured TEC hydrogels was significantly enhanced compared to controls. When quantified using Fast Fourier Transform (FFT) algorithms, the collagen alignment in the surface region of the bioreactor-cultured TEC hydrogels was remarkably similar to the alignment pattern of collagen in the superficial zone of native articular cartilage. To formally test the hypothesis that the aforementioned effects of Couette flow are related to interstitial flow fields, the interstitial flow velocity profiles within TEC hydrogels were experimentally measured as a function of flow rate through a parallel plate (Poiseuille flow) bioreactor using a flow visualization technique based on Fluorescence Recovery After Photobleaching (FRAP). Experimental measurements of the fluid velocity profile over a range of flow rates demonstrated that Poiseuille flow induced measurable interstitial flow fields near the flow-exposed surface of…

Subjects/Keywords: Collagen alignment; Chondrocyte; TNF-&alpha

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

APA (6^th Edition):

Chen, T. (. -. ). (2011). The Role of interstitial fluid flow as a mediator of matrix anisotropy and as a protective mechanism against inflammation in cartilage tissue engineering. (Doctoral Dissertation). University of Rochester. Retrieved from http://hdl.handle.net/1802/14143

Chicago Manual of Style (16^th Edition):

Chen, Tony (1981 - ). “The Role of interstitial fluid flow as a mediator of matrix anisotropy and as a protective mechanism against inflammation in cartilage tissue engineering.” 2011. Doctoral Dissertation, University of Rochester. Accessed January 26, 2021. http://hdl.handle.net/1802/14143.

MLA Handbook (7^th Edition):

Chen, Tony (1981 - ). “The Role of interstitial fluid flow as a mediator of matrix anisotropy and as a protective mechanism against inflammation in cartilage tissue engineering.” 2011. Web. 26 Jan 2021.

Vancouver:

Chen T(-). The Role of interstitial fluid flow as a mediator of matrix anisotropy and as a protective mechanism against inflammation in cartilage tissue engineering. [Internet] [Doctoral dissertation]. University of Rochester; 2011. [cited 2021 Jan 26]. Available from: http://hdl.handle.net/1802/14143.

Council of Science Editors:

Chen T(-). The Role of interstitial fluid flow as a mediator of matrix anisotropy and as a protective mechanism against inflammation in cartilage tissue engineering. [Doctoral Dissertation]. University of Rochester; 2011. Available from: http://hdl.handle.net/1802/14143

University of Alberta

5. Srivastava, Nutan. NEUTROPHIL SECRETION OF THE PROINFLAMMATORY CYTOKINE TNF VIA RECYCLING ENDOSOMES.

Degree: MS, Department of Medicine, 2015, University of Alberta

URL: https://era.library.ualberta.ca/files/mp48sg31c

► Neutrophils are highly abundant innate immune cells that are important in immediate responses to injury and infection, and secrete the proinflammatory cytokine tumor necrosis factor… (more)

Subjects/Keywords: Neutrophil; Recycling endosomes; TNF-alpha

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

APA (6^th Edition):

Srivastava, N. (2015). NEUTROPHIL SECRETION OF THE PROINFLAMMATORY CYTOKINE TNF VIA RECYCLING ENDOSOMES. (Masters Thesis). University of Alberta. Retrieved from https://era.library.ualberta.ca/files/mp48sg31c

Chicago Manual of Style (16^th Edition):

Srivastava, Nutan. “NEUTROPHIL SECRETION OF THE PROINFLAMMATORY CYTOKINE TNF VIA RECYCLING ENDOSOMES.” 2015. Masters Thesis, University of Alberta. Accessed January 26, 2021. https://era.library.ualberta.ca/files/mp48sg31c.

MLA Handbook (7^th Edition):

Srivastava, Nutan. “NEUTROPHIL SECRETION OF THE PROINFLAMMATORY CYTOKINE TNF VIA RECYCLING ENDOSOMES.” 2015. Web. 26 Jan 2021.

Vancouver:

Srivastava N. NEUTROPHIL SECRETION OF THE PROINFLAMMATORY CYTOKINE TNF VIA RECYCLING ENDOSOMES. [Internet] [Masters thesis]. University of Alberta; 2015. [cited 2021 Jan 26]. Available from: https://era.library.ualberta.ca/files/mp48sg31c.

Council of Science Editors:

Srivastava N. NEUTROPHIL SECRETION OF THE PROINFLAMMATORY CYTOKINE TNF VIA RECYCLING ENDOSOMES. [Masters Thesis]. University of Alberta; 2015. Available from: https://era.library.ualberta.ca/files/mp48sg31c

Universidade do Rio Grande do Sul

6. Jardim, Fernanda Rafaela. Ação da adenosina extracelular sobre uma linhagem de célula estrelada hepática tratada com TNF-[alfa] : papel do receptor A2B.

Degree: 2008, Universidade do Rio Grande do Sul

URL: http://hdl.handle.net/10183/14831

► Fibrose hepática é caracterizada pelo acúmulo de matriz extracelular fibrótica, cuja presença danifica as funções do fígado. Células estreladas hepáticas (HSCs) participam ativamente deste processo,… (more)

▼ Fibrose hepática é caracterizada pelo acúmulo de matriz extracelular fibrótica, cuja presença danifica as funções do fígado. Células estreladas hepáticas (HSCs) participam ativamente deste processo, modificando seu fenótipo quiescente, rico em lipídios no citoplasma, para o fenótipo ativado, em resposta ao insulto fibrogênico. A regressão do processo fibrótico pode, inclusive, estar relacionada com a apoptose das HSCs e também com sua reversão fenotípica, do estado ativado ao estado quiescente. Adenosina tem papel hepatoprotetor bem conhecido e medeia várias ações antiinflamatórias em diferentes tipos celulares e condições patológicas. TNF-α é uma citocina pró-inflamatória com importantes funções no início e perpetuação do processo fibrogênico. Tendo em vista o papel antiinflamatório da adenosina, este trabalho investigou, em linhagem de HSC em cultura - GRX -, as ações desse nucleosídeo em presença ou ausência dos sinais inflamatórios que acompanham o tratamento com TNF- α. Assim, foram analisados os efeitos da adenosina extracelular na síntese lipídica, avaliando a reversão fenotípica da GRX, e a apoptose em resposta à adenosina e/ou TNF-α. Além disso, a regulação dos níveis de adenosina extracelular, bem como a presença dos receptores de adenosina foram investigadas. O efeito de adenosina e/ou TNF-α sobre a produção de óxido nítrico (NO) e atividade e expressão de gelatinases (MMP-9 e -2), ambos importantes mediadores na fibrose hepática, também foram alvo deste estudo. Nossos resultados mostram a presença do receptor de adenosina A2B (A2BR), e a regulação dos níveis extracelulares de adenosina por TNF-α, através do aumento da atividade ecto-adenosina deaminase. Além disso, demontramos que adenosina extracelular não modifica a síntese de lipídios nas células GRX. Os dados ainda indicam que adenosina, em presença ou ausência de TNF-α, não resulta em apoptose, e que esta citocina também não induz à formação de corpos apoptóticos nas células tratadas. O estudo mostra que a produção de NO foi aumentada com TNF-α, com potencialização deste efeito na presença de adenosina, provavelmente mediado pelo A2BR e não por inosina, produto da hidrólise de adenosina. Com relação às gelatinases, o tratamento com adenosina diminui a atividade de MMP-9 tanto em ausência, quanto em presença de TNF-α, revertendo a ação da citocina, a níveis de controle, com o envolvimento do receptor A2BR mediando os efeitos do nucleosídeo. No entanto, a expressão da MMP-9 não foi afetada pelo tratamento com adenosina, porém, o nucleosídeo diminui os efeitos de TNF-α sobre a expressão da gelatinase. Com relação à MMP-2, ambos tratamentos com adenosina e com TNF-α, bem como o tratamento com adenosina, em presença da citocina, diminuem a atividade da gelatinase, sem efeitos aditivos. A expressão do mRNA de MMP-2 aumentou em resposta aos tratamentos com adenosina e TNF-α, isolados ou em associação, indicando a presença de mecanismo pós-transcricional de regulação para MMP-2. Este trabalho mostra, claramente, que adenosina extracelular e TNF-α estão… Advisors/Committee Members: Bernard, Elena Aida.

Subjects/Keywords: Adenosina; TNF-alfa; Cirrose hepática

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

APA (6^th Edition):

Jardim, F. R. (2008). Ação da adenosina extracelular sobre uma linhagem de célula estrelada hepática tratada com TNF-[alfa] : papel do receptor A2B. (Thesis). Universidade do Rio Grande do Sul. Retrieved from http://hdl.handle.net/10183/14831

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):

Jardim, Fernanda Rafaela. “Ação da adenosina extracelular sobre uma linhagem de célula estrelada hepática tratada com TNF-[alfa] : papel do receptor A2B.” 2008. Thesis, Universidade do Rio Grande do Sul. Accessed January 26, 2021. http://hdl.handle.net/10183/14831.

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

MLA Handbook (7^th Edition):

Jardim, Fernanda Rafaela. “Ação da adenosina extracelular sobre uma linhagem de célula estrelada hepática tratada com TNF-[alfa] : papel do receptor A2B.” 2008. Web. 26 Jan 2021.

Vancouver:

Jardim FR. Ação da adenosina extracelular sobre uma linhagem de célula estrelada hepática tratada com TNF-[alfa] : papel do receptor A2B. [Internet] [Thesis]. Universidade do Rio Grande do Sul; 2008. [cited 2021 Jan 26]. Available from: http://hdl.handle.net/10183/14831.

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

Council of Science Editors:

Jardim FR. Ação da adenosina extracelular sobre uma linhagem de célula estrelada hepática tratada com TNF-[alfa] : papel do receptor A2B. [Thesis]. Universidade do Rio Grande do Sul; 2008. Available from: http://hdl.handle.net/10183/14831

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

Vanderbilt University

7. Ardestani, Shidrokh. New insights into tumor necrosis factor-alpha in cancer: distinct isoforms exert opposing effects on tumor associated myeloid cells and tumorigenesis.

Degree: PhD, Pathology, 2013, Vanderbilt University

URL: http://hdl.handle.net/1803/13448

► TNF-α, produced by most malignant cells, orchestrates the interplay between malignant cells and myeloid cells, which have been linked to tumor growth and metastasis. Although… (more)

▼ TNF-α, produced by most malignant cells, orchestrates the interplay between malignant cells and myeloid cells, which have been linked to tumor growth and metastasis. Although TNF-α can exist as one of two isoforms, a 26-kDa membrane tethered form (mTNF-α) or a soluble 17-kDa cytokine (sTNF-α), the vast majority of published studies have only investigated the biological effects of the soluble form. We demonstrate for the first time that membrane and soluble isoforms have diametrically opposing effects on both tumor growth and myeloid content. Mouse lung and melanoma tumor lines expressing mTNF-α, generated small tumors devoid of monocytes versus respective control lines or lines expressing sTNF-α. The lack of myeloid cells was due to a direct effect of mTNF-α on myeloid survival via induction of cell necrosis by increasing reactive oxygen species. Using cultured RAW 264.7 monocytic cell line and L929 fibroblasts we showed that mTNF-α increased reactive oxygen species (ROS)-mediated cytotoxicity, independent of caspase-3 activity. Although TNF-α receptors (TNFR) on target cells were required for this effect, we observed that mTNF-α-induced cell death could be mediated through both TNFR-1 and the death domain-lacking TNFR-2. ROS generation and cytotoxicity were inhibited by a mitochondrial respiratory chain inhibitor but not by an inhibitor of NADPH oxidase. Furthermore, mTNF-α mediated cytotoxicity was independent of RIP-1, a serine/threonine kinase which serves as a main adaptor protein of sTNF-α induced programmed necrosis, but rather depended on ceramide signaling pathways. Furthermore, we found that human none-small-cells lung carcinomas (NSCLCs) expressed varying levels of both soluble and membrane TNF-α. Analysis of publicly accessible NSCLC microarray database showed that gene expression patterns favoring mTNF-α were predictive of improved lung cancer survival. Advisors/Committee Members: Sarki Abdulkadir (committee member), Jin Chen (committee member), Ambra Pozzi (committee member), Bill Valentine (Committee Chair).

Subjects/Keywords: ROS; Myeloid cells; TNF-alpha

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

APA (6^th Edition):

Ardestani, S. (2013). New insights into tumor necrosis factor-alpha in cancer: distinct isoforms exert opposing effects on tumor associated myeloid cells and tumorigenesis. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/13448

Chicago Manual of Style (16^th Edition):

Ardestani, Shidrokh. “New insights into tumor necrosis factor-alpha in cancer: distinct isoforms exert opposing effects on tumor associated myeloid cells and tumorigenesis.” 2013. Doctoral Dissertation, Vanderbilt University. Accessed January 26, 2021. http://hdl.handle.net/1803/13448.

MLA Handbook (7^th Edition):

Ardestani, Shidrokh. “New insights into tumor necrosis factor-alpha in cancer: distinct isoforms exert opposing effects on tumor associated myeloid cells and tumorigenesis.” 2013. Web. 26 Jan 2021.

Vancouver:

Ardestani S. New insights into tumor necrosis factor-alpha in cancer: distinct isoforms exert opposing effects on tumor associated myeloid cells and tumorigenesis. [Internet] [Doctoral dissertation]. Vanderbilt University; 2013. [cited 2021 Jan 26]. Available from: http://hdl.handle.net/1803/13448.

Council of Science Editors:

Ardestani S. New insights into tumor necrosis factor-alpha in cancer: distinct isoforms exert opposing effects on tumor associated myeloid cells and tumorigenesis. [Doctoral Dissertation]. Vanderbilt University; 2013. Available from: http://hdl.handle.net/1803/13448

North Carolina State University

8. Harris, Virginia Gail. The intracellular targeting of cPLA2.

Degree: MS, Microbiology, 2002, North Carolina State University

URL: http://www.lib.ncsu.edu/resolver/1840.16/1243

► Tumor necrosis factor-α (TNF) is an inflammatory cytokine that can induce apoptosis in virus-infected cells, susceptible tumor cells, and cells whose transcriptional or translational processes… (more)

▼ Tumor necrosis factor-α (TNF) is an inflammatory cytokine that can induce apoptosis in virus-infected cells, susceptible tumor cells, and cells whose transcriptional or translational processes have been disrupted. The apoptotic pathway that is activated by TNF is dependent on the activity of the enzyme cytosolic phospholipase A2 (cPLA2). This enzyme cleaves arachidonic acid from membrane phospholipid, which in turn causes mitochondrial dysfunction leading to cell death. The goal of this research project was to identify the specific intracellular membrane to which cPLA2 binds during TNF-induced apoptosis. The membrane site for cPLA2 interaction during apoptosis would be a possible target for anti-apoptotic drug development. Three methods were tested in an attempt to identify the membrane location, including; immunofluorescence, biochemical fractionation, and GC/MS. Our results with immunofluorescence suggested that cPLA2 translocates to the nuclear membrane during apoptosis. The identity of the nuclear membrane was confirmed by staining with an antibody to the nuclear pore complex. In addition, cPLA2 staining was noted within the nucleus, perhaps indicating an interaction with chromatin, and small areas of punctate staining were noted in the perinuclear region. Biochemical fractionation indicated that the association of cPLA2 with the nuclear membrane was calcium-dependent since this association could not be stabilized in the absence of calcium. GC/MS, which was used in an attempt to find amputated phospholipids remaining in membranes as a result of cPLA2 activity, instead revealed higher levels of arachidonic acid suggesting that cells may increase the synthesis or repair of arachidonic acid containing membranes following the activation of cPLA2. Finally, our results revealed several novel, lower molecular weight forms of cPLA2 that were associated with nuclei in a calcium-independent fashion. Taken together these results suggest that it will be important to understand the mechanisms controlling the association of cPLA2 with nuclei. Advisors/Committee Members: Scott Laster, Committee Member (advisor), Amy Grunden, Committee Member (advisor), Geraldine Luginbuhl, Committee Member (advisor).

Subjects/Keywords: cPLA2; TNF

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

APA (6^th Edition):

Harris, V. G. (2002). The intracellular targeting of cPLA2. (Thesis). North Carolina State University. Retrieved from http://www.lib.ncsu.edu/resolver/1840.16/1243

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):

Harris, Virginia Gail. “The intracellular targeting of cPLA2.” 2002. Thesis, North Carolina State University. Accessed January 26, 2021. http://www.lib.ncsu.edu/resolver/1840.16/1243.

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

MLA Handbook (7^th Edition):

Harris, Virginia Gail. “The intracellular targeting of cPLA2.” 2002. Web. 26 Jan 2021.

Vancouver:

Harris VG. The intracellular targeting of cPLA2. [Internet] [Thesis]. North Carolina State University; 2002. [cited 2021 Jan 26]. Available from: http://www.lib.ncsu.edu/resolver/1840.16/1243.

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

Council of Science Editors:

Harris VG. The intracellular targeting of cPLA2. [Thesis]. North Carolina State University; 2002. Available from: http://www.lib.ncsu.edu/resolver/1840.16/1243

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

University of Debrecen

9. Nemes, Olívia. Tumor nekrózis faktor-alfa (TNF-α) szerepe .

Degree: DE – Természettudományi és Technológiai Kar – Biológiai és Ökológiai Intézet, University of Debrecen

URL: http://hdl.handle.net/2437/211769

► A TNF-α egy gyulladást keltő citokin, amelynek kettő formája ismert, egy szolubilis és egy membrán kötött. Részt vesznek a fertőzés és a daganatok elleni védekezésben,… (more)

Subjects/Keywords: TNF; TNF-R1; TNF-R2; TNF-R signaling

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APA (6^th Edition):

Nemes, O. (n.d.). Tumor nekrózis faktor-alfa (TNF-α) szerepe . (Thesis). University of Debrecen. Retrieved from http://hdl.handle.net/2437/211769

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):

Nemes, Olívia. “Tumor nekrózis faktor-alfa (TNF-α) szerepe .” Thesis, University of Debrecen. Accessed January 26, 2021. http://hdl.handle.net/2437/211769.

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):

Nemes, Olívia. “Tumor nekrózis faktor-alfa (TNF-α) szerepe .” Web. 26 Jan 2021.

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

Vancouver:

Nemes O. Tumor nekrózis faktor-alfa (TNF-α) szerepe . [Internet] [Thesis]. University of Debrecen; [cited 2021 Jan 26]. Available from: http://hdl.handle.net/2437/211769.

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:

Nemes O. Tumor nekrózis faktor-alfa (TNF-α) szerepe . [Thesis]. University of Debrecen; Available from: http://hdl.handle.net/2437/211769

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

University of Debrecen

10. Hajdu, Dorottya Zsuzsanna. Az antipszichotikumok makrofágok funkcionális aktivitására gyakorolt hatása .

Degree: DE – Természettudományi és Technológiai Kar – Biológiai és Ökológiai Intézet, 2014, University of Debrecen

URL: http://hdl.handle.net/2437/191161

► Célom volt az atípusos antipszichotikumok hatásának vizsgálata humán monocita-makrofág differenciálódásra. Kísérleteim során használt gyógyszerek a Quetiapin, Aripiprasol, Ziprasidon, Risperidon, Clozapin és Olanzapin, a Haloperidol antipszichotikumok… (more)

Subjects/Keywords: monocita; differenciálódás; TNF-alfa

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

APA (6^th Edition):

Hajdu, D. Z. (2014). Az antipszichotikumok makrofágok funkcionális aktivitására gyakorolt hatása . (Thesis). University of Debrecen. Retrieved from http://hdl.handle.net/2437/191161

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):

Hajdu, Dorottya Zsuzsanna. “Az antipszichotikumok makrofágok funkcionális aktivitására gyakorolt hatása .” 2014. Thesis, University of Debrecen. Accessed January 26, 2021. http://hdl.handle.net/2437/191161.

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

MLA Handbook (7^th Edition):

Hajdu, Dorottya Zsuzsanna. “Az antipszichotikumok makrofágok funkcionális aktivitására gyakorolt hatása .” 2014. Web. 26 Jan 2021.

Vancouver:

Hajdu DZ. Az antipszichotikumok makrofágok funkcionális aktivitására gyakorolt hatása . [Internet] [Thesis]. University of Debrecen; 2014. [cited 2021 Jan 26]. Available from: http://hdl.handle.net/2437/191161.

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

Council of Science Editors:

Hajdu DZ. Az antipszichotikumok makrofágok funkcionális aktivitására gyakorolt hatása . [Thesis]. University of Debrecen; 2014. Available from: http://hdl.handle.net/2437/191161

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

11. Silva, Mariana Machado da. Polimorfismo da região do fator de necrose tumoral (TNF) na síndrome da lipodistrofia associada à terapia anti-retroviral em portadores do HIV-1.

Degree: Mestrado, Enfermagem Fundamental, 2008, University of São Paulo

URL: http://www.teses.usp.br/teses/disponiveis/22/22132/tde-27052008-144002/ ;

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Apesar de causar um enorme impacto na história da evolução e prognóstico a partir da infecção pelo HIV, a terapia anti-retroviral altamente potente prolongada apresenta… (more)

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Apesar de causar um enorme impacto na história da evolução e prognóstico a partir da infecção pelo HIV, a terapia anti-retroviral altamente potente prolongada apresenta vários efeitos colaterais. Dentre esses, a síndrome da lipodistrofia (SL) caracterizada por alterações metabólicas e morfológicas. Embora tenha sido descrito que a adesão à terapia esteja associada, sua patogenia ainda permanece desconhecida. Um enfoque têm sido dado aos mediadores pró-inflamatórios, como o Fator de Necrose Tumoral (TNF), sugerindo que o aumento nos níveis dessa citocina esteja associado com o desenvolvimento da SL. Como os sítios polimórficos têm sido associados com a magnitude da produção de citocinas, no presente estudo avaliamos a freqüência de alguns sítios polimórficos na região do gene que codifica o TNF em portadores do HIV/aids apresentando ou não a SL. Para avaliar o polimorfismo genético dos microssatélites TNFa-e e da região promotora do TNF (TNF-308 e TNF-238) foram estudados 117 portadores do HIV-1 usando terapia anti-retroviral (67 com SL e 50 sem SL) e 131 controles saudáveis. Os microssatélites e região promotora do TNF foram tipificados usando DNA genômico hibridizado com iniciadores específicos. Os pacientes foram arrolados no Hospital das Clínicas da Universidade de São Paulo (HCFMRP-USP). A analise estatística foi realizada utilizando-se o teste exato de Fisher. Quando consideramos as comparações das freqüências dos alelos dos microssatélites da região do TNF podemos inferir que a presença do alelo TNFa5 pode conferir proteção aos indivíduos portadores do HIV/aids no desenvolvimento da SL. Já as comparações dos alelos da região promotora do TNF nos sugerem que a presença do alelo TNF-308G, assim como seu homozigoto TNF-308GG, podem conferir susceptibilidade para o desenvolvimento da SL. A presença do haplótipo TNFe3 d3 -238G -308A c1 a5 b7 sugere proteção para o desenvolvimento dessa síndrome. Esse é o primeiro estudo associando o polimorfismo dos microssatelites do TNF com a SL e aponta diversas associações entre alelos da região do gene que codifica o TNF com a SL. Embora os mecanismos relacionados com a participação do TNF no desenvolvimento da SL não estejam bem esclarecidos, este estudo sugere que fatores imunogenéticos associados com a magnitude de expressão do TNF e, provavelmente da expressão de outras citocinas pró-inflamatórias, estejam envolvidas no desenvolvimento da SL em portadores do HIV/aids.

Despite causing a significant impact in the history of evolution and prognosis after HIV infection, the highly potent antiretroviral therapy causes various side effects, which include lipodystrophy syndrome (LS), characterized by metabolic and morphologic changes. Although it has been reported that treatment compliance is associated, LS pathogenesis remains unknown. Special attention has been given to proinflammatory mediators, such as the Tumoral Necrosis Factor (TNF), suggesting that the increase in levels of this cytokine is associated with the development of LS. Since polymorphic sites have been…

Advisors/Committee Members: Morais, Ana Paula de Souza.

Subjects/Keywords: HIV; HIV; Lipodystrophy Syndrome; Microsatellites; Microssatélites; Síndrome da Lipodistrofia; TNF; TNF

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

APA (6^th Edition):

Silva, M. M. d. (2008). Polimorfismo da região do fator de necrose tumoral (TNF) na síndrome da lipodistrofia associada à terapia anti-retroviral em portadores do HIV-1. (Masters Thesis). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/22/22132/tde-27052008-144002/ ;

Chicago Manual of Style (16^th Edition):

Silva, Mariana Machado da. “Polimorfismo da região do fator de necrose tumoral (TNF) na síndrome da lipodistrofia associada à terapia anti-retroviral em portadores do HIV-1.” 2008. Masters Thesis, University of São Paulo. Accessed January 26, 2021. http://www.teses.usp.br/teses/disponiveis/22/22132/tde-27052008-144002/ ;.

MLA Handbook (7^th Edition):

Silva, Mariana Machado da. “Polimorfismo da região do fator de necrose tumoral (TNF) na síndrome da lipodistrofia associada à terapia anti-retroviral em portadores do HIV-1.” 2008. Web. 26 Jan 2021.

Vancouver:

Silva MMd. Polimorfismo da região do fator de necrose tumoral (TNF) na síndrome da lipodistrofia associada à terapia anti-retroviral em portadores do HIV-1. [Internet] [Masters thesis]. University of São Paulo; 2008. [cited 2021 Jan 26]. Available from: http://www.teses.usp.br/teses/disponiveis/22/22132/tde-27052008-144002/ ;.

Council of Science Editors:

Silva MMd. Polimorfismo da região do fator de necrose tumoral (TNF) na síndrome da lipodistrofia associada à terapia anti-retroviral em portadores do HIV-1. [Masters Thesis]. University of São Paulo; 2008. Available from: http://www.teses.usp.br/teses/disponiveis/22/22132/tde-27052008-144002/ ;

12. Kouris, Anargyros. Ψωρίαση: διερεύνηση μεταβολών των Τ-λεμφοκυττάρων στην ανοσολογική διαταραχή των ασθενών με ψωρίαση.

Degree: 2014, National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ)

URL: http://hdl.handle.net/10442/hedi/42257

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Psoriasis is one of the most common immune-mediated chronic inflammatory skin diseases, in which proinflammatory cytokines, such as, TNF-α, IL-17, IL-1β, IL-6 and IL-22 play… (more)

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Psoriasis is one of the most common immune-mediated chronic inflammatory skin diseases, in which proinflammatory cytokines, such as, TNF-α, IL-17, IL-1β, IL-6 and IL-22 play an important pathogenetic role.-The aim of this study is to assess whether proinflammatory cytokines TNF-α, IL-17, IL-1β, IL-6 and IL-22 are released systemically during psoriasis, arguing for a generalized inflammatory reaction. Peripheral blood mononuclear cells (PBMCs) were isolated from 30 patients with psoriasis and from 30 healthy volunteers. Cytokine production was assessed in supernatants after stimulation of PBMCs with microbial stimuli by an enzyme immunoassay. In addition, flow cytometry was used to determine the subsets of monocytes involved and-the intracellular TNF-α production in monocytes. IL-17 levels were-significantly higher in supernatants of PBMCs of psoriatic patients compared to controls after stimulation with PHA (p= 0.042).TNF-α production was-significantly higher in cells of psoriatic patients compared to controls after-stimulation with all stimuli.-A statistically significant difference was observed between-patients and controls for CD14+/CD16+ monocytes (p<0.0001) and CD14-/CD16+ monocytes-(p=0.002). TNF-α produced by monocytes and the absolute counts of CD14-/CD16+ monocytes were greater in psoriatic patients compared to healthy controls.-There is evidence that this subpopulation may be responsible for the increased TNF-α production by monocytes.

Η ψωρίαση είναι μία χρόνια φλεγμονώδης δερματοπάθεια, στην οποία οι προφλεγμονώδεις κυτοκίνες, όπως TNF-α, IL-17, IL-1β, IL-6 και IL-22 παίζουν σημαντικό ρόλο στην παθογένεια της. Ο σκοπός αυτής της μελέτης είναι να εκτιμήσει κατά πόσον οι προφλεγμονώδεις κυτοκίνες TNF-α, IL-17, IL-1β,IL-6 και IL-22 απελευθερώνονται συστηματικά κατά τη διάρκεια της ψωρίασης, υποστηρίζοντας μια γενικευμένη φλεγμονώδη αντίδραση. Μονοπύρηνα κύτταρα περιφερικού αίματος (PBMCs) απομονώθηκαν από 30 ασθενείς με ψωρίαση και από 30 υγιείς μάρτυρες. Η παραγωγή της κυτοκίνης εκτιμήθηκε στα υπερκείμενα μετά από διέγερση των PBMCs με μικροβιακούς διεγέρτες και μέτρησή της με την μέθοδο Elisa. Επιπλέον, η κυτταρομετρία ροής χρησιμοποιήθηκε για τον προσδιορισμό των υποσυνόλων των μονοκυττάρων που εμπλέκονται και την παραγωγή ενδοκυτταρικού ΤΝF-α στα μονοκύτταρα. Τα επίπεδα της IL-17 ήταν σημαντικά υψηλότερα στα υπερκείμενα των PBMCs των ψωριασικών ασθενών σε σύγκριση με τους μάρτυρες μετά από διέγερση με ΡΗΑ (p=0,042). Ο TNF-α ήταν στατιστικώς σημαντικά υψηλότερος στα κύτταρα των ψωριασικών ασθενών σε σύγκριση με τους μάρτυρες μετά από διέγερση με όλους τους διεγέρτες. Στατιστικά σημαντική διαφορά παρατηρήθηκε μεταξύ των ασθενών και των μαρτύρων για τα CD14+/CD16+ μονοκύτταρα (p <0,0001) και τα CD14-/CD16+ μονοκύτταρα (p = 0,002). Ο ΤΝF-α που παράγεται από τα μονοκύτταρα και τον απόλυτο αριθμό των CD14-/CD16+ μονοκυττάρων ήταν μεγαλύτερος στους ψωριασικούς ασθενείς σε σύγκριση με υγιείς μάρτυρες. Υπάρχουν ενδείξεις ότι αυτός ο υποπληθυσμός μπορεί να είναι υπεύθυνος για την αυξημένη παραγωγή ΤΝF-α από τα…

Subjects/Keywords: Ψωράση; TNF-α; Μονοκύτταρα; Psoriasis; Monocytes; TNF-α

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

APA (6^th Edition):

Kouris, A. (2014). Ψωρίαση: διερεύνηση μεταβολών των Τ-λεμφοκυττάρων στην ανοσολογική διαταραχή των ασθενών με ψωρίαση. (Thesis). National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ). Retrieved from http://hdl.handle.net/10442/hedi/42257

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):

Kouris, Anargyros. “Ψωρίαση: διερεύνηση μεταβολών των Τ-λεμφοκυττάρων στην ανοσολογική διαταραχή των ασθενών με ψωρίαση.” 2014. Thesis, National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ). Accessed January 26, 2021. http://hdl.handle.net/10442/hedi/42257.

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

MLA Handbook (7^th Edition):

Kouris, Anargyros. “Ψωρίαση: διερεύνηση μεταβολών των Τ-λεμφοκυττάρων στην ανοσολογική διαταραχή των ασθενών με ψωρίαση.” 2014. Web. 26 Jan 2021.

Vancouver:

Kouris A. Ψωρίαση: διερεύνηση μεταβολών των Τ-λεμφοκυττάρων στην ανοσολογική διαταραχή των ασθενών με ψωρίαση. [Internet] [Thesis]. National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ); 2014. [cited 2021 Jan 26]. Available from: http://hdl.handle.net/10442/hedi/42257.

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

Council of Science Editors:

Kouris A. Ψωρίαση: διερεύνηση μεταβολών των Τ-λεμφοκυττάρων στην ανοσολογική διαταραχή των ασθενών με ψωρίαση. [Thesis]. National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ); 2014. Available from: http://hdl.handle.net/10442/hedi/42257

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

Univerzitet u Beogradu

13. Ilić, Branislav B., 1981-. Ispitivanje polimorfizama gena za metilentetrahidrofolat reduktazu, glutation transferazu, faktor nekroze tumora alfa i njegove receptore u epitelnim tumorima usne duplje.

Degree: Stomatološki fakultet, 2016, Univerzitet u Beogradu

URL: https://fedorabg.bg.ac.rs/fedora/get/o:13271/bdef:Content/get

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oralna hirurgija - onkogenetika / oral surgery - oncogenetic

Uvod: Odontogeni keratocistični tumor (OKT) i oralni planocelularni karcinom (OPK) pripadaju grupi oralnih epitelnih tumora. Iako… (more)

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oralna hirurgija - onkogenetika / oral surgery - oncogenetic

Uvod: Odontogeni keratocistični tumor (OKT) i oralni planocelularni karcinom (OPK) pripadaju grupi oralnih epitelnih tumora. Iako je prvi benignog, a drugi malignog karaktera, odlikuje ih agresivan rast, složena patogeneza i relativno visok stepen recidiva nakon hirurške intervencije. Nasledne (germinativne) promene koje su deo genetičke konstitucije svakog pojedinca, a koje uključuju i polimorfizme gena, imaju značajnu ulogu u etiologiji ovih tumora. Cilj: Utvrditi da li polimorfizmi gena odgovornog za sintezu i metilaciju DNK (MTHFR -677C>T), gena odgovornog za detoksifikaciju (GSTM1/T1) i gena odgovornog za imunomodulaciju (TNF-α -308G>A; TNF-α R1 -36A>G; TNF-α R2 -676T>G) predstavljaju faktore rizika za nastanak epitelnih tumora usne duplje. Materijal i metode: Ispitivanja su rađena na uzorku od 71 pacijenta lečenog zbog OKT i 78 pacijenata lečenih zbog OPK. Kontrolnu grupu sačinjavalo je 182 zdravih osoba kod kojih je DNK dobijena brisom bukalne sluzokože. Genotipizacija je vršena pomoću lančane reakcije polimeraze (PCR) i analize restrikcionih fragmenata (RFLP). Chi kvadrat i Fišerov test su korišćeni kako bi se utvrdile eventualne razlike u genotipovima i alelnim učestalostima. Povezanost različitih genetskih oblika sa rizikom za nastanak ova dva epitelna tumora vršena je upotrebom logističke regresione analize izračunavanjem odnos šansi (odds ratios) i 95% intervala pouzdanosti (confidence intervals). P vrednosti manje od 0.05 smatrane su za statistički značajne. Rezultati: U okviru grupe ispitanika obolelih od OKT, postojala je visoka statistička značajnost između genotipova i alelnih učestalosti (kod obolelih i zdravih ispitanika), za analizirani TNF alfa (p=0.00) i TNF alfa receptor 1 polimorfizam (p=0.00). Nosioci alela A za TNF alfa, imali su izrazito visok rizik za nastanak OKT (OR 4.41, CI 2.66-7.27, p=0.00). Ostali ispitivani polimorfizmi nisu pokazali statistički značajnu razliku između ispitivanih grupa. U okviru grupe ispitanika obolelih od OPK, postojala je visoka statistička značajnost između genotipova i alelnih učestalosti (kod obolelih i zdravih ispitanika), za analizirani GST1 polimorfizam (p=0.00). Ispitanici kod kojih je bila ispoljena delecija gena, imali su izrazito visok rizik za nastanak OKT (OR 3.56, CI 1.94-6.50, p=0.00). Ostali ispitivani polimorfizmi nisu pokazali statistički značajnu razliku između ispitivanih grupa...

Advisors/Committee Members: Milašin, Jelena, 1957-.

Subjects/Keywords: oral epithelial tumors; KCOT; OSCC; gene polymorphisms; MTHFR; GST; TNF α; TNF α R1; TNF α R2

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

APA (6^th Edition):

Ilić, Branislav B., 1. (2016). Ispitivanje polimorfizama gena za metilentetrahidrofolat reduktazu, glutation transferazu, faktor nekroze tumora alfa i njegove receptore u epitelnim tumorima usne duplje. (Thesis). Univerzitet u Beogradu. Retrieved from https://fedorabg.bg.ac.rs/fedora/get/o:13271/bdef:Content/get

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):

Ilić, Branislav B., 1981-. “Ispitivanje polimorfizama gena za metilentetrahidrofolat reduktazu, glutation transferazu, faktor nekroze tumora alfa i njegove receptore u epitelnim tumorima usne duplje.” 2016. Thesis, Univerzitet u Beogradu. Accessed January 26, 2021. https://fedorabg.bg.ac.rs/fedora/get/o:13271/bdef:Content/get.

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

MLA Handbook (7^th Edition):

Ilić, Branislav B., 1981-. “Ispitivanje polimorfizama gena za metilentetrahidrofolat reduktazu, glutation transferazu, faktor nekroze tumora alfa i njegove receptore u epitelnim tumorima usne duplje.” 2016. Web. 26 Jan 2021.

Vancouver:

Ilić, Branislav B. 1. Ispitivanje polimorfizama gena za metilentetrahidrofolat reduktazu, glutation transferazu, faktor nekroze tumora alfa i njegove receptore u epitelnim tumorima usne duplje. [Internet] [Thesis]. Univerzitet u Beogradu; 2016. [cited 2021 Jan 26]. Available from: https://fedorabg.bg.ac.rs/fedora/get/o:13271/bdef:Content/get.

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

Council of Science Editors:

Ilić, Branislav B. 1. Ispitivanje polimorfizama gena za metilentetrahidrofolat reduktazu, glutation transferazu, faktor nekroze tumora alfa i njegove receptore u epitelnim tumorima usne duplje. [Thesis]. Univerzitet u Beogradu; 2016. Available from: https://fedorabg.bg.ac.rs/fedora/get/o:13271/bdef:Content/get

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

14. Γεωργιάδου, Μαρία. Μελέτη των υποδοχέων του TNFα στα κύτταρα Kupffer και στο ηπατοκυτταρικό καρκίνωμα.

Degree: 2011, University of Crete (UOC); Πανεπιστήμιο Κρήτης

URL: http://hdl.handle.net/10442/hedi/26069

► Tumor necrosis factor (TNF), a pleiotropic cytokine involved in a broad spectrum of inflammatory and immune responses, exerts its biological effects by engaging two distinct… (more)

▼ Tumor necrosis factor (TNF), a pleiotropic cytokine involved in a broad spectrum of inflammatory and immune responses, exerts its biological effects by engaging two distinct cell surface receptors, the 55-kD TNFR1 and the 75-kD TNFR2. Both TNF Receptors (TNFRs) have the ability to mediate cell death via various mechanisms. TNFR1 stimulation may also result in inhibition of apoptosis through induction of the transcription factor NF-kappaB, specifically the heterodimer p50/p65. In response to TNF, p65 undergoes several post-translational modifications, including phosphorylation on serines 536 and 468, and translocates to the nucleus, where it typically mediates expression of many pro-survival genes. Depending on the cell type and the stimulus involved, NF-kappaB may also have a proapoptotic function. TNF in liver is mainly produced by Kupffer cells (KC), the resident liver macrophages, and has a pivotal role in hepatic homeostasis and pathophysiology, since it holds the capacity to induce both hepatocyte cell death and proliferation. KC have been demonstrated to be implicated in the defence against the development of hepatic metastases from various extrahepatic tumors, but on the other hand, they may also be detrimental in the development of liver cancer. Hepatocellular carcinoma (HCC), the main histological type of liver cancer, is a major cause of morbidity and mortality worldwide. Because of its innate resistance to the conventional treatment regiments, the investigation of new therapeutic agents is required. A large number of clinical and experimental data indicate that Octreotide, a potent synthetic somatostatin analogue with antiproliferative, antisecretory and immunomodulatory properties, may be a promising anti-cancer therapeutic agent. Octreotide has been reported to prolong survival in approximately 40% of patients with unresectable hepatocellular carcinoma. Although the favourable findings have been disputed, these negative studies have been criticized for the selection of the participating patients. Previous work in our laboratory has demonstrated that Octreotide has a direct antiproliferative effect on human hepatoma cells HepG2 and modulates the expression of pro- or antifibrotic agents, inflammatory mediators, chemokines and apoptosis related proteins in rat KC. To further explore the mechanisms by which Octreotide exerts its antineoplastic actions, we evaluated its influence, at the clinically feasible concentration of 10-8 Μ, on TNFRs expression, NF-kappaB activation and apoptotic response of KC and HepG2/Hep3B human hepatoma cells to TNF. Rat KC were isolated by centrifugal elutriation. TNFR1 and TNFR2 expression was studied by RT-PCR, quantitative PCR, Western Blot and immunofluorescence. TNF mRNA expression in KC was also assessed by semiquantitative PCR. Intracellular localization of NF-kappaB in HepG2/Hep3B was detected by immunofluorescent analysis and a cell-based ELISA assay was used to quantitate total and active (phosphorylated at serine 536 and serine 468) p65. Apoptosis was examined by a…

Subjects/Keywords: Ηπατοκυτταρικό καρκίνωμα; Οκτρεοτίδη; Υποδοχείς TNF; Απόπτωση; Hepatocellular carcinoma; Kupffer cells; Octreotide; TNF; TNF receptors; p65; Apoptosis

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

APA (6^th Edition):

Γεωργιάδου, . �. (2011). Μελέτη των υποδοχέων του TNFα στα κύτταρα Kupffer και στο ηπατοκυτταρικό καρκίνωμα. (Thesis). University of Crete (UOC); Πανεπιστήμιο Κρήτης. Retrieved from http://hdl.handle.net/10442/hedi/26069

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):

Γεωργιάδου, Μαρία. “Μελέτη των υποδοχέων του TNFα στα κύτταρα Kupffer και στο ηπατοκυτταρικό καρκίνωμα.” 2011. Thesis, University of Crete (UOC); Πανεπιστήμιο Κρήτης. Accessed January 26, 2021. http://hdl.handle.net/10442/hedi/26069.

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

MLA Handbook (7^th Edition):

Γεωργιάδου, Μαρία. “Μελέτη των υποδοχέων του TNFα στα κύτταρα Kupffer και στο ηπατοκυτταρικό καρκίνωμα.” 2011. Web. 26 Jan 2021.

Vancouver:

Γεωργιάδου �. Μελέτη των υποδοχέων του TNFα στα κύτταρα Kupffer και στο ηπατοκυτταρικό καρκίνωμα. [Internet] [Thesis]. University of Crete (UOC); Πανεπιστήμιο Κρήτης; 2011. [cited 2021 Jan 26]. Available from: http://hdl.handle.net/10442/hedi/26069.

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

Council of Science Editors:

Γεωργιάδου �. Μελέτη των υποδοχέων του TNFα στα κύτταρα Kupffer και στο ηπατοκυτταρικό καρκίνωμα. [Thesis]. University of Crete (UOC); Πανεπιστήμιο Κρήτης; 2011. Available from: http://hdl.handle.net/10442/hedi/26069

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

University of Rochester

15. Fahrenthold, Berkeley Kristyn. Assessment of the Involvement of Intrinsic and Extrinsic Cell Death Pathways in Retinal Ganglion Cell Death after Excitotoxic Injury.

Degree: PhD, 2017, University of Rochester

URL: http://hdl.handle.net/1802/32924

► Excitotoxicity leads to disruption of the intracellular environment and activation of cytotoxic cascades that cause neuronal death. Multiple cell types, including both neurons and glia,… (more)

▼ Excitotoxicity leads to disruption of the intracellular environment and activation of cytotoxic cascades that cause neuronal death. Multiple cell types, including both neurons and glia, are affected by excitotoxic insult. In the mammalian retina, cells that die following this insult are retinal ganglion (RGCs) and amacrine cells. Both intrinsic and extrinsic signals have been hypothesized to activate injury response and cell death pathways that ultimately result in RGC death. Here, I test the importance of a TNF-dependent extrinsic apoptotic pathway and JNK signaling, an intrinsic cell death pathway shown to result in RGC apoptosis after diverse insults, in excitotoxicity induced RGC death. Tumor necrosis factor (TNF), through BID-dependent signaling, is known to be a key extrinsic mediator of neuronal degeneration. TNF released by Müller glial cells has also been suggested to be important in RGC death after an excitotoxic injury. To critically test the importance of TNF in RGC death after excitotoxic injury, the excitotoxin N-methyl-D-aspartate (NMDA) was intravitreally injected into mice deficient in TNF. Absence of Tnf did not confer short- or long-term protection to RGCs. Further suggesting that TNF mediated extrinsic cell death pathways are not required for excitotoxic RGC death, Bid deficiency did not protect RGCs nor did it prevent cytochrome c release. Thus, a key extrinsic pathway that has been implicated in RGC death was found to not be necessary for RGC death after excitotoxic injury. Intrinsic cell signaling pathways have also been implicated in excitotoxic neuronal death. JNK signaling is known to be a critical mediator of NMDA-induced cell death in other neuronal cell types. JNK signaling is also known to be critical for RGC death after a variety injuries and is activated in RGCs after excitotoxic injury. To test the importance of JNK signaling in RGC death after an excitotoxic insult, mice deficient in various JNK isoforms were used. Despite known expression in RGCs, involvement in excitotoxic injury in other neurons, and a prominent role in mediating RGC death after other insults, attenuating JNK signaling did not prevent RGC death after excitotoxic insult. Collectively, these results indicate that the cell death pathways that orchestrate RGC death after diverse pathological insults are not analogous. Future studies aimed at using a combinatorial approach to target multiple cell death pathways simultaneously will be needed to shed light on the mechanisms that lead to RGC death after an excitotoxic insult.

Subjects/Keywords: Retina; Excitotoxicity; NMDA; TNF; JNK; CHOP

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

APA (6^th Edition):

Fahrenthold, B. K. (2017). Assessment of the Involvement of Intrinsic and Extrinsic Cell Death Pathways in Retinal Ganglion Cell Death after Excitotoxic Injury. (Doctoral Dissertation). University of Rochester. Retrieved from http://hdl.handle.net/1802/32924

Chicago Manual of Style (16^th Edition):

Fahrenthold, Berkeley Kristyn. “Assessment of the Involvement of Intrinsic and Extrinsic Cell Death Pathways in Retinal Ganglion Cell Death after Excitotoxic Injury.” 2017. Doctoral Dissertation, University of Rochester. Accessed January 26, 2021. http://hdl.handle.net/1802/32924.

MLA Handbook (7^th Edition):

Fahrenthold, Berkeley Kristyn. “Assessment of the Involvement of Intrinsic and Extrinsic Cell Death Pathways in Retinal Ganglion Cell Death after Excitotoxic Injury.” 2017. Web. 26 Jan 2021.

Vancouver:

Fahrenthold BK. Assessment of the Involvement of Intrinsic and Extrinsic Cell Death Pathways in Retinal Ganglion Cell Death after Excitotoxic Injury. [Internet] [Doctoral dissertation]. University of Rochester; 2017. [cited 2021 Jan 26]. Available from: http://hdl.handle.net/1802/32924.

Council of Science Editors:

Fahrenthold BK. Assessment of the Involvement of Intrinsic and Extrinsic Cell Death Pathways in Retinal Ganglion Cell Death after Excitotoxic Injury. [Doctoral Dissertation]. University of Rochester; 2017. Available from: http://hdl.handle.net/1802/32924

16. Izadi, Hooman. Innate immune responses to B. burgdorferi mediated by JNK1 and the cochaperone, methylation controlled DNAJ (MCJ).

Degree: PhD, Animal Biotechnology & Biomedical Sciences, 2011, U of Massachusetts : PhD

URL: https://scholarworks.umass.edu/open_access_dissertations/360

► The infections agent of Lyme disease, Borrelia Burgdorferi is a complex microorganism with a highly diverse genome. One of the most remarkable aspects of… (more)

▼ The infections agent of Lyme disease, Borrelia Burgdorferi is a complex microorganism with a highly diverse genome. One of the most remarkable aspects of the B. burgdorferi genome is the large number of sequences encoding predicted or known lipoproteins, including outer-surface proteins. The B. burgdorferi genome encodes no recognizable toxins. Instead, this extracellular pathogen causes pathology by migration through tissues, adhesion to host cells, and evasion of immune clearance. Inflammation elicited by infection with B. burgdorferi depends on the ability of the spirochete to survive in the mammalian host, as well as the immune response that arises upon the interaction of the bacterium with phagocytic, T and other cell types. Innate immune responses are critical in recognition and clearance of pathogens, and also play an important role in the outcome of adaptive immune responses. The regulation of innate immune responses to pathogens occurs through the interaction of Toll-like receptors (TLRs) with pathogen-associated molecular patterns (PAMPs) and the activation of several signaling pathways whose contribution to the overall innate immune response to pathogens is poorly understood. In this study we demonstrate a mechanism of control of murine macrophage responses mediated by TLR1/2 heterodimers through c-Jun N-terminal kinase 1 (JNK1) activity. JNK also controls tumor necrosis factor production and TLR-mediated macrophage responses to B. burgdorferi. We also show that the proximal promoter region of the human tlr1 gene contains an AP-1 binding site that is subjected to regulation by the kinase and binds two complexes that involve the JNK substrates c-Jun, JunD, and ATF-2. These results demonstrate that JNK1 regulates the response to TLR1/2 ligands and suggest a positive feedback loop that may serve to increase the innate immune response to the spirochete. MCJ is a newly identified member of the DnaJ protein family of cochaperones that contains unique features different than the normally described DnaJ proteins. However, there is little known about its function and the role it plays in different cells and systems. It has been previously shown that MCJ is required for the repression of the ABCB1 drug transporter expression in breast cancer cells, and that this repression is mediated through the control of c-Jun protein stability. We were therefore interested in determining the role that MCJ plays in macrophages in response to B. burgdorferi antigens. We now provide evidence that MCJ controls inflammatory responses of macrophages through the regulation of c-Jun protein stability, and the expression and release of the inflammatory cytokine TNF through the regulation of the expression of TNF converting enzyme (TACE) inhibitor tissue inhibitor of metalloproteinase 3 (TIMP-3). Advisors/Committee Members: Juan Anguita, Barbara A. Osborne, Wilmore Webley.

Subjects/Keywords: JNK1; MCJ; TLR; TNF; Animal Sciences; Biotechnology

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

APA (6^th Edition):

Izadi, H. (2011). Innate immune responses to B. burgdorferi mediated by JNK1 and the cochaperone, methylation controlled DNAJ (MCJ). (Doctoral Dissertation). U of Massachusetts : PhD. Retrieved from https://scholarworks.umass.edu/open_access_dissertations/360

Chicago Manual of Style (16^th Edition):

Izadi, Hooman. “Innate immune responses to B. burgdorferi mediated by JNK1 and the cochaperone, methylation controlled DNAJ (MCJ).” 2011. Doctoral Dissertation, U of Massachusetts : PhD. Accessed January 26, 2021. https://scholarworks.umass.edu/open_access_dissertations/360.

MLA Handbook (7^th Edition):

Izadi, Hooman. “Innate immune responses to B. burgdorferi mediated by JNK1 and the cochaperone, methylation controlled DNAJ (MCJ).” 2011. Web. 26 Jan 2021.

Vancouver:

Izadi H. Innate immune responses to B. burgdorferi mediated by JNK1 and the cochaperone, methylation controlled DNAJ (MCJ). [Internet] [Doctoral dissertation]. U of Massachusetts : PhD; 2011. [cited 2021 Jan 26]. Available from: https://scholarworks.umass.edu/open_access_dissertations/360.

Council of Science Editors:

Izadi H. Innate immune responses to B. burgdorferi mediated by JNK1 and the cochaperone, methylation controlled DNAJ (MCJ). [Doctoral Dissertation]. U of Massachusetts : PhD; 2011. Available from: https://scholarworks.umass.edu/open_access_dissertations/360

Temple University

17. Pozniak, Paul Daniel. TNF-alpha-Induced Neuroregeneration through an NF-kappaB-dependent Pathway: A New Mechanism Involving EphB2 in the Context of HIV-1 Neuroinflammation.

Degree: PhD, 2016, Temple University

URL: http://digital.library.temple.edu/u?/p245801coll10,386002

►

Biomedical Neuroscience

The use of highly active antiretroviral therapy (HAART) has significantly decreased the mortality rate of HIV-1 patients, however the increased survival has led… (more)

▼

Biomedical Neuroscience

The use of highly active antiretroviral therapy (HAART) has significantly decreased the mortality rate of HIV-1 patients, however the increased survival has led to the development of complications associated with the persistence of the viral infection. Nearly half of HIV-1-infected individuals develop HIV-associated neurocognitive disorders (HAND) as the effects of the chronic infection leads to neuronal injury and synaptic loss in the central nervous system (CNS). The neurotoxicity of HIV-1 has largely been attributed to the inflammation caused by viral replication and the altered signaling of astrocytes, microglia, and macrophages. Although HAART has improved the control of viral replication, the effects from inflammation remain a concern, particularly those of the pro-inflammatory cytokine, tumor necrosis factor alpha (TNF-α). TNF-α has been a therapeutic target for other diseases associated with chronic inflammation, such as rheumatoid arthritis, but emerging evidence has suggested that TNF-α signaling can have a dual role, especially in the CNS, proving the complexity in the modulation of the TNF-α pathway. Although the detrimental effects of TNF-α have been well-characterized, we lack a complete understanding of the beneficial role of TNF-α. TNF-α signaling has largely been considered to be neurotoxic but has been able to regulate neurite outgrowth in the context of neural development. Since TNF-α is upregulated in various neurodegenerative conditions, we considered potential outcomes of TNF-α on neurite outgrowth following injury. Initially, most would assume that TNF-α would prevent neurite outgrowth as apoptosis is a common outcome of TNF-α-induced signaling. If TNF-α signaling strictly prevents neurite outgrowth, anti-TNFα therapies could be considered to reverse this effect. However, upon induced injury, we observed an increase in neurite regrowth following induced injury in human primary fetal neurons, demonstrating a strong need for a deeper understanding of this dual role of TNF-α. Anti-TNF-α therapies have been considered for HIV-1-infected patients to reduce the chronic inflammation, however inhibiting TNF-α signaling could have side-effects that could prevent neuronal recovery from HIV-1 effects. Targeting pathways downstream of TNF-α signaling would be more advantageous to mediate the beneficial role of TNF-α in the CNS. We investigated the transcriptional effects of TNF-α treatment on neurons to uncover a potential pathway to promote neurite outgrowth. One pathway we have discovered to be beneficial in primary human fetal neurons is TNF-α-induced Ephrin B2 upregulation. Ephrin B2 (EphB2) receptors are important mediators of neuronal development and synaptic plasticity, however little has been established in regards to their role in HIV and inflammation, particularly in the CNS. EphB2 can mediate axonal development by providing retractive cues to assist the axon to reach the target, but EphB2 can also promote dendritic branching to improve learning and memory, which would…

Advisors/Committee Members: Khalili, Kamel;, Gordon, Jennifer, Ph.D., Hu, Wenhui, Langford, Dianne, Smith, George M., Wigdahl, Brian;.

Subjects/Keywords: Neurosciences;

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

APA (6^th Edition):

Pozniak, P. D. (2016). TNF-alpha-Induced Neuroregeneration through an NF-kappaB-dependent Pathway: A New Mechanism Involving EphB2 in the Context of HIV-1 Neuroinflammation. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,386002

Chicago Manual of Style (16^th Edition):

Pozniak, Paul Daniel. “TNF-alpha-Induced Neuroregeneration through an NF-kappaB-dependent Pathway: A New Mechanism Involving EphB2 in the Context of HIV-1 Neuroinflammation.” 2016. Doctoral Dissertation, Temple University. Accessed January 26, 2021. http://digital.library.temple.edu/u?/p245801coll10,386002.

MLA Handbook (7^th Edition):

Pozniak, Paul Daniel. “TNF-alpha-Induced Neuroregeneration through an NF-kappaB-dependent Pathway: A New Mechanism Involving EphB2 in the Context of HIV-1 Neuroinflammation.” 2016. Web. 26 Jan 2021.

Vancouver:

Pozniak PD. TNF-alpha-Induced Neuroregeneration through an NF-kappaB-dependent Pathway: A New Mechanism Involving EphB2 in the Context of HIV-1 Neuroinflammation. [Internet] [Doctoral dissertation]. Temple University; 2016. [cited 2021 Jan 26]. Available from: http://digital.library.temple.edu/u?/p245801coll10,386002.

Council of Science Editors:

Pozniak PD. TNF-alpha-Induced Neuroregeneration through an NF-kappaB-dependent Pathway: A New Mechanism Involving EphB2 in the Context of HIV-1 Neuroinflammation. [Doctoral Dissertation]. Temple University; 2016. Available from: http://digital.library.temple.edu/u?/p245801coll10,386002

Universidade do Rio Grande do Norte

18. Carvalho, Fabiana Maria Coimbra de. Efeito anti-inflamatório de proteínas sacietogênicas da semente de tamarindo em modelo experimental de síndrome metabólica .

Degree: 2016, Universidade do Rio Grande do Norte

URL: http://repositorio.ufrn.br/handle/123456789/21674

► Trypsin inhibitors are studied in a variety of models for their anti-obesity and anti-inflammatory bioactive properties. Our group has previously demonstrated the satietogenic effect of… (more)

Subjects/Keywords: Obesidade; Dieta de cafeteria; TNF-α; Glicemia

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

APA (6^th Edition):

Carvalho, F. M. C. d. (2016). Efeito anti-inflamatório de proteínas sacietogênicas da semente de tamarindo em modelo experimental de síndrome metabólica . (Masters Thesis). Universidade do Rio Grande do Norte. Retrieved from http://repositorio.ufrn.br/handle/123456789/21674

Chicago Manual of Style (16^th Edition):

Carvalho, Fabiana Maria Coimbra de. “Efeito anti-inflamatório de proteínas sacietogênicas da semente de tamarindo em modelo experimental de síndrome metabólica .” 2016. Masters Thesis, Universidade do Rio Grande do Norte. Accessed January 26, 2021. http://repositorio.ufrn.br/handle/123456789/21674.

MLA Handbook (7^th Edition):

Carvalho, Fabiana Maria Coimbra de. “Efeito anti-inflamatório de proteínas sacietogênicas da semente de tamarindo em modelo experimental de síndrome metabólica .” 2016. Web. 26 Jan 2021.

Vancouver:

Carvalho FMCd. Efeito anti-inflamatório de proteínas sacietogênicas da semente de tamarindo em modelo experimental de síndrome metabólica . [Internet] [Masters thesis]. Universidade do Rio Grande do Norte; 2016. [cited 2021 Jan 26]. Available from: http://repositorio.ufrn.br/handle/123456789/21674.

Council of Science Editors:

Carvalho FMCd. Efeito anti-inflamatório de proteínas sacietogênicas da semente de tamarindo em modelo experimental de síndrome metabólica . [Masters Thesis]. Universidade do Rio Grande do Norte; 2016. Available from: http://repositorio.ufrn.br/handle/123456789/21674

19. Papazian, Irini. Μελέτη του ρόλου του διαλυτού και διαμεμβρανικού TNF κατά την παθολογία του ΚΝΣ.

Degree: 2019, National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ)

URL: http://hdl.handle.net/10442/hedi/45595

► TNF is a member of a large family of cytokines and has multiple roles in the CNS. Regulated TNF production is necessary for successful host… (more)

▼ TNF is a member of a large family of cytokines and has multiple roles in the CNS. Regulated TNF production is necessary for successful host defense responses against infection and for tissue repair mechanisms. On the other hand, deregulation of TNF production and molecular signaling leads to chronic inflammation and immune activation, which can lead to autoimmunity. Increased TNF levels have been associated with inflammatory autoimmune diseases, including neurodegenerative CNS disorders such as multiple sclerosis (MS). However, while TNF inhibitors are blockbuster drugs for chronic immune diseases in the periphery, such as rheumatoid arthritis, they exacerbate disease in MS patients, induce de novo demyelination in patients treated for other diseases, and even cause MS. These clinical data clearly show that TNF has overall beneficial effects in the CNS. In experimental models for MS, TNF receptor 1 (TNFR1) mediates the detrimental pro- inflammatory effects of soluble TNF (solTNF), whereas TNFR2 and transmembrane TNF (tmTNF) are essential for beneficial effects, mainly in myelin maintenance and repair. This mechanistic framework supports the use of novel selective inhibitors of solTNF and/or TNFR1, or TNFR2 agonists, for safer therapy of chronic inflammatory diseases including those of the CNS. A potential obstacle to such an approach is substantial evidence that TNF has neuroprotective effects against a wide variety of oxidative and excitotoxic stimuli when used to pretreat cultured neurons, and that protection involves both TNFR1 and TNFR2. However, the relevance of these effects for CNS protection in vivo have yet to be proven and is this subject of this thesis. In a separate line of investigation, previous studies in our lab show that, similar to TNF, conditioned medium from MSC has neuroprotective effects against glutamate excitotoxicity when used to pretreat cultured neurons. MSC provide therapeutic effects in experimental CNS disease models and therefore show promise as cell-based therapies for humans. However, their modes of action, and whether TNF is secreted and involved in their neuroprotection, need to be elucidated. To address the questions described above, we used a genetic approach, combining mice with conventionally and conditionally targeted genes for TNF and its receptors, with an in vitro of glutamate excitotoxicity and in vivo models for multiple sclerosis. Glutamate, and specifically NMDA excitotoxicity, was used because it is directly relevant for neuronal death in a wide variety of neurodegenerative disorders including MS. The NMDA, AMPA and kainate receptors belong to the family of ionotropic glutamate receptors and bind glutamate, which is the major excitatory neurotransmitter in the mammalian CNS. Under certain conditions, dysregulated glutamate function can lead to pathology. High levels of glutamate are toxic for neurons and induce so-called excitotoxic death resulting from increased calcium influx into the cell via the NMDA receptors. First the neuroprotective function of TNF against…

Subjects/Keywords: TNF υποδοχείς; TNF; Νευροεκφυλισμός; Νευροπροστασία; Σκλήρυνση κατά πλάκας; Γλουταμινικοί υποδοχείς; Απομυελίνωση απο κουπριζόνη; Πειραματική αυτοάνοση εγκεφαλομυελίτιδα; TNF receptors; TNF; Neurodegeneration; Neuroprotection; Multiple sclerosis; Glutamate receptors; Cuprizone model; Experimental autoimmune encephalomyelitis

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

APA (6^th Edition):

Papazian, I. (2019). Μελέτη του ρόλου του διαλυτού και διαμεμβρανικού TNF κατά την παθολογία του ΚΝΣ. (Thesis). National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ). Retrieved from http://hdl.handle.net/10442/hedi/45595

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):

Papazian, Irini. “Μελέτη του ρόλου του διαλυτού και διαμεμβρανικού TNF κατά την παθολογία του ΚΝΣ.” 2019. Thesis, National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ). Accessed January 26, 2021. http://hdl.handle.net/10442/hedi/45595.

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

MLA Handbook (7^th Edition):

Papazian, Irini. “Μελέτη του ρόλου του διαλυτού και διαμεμβρανικού TNF κατά την παθολογία του ΚΝΣ.” 2019. Web. 26 Jan 2021.

Vancouver:

Papazian I. Μελέτη του ρόλου του διαλυτού και διαμεμβρανικού TNF κατά την παθολογία του ΚΝΣ. [Internet] [Thesis]. National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ); 2019. [cited 2021 Jan 26]. Available from: http://hdl.handle.net/10442/hedi/45595.

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

Council of Science Editors:

Papazian I. Μελέτη του ρόλου του διαλυτού και διαμεμβρανικού TNF κατά την παθολογία του ΚΝΣ. [Thesis]. National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ); 2019. Available from: http://hdl.handle.net/10442/hedi/45595

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

Vanderbilt University

20. Hilliard, Valda Catherine. TNF-alpha converting enzyme-dependent ErbB4 transactivation by TNF promotes colonic epithelial cell survival.

Degree: PhD, Cell and Developmental Biology, 2011, Vanderbilt University

URL: http://hdl.handle.net/1803/13315

► Disruption of intestinal epithelial homeostasis, including enhanced apoptosis, is a hallmark of inflammatory bowel disease (IBD). We have shown that tumor necrosis factor (TNF) increases… (more)

Subjects/Keywords: colon; ADAM17; TACE; TNF; ErbB4; apoptosis

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APA (6^th Edition):

Hilliard, V. C. (2011). TNF-alpha converting enzyme-dependent ErbB4 transactivation by TNF promotes colonic epithelial cell survival. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/13315

Chicago Manual of Style (16^th Edition):

Hilliard, Valda Catherine. “TNF-alpha converting enzyme-dependent ErbB4 transactivation by TNF promotes colonic epithelial cell survival.” 2011. Doctoral Dissertation, Vanderbilt University. Accessed January 26, 2021. http://hdl.handle.net/1803/13315.

MLA Handbook (7^th Edition):

Hilliard, Valda Catherine. “TNF-alpha converting enzyme-dependent ErbB4 transactivation by TNF promotes colonic epithelial cell survival.” 2011. Web. 26 Jan 2021.

Vancouver:

Hilliard VC. TNF-alpha converting enzyme-dependent ErbB4 transactivation by TNF promotes colonic epithelial cell survival. [Internet] [Doctoral dissertation]. Vanderbilt University; 2011. [cited 2021 Jan 26]. Available from: http://hdl.handle.net/1803/13315.

Council of Science Editors:

Hilliard VC. TNF-alpha converting enzyme-dependent ErbB4 transactivation by TNF promotes colonic epithelial cell survival. [Doctoral Dissertation]. Vanderbilt University; 2011. Available from: http://hdl.handle.net/1803/13315

University of Saskatchewan

21. Brymer, Kyle Jordan 1991-. Examining the Antidepressant Potential of TNF-alpha and Reelin on Associated Behavioural and Neurobiological Markers in a Preclinical Model of Depression.

Degree: 2019, University of Saskatchewan

URL: http://hdl.handle.net/10388/12264

► Depression is a debilitating psychiatric disorder affecting approximately 10% of the world’s population. Cognitive dysfunction is an often ignored aspect of depression, and predicts patient… (more)

▼ Depression is a debilitating psychiatric disorder affecting approximately 10% of the world’s population. Cognitive dysfunction is an often ignored aspect of depression, and predicts patient response to antidepressants. While several classes of antidepressants have been developed for the treatment of depression, over one-third of patients do not respond to conventional antidepressants, and all currently available antidepressants require weeks of continuous administration to achieve therapeutic effects. The delay in the onset of therapeutic effects from the time of taking antidepressants can put patients at risk for suicide. Therefore, there is a need in the literature to develop and identify novel antidepressants that do not work on conventional targets and that have fast-acting properties. The primary goals of this dissertation were to investigate the pattern of cognitive impairments following CORT treatment and to examine the antidepressant potential of TNF-α receptor inhibition and reelin. To begin, in Chapter 2, I examined the effect of repeated CORT injections on depression-like behaviour using the forced swim test, the object-location, object-in-place, and object-recognition memory tests, and sensorimotor gating using prepulse inhibition. These data suggested that CORT increases depression-like behaviour while simultaneously impairing hippocampal and prefrontal cortex-dependent memory and sensorimotor gating. In Chapter 3, I examined the effects of the TNF-α inhibitor etanercept on CORT induced depression-like behaviour, cognition, and markers of synaptic plasticity through post-mortem analysis of brain tissue. I found that CORT increased depression-like behaviour on the forced swim test and impaired object memory. CORT also impaired several post-mortem markers of hippocampal plasticity, and etanercept restored these measures back to control levels. In Chapter 4 I examined the antidepressant potential of intrahippocampal reelin infusions and its effects on cognition and markers of synaptic plasticity. I found CORT treatment increased depression-like behaviour on the forced swim test and impaired object memory. Reelin treatment restored both of these measures back to control levels within one day. CORT also decreased markers of hippocampal plasticity, and reelin restored these measures back to control levels. Finally, in Chapter 5, I examined the contribution of AMPA signaling to the antidepressant effects of reelin. I found that infusion of the AMPA antagonist CNQX blocked reelin’s antidepressant effects on the forced swim test, without altering CORT’s pattern of changes on markers of hippocampal plasticity. The results of this dissertation reveal novel compounds with antidepressant properties that warrant further investigation into their potential use in humans Advisors/Committee Members: Kalynchuk, Lisa E, Caruncho, Hector J, Paterson, Phyllis, Cummings, Jorden, Hunter, Paulette.

Subjects/Keywords: Stress; Depression; Reelin; TNF; Neurogenesis; Glutamate

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APA (6^th Edition):

Brymer, K. J. 1. (2019). Examining the Antidepressant Potential of TNF-alpha and Reelin on Associated Behavioural and Neurobiological Markers in a Preclinical Model of Depression. (Thesis). University of Saskatchewan. Retrieved from http://hdl.handle.net/10388/12264

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):

Brymer, Kyle Jordan 1991-. “Examining the Antidepressant Potential of TNF-alpha and Reelin on Associated Behavioural and Neurobiological Markers in a Preclinical Model of Depression.” 2019. Thesis, University of Saskatchewan. Accessed January 26, 2021. http://hdl.handle.net/10388/12264.

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

MLA Handbook (7^th Edition):

Brymer, Kyle Jordan 1991-. “Examining the Antidepressant Potential of TNF-alpha and Reelin on Associated Behavioural and Neurobiological Markers in a Preclinical Model of Depression.” 2019. Web. 26 Jan 2021.

Vancouver:

Brymer KJ1. Examining the Antidepressant Potential of TNF-alpha and Reelin on Associated Behavioural and Neurobiological Markers in a Preclinical Model of Depression. [Internet] [Thesis]. University of Saskatchewan; 2019. [cited 2021 Jan 26]. Available from: http://hdl.handle.net/10388/12264.

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

Council of Science Editors:

Brymer KJ1. Examining the Antidepressant Potential of TNF-alpha and Reelin on Associated Behavioural and Neurobiological Markers in a Preclinical Model of Depression. [Thesis]. University of Saskatchewan; 2019. Available from: http://hdl.handle.net/10388/12264

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

Boston University

22. Bhambhani, Vijeta. Micro-RNA mediated regulation of a cytokine factor: TNF-alpha: an exploration of gene expression control in proliferating and quiescent cells.

Degree: MS, Medical Sciences, 2015, Boston University

URL: http://hdl.handle.net/2144/16241

► Two types mechanisms that control gene expression involve cis-regulatory factors and trans-regulatory factors. Cis-acting regulatory RNAs include targeted messenger RNA (mRNA) specificity and AU-rich elements… (more)

Subjects/Keywords: Biology; eIF5B; FXR1; miRNA; TNF-alpha; Translation

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APA (6^th Edition):

Bhambhani, V. (2015). Micro-RNA mediated regulation of a cytokine factor: TNF-alpha: an exploration of gene expression control in proliferating and quiescent cells. (Masters Thesis). Boston University. Retrieved from http://hdl.handle.net/2144/16241

Chicago Manual of Style (16^th Edition):

Bhambhani, Vijeta. “Micro-RNA mediated regulation of a cytokine factor: TNF-alpha: an exploration of gene expression control in proliferating and quiescent cells.” 2015. Masters Thesis, Boston University. Accessed January 26, 2021. http://hdl.handle.net/2144/16241.

MLA Handbook (7^th Edition):

Bhambhani, Vijeta. “Micro-RNA mediated regulation of a cytokine factor: TNF-alpha: an exploration of gene expression control in proliferating and quiescent cells.” 2015. Web. 26 Jan 2021.

Vancouver:

Bhambhani V. Micro-RNA mediated regulation of a cytokine factor: TNF-alpha: an exploration of gene expression control in proliferating and quiescent cells. [Internet] [Masters thesis]. Boston University; 2015. [cited 2021 Jan 26]. Available from: http://hdl.handle.net/2144/16241.

Council of Science Editors:

Bhambhani V. Micro-RNA mediated regulation of a cytokine factor: TNF-alpha: an exploration of gene expression control in proliferating and quiescent cells. [Masters Thesis]. Boston University; 2015. Available from: http://hdl.handle.net/2144/16241

University of Toronto

23. Wong, Aaron. Dissecting The Role Of TNFα In Kawasaki Disease: Alteration Of Cell Fate By TNFα After Superantigen Activation.

Degree: 2011, University of Toronto

URL: http://hdl.handle.net/1807/31634

►

Kawasaki disease (KD) is an acute inflammatory disease characterized by persistent inflammation of the coronary arteries. KD is characterized by the release of cytokines such… (more)

Subjects/Keywords: Kawasaki Disease; TNF; Superantigen; apoptosis; 0982; 0379

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APA (6^th Edition):

Wong, A. (2011). Dissecting The Role Of TNFα In Kawasaki Disease: Alteration Of Cell Fate By TNFα After Superantigen Activation. (Masters Thesis). University of Toronto. Retrieved from http://hdl.handle.net/1807/31634

Chicago Manual of Style (16^th Edition):

Wong, Aaron. “Dissecting The Role Of TNFα In Kawasaki Disease: Alteration Of Cell Fate By TNFα After Superantigen Activation.” 2011. Masters Thesis, University of Toronto. Accessed January 26, 2021. http://hdl.handle.net/1807/31634.

MLA Handbook (7^th Edition):

Wong, Aaron. “Dissecting The Role Of TNFα In Kawasaki Disease: Alteration Of Cell Fate By TNFα After Superantigen Activation.” 2011. Web. 26 Jan 2021.

Vancouver:

Wong A. Dissecting The Role Of TNFα In Kawasaki Disease: Alteration Of Cell Fate By TNFα After Superantigen Activation. [Internet] [Masters thesis]. University of Toronto; 2011. [cited 2021 Jan 26]. Available from: http://hdl.handle.net/1807/31634.

Council of Science Editors:

Wong A. Dissecting The Role Of TNFα In Kawasaki Disease: Alteration Of Cell Fate By TNFα After Superantigen Activation. [Masters Thesis]. University of Toronto; 2011. Available from: http://hdl.handle.net/1807/31634

Universidade Nova

24. Raposeiro, Rita Maria Mendes. Osteoclast activity in ankylosing spondylitis patients before and after TNF-blocking therapy.

Degree: 2014, Universidade Nova

URL: http://www.rcaap.pt/detail.jsp?id=oai:run.unl.pt:10362/13804

► Ankylosing spondylitis (AS) is a chronic inflammatory rheumatic disease of the axial skeleton. The major outcome of this disease is defined by new bone formation,… (more)

Subjects/Keywords: Ankylosing spondylitis; Inflammation; Osteoclastogenesis; TNF-blocking therapy

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APA (6^th Edition):

Raposeiro, R. M. M. (2014). Osteoclast activity in ankylosing spondylitis patients before and after TNF-blocking therapy. (Thesis). Universidade Nova. Retrieved from http://www.rcaap.pt/detail.jsp?id=oai:run.unl.pt:10362/13804

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):

Raposeiro, Rita Maria Mendes. “Osteoclast activity in ankylosing spondylitis patients before and after TNF-blocking therapy.” 2014. Thesis, Universidade Nova. Accessed January 26, 2021. http://www.rcaap.pt/detail.jsp?id=oai:run.unl.pt:10362/13804.

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

MLA Handbook (7^th Edition):

Raposeiro, Rita Maria Mendes. “Osteoclast activity in ankylosing spondylitis patients before and after TNF-blocking therapy.” 2014. Web. 26 Jan 2021.

Vancouver:

Raposeiro RMM. Osteoclast activity in ankylosing spondylitis patients before and after TNF-blocking therapy. [Internet] [Thesis]. Universidade Nova; 2014. [cited 2021 Jan 26]. Available from: http://www.rcaap.pt/detail.jsp?id=oai:run.unl.pt:10362/13804.

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

Council of Science Editors:

Raposeiro RMM. Osteoclast activity in ankylosing spondylitis patients before and after TNF-blocking therapy. [Thesis]. Universidade Nova; 2014. Available from: http://www.rcaap.pt/detail.jsp?id=oai:run.unl.pt:10362/13804

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

25. Moriya, Takashi; Kitamori, Kazuya; Naito, Hisao; Yanagiba, Yukie; Ito, Yuki; Yamagishi, Nozomi; Tamada, Hazuki; Jia, Xiaofang; Tsuchikura, Satoru; Ikeda, Katsumi; Yamori, Yukio. Simultaneous changes in high-fat and high-cholesterol diet-induced steatohepatitis and severe fibrosis and those underlying molecular mechanisms in novel SHRSP5/Dmcr rat.

Degree: 2018, Nagoya University / 名古屋大学

URL: http://hdl.handle.net/2237/16803

►

Objectives: The aim of this study was to identify the molecular mechanisms underlying high-fat and high-cholesterol (HFC) diet-induced steatohepatitis and associated liver fibrosis progression in… (more)

▼

Objectives: The aim of this study was to identify the molecular mechanisms underlying high-fat and high-cholesterol (HFC) diet-induced steatohepatitis and associated liver fibrosis progression in a novel stroke-prone, spontaneously hypertensive 5/Dmcr (SHRSP5/Dmcr) rat model. Methods: SHRSP5/Dmcr rats were given the control or HFC-diet for 2, 8, and 16 weeks. Plasma and hepatic gene expression of key molecules involved in fatty acid oxidation, inflammation, oxidative stress, and fibrosis were subsequently analyzed. Results: Rats fed the HFC-diet showed increased plasma tumor necrosis factor-α (TNF-α) and hepatic p50/p65 signals, but reduced hepatic Cu2+/Zn2+-superoxide dismutase across the treatment period and reduced plasma total adiponectin at 8 weeks. In HFC-diet-fed rats, transforming growth factor-β1 (TGF-β1) was elevated prior to the appearance of obvious liver fibrosis pathology at 2 weeks, followed by elevations in platelet-derived growth factor-B (PDGF-B) and α-smooth muscle actin (α-SMA), corresponding to evident liver fibrosis, at 8 weeks and by α1 type I collagen production at 16 weeks. The HFC-diet increased hepatic total cholesterol accumulation, although hepatic triglyceride declined by 0.3-fold from 2 to 16 weeks due to reduced hepatic triglyceride synthesis, as suggested by the diacylglycerol acyltransferase 1 and 2 measurements. Conclusions: TNF-α and p50/p65 molecular signals appeared to be major factors for HFC-diet-induced hepatic inflammation and oxidative stress facilitating liver disease progression. While the up-regulation of TGF-β1 prior to the appearance of any evident liver fibrosis could be an early signal for progressive liver fibrosis, elevated PDGF-B and α-SMA levels signified evident liver fibrosis at 8 weeks, and subsequent increased α1 type I collagen production and reduced triglyceride synthesis indicated extensive liver fibrosis at 16 weeks in this novel SHRSP5/Dmcr model.

名古屋大学博士学位論文学位の種類 : 博士(医学)(課程) 学位授与年月日:平成24年4月27日森谷隆氏の博士論文として提出された

First published online: 2012-03-10

Subjects/Keywords: Steatohepatitis; Inflammation; TNF-α; NF-κb; Fibrosis

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APA (6^th Edition):

Moriya, Takashi; Kitamori, Kazuya; Naito, Hisao; Yanagiba, Yukie; Ito, Yuki; Yamagishi, Nozomi; Tamada, Hazuki; Jia, Xiaofang; Tsuchikura, Satoru; Ikeda, Katsumi; Yamori, Y. (2018). Simultaneous changes in high-fat and high-cholesterol diet-induced steatohepatitis and severe fibrosis and those underlying molecular mechanisms in novel SHRSP5/Dmcr rat. (Thesis). Nagoya University / 名古屋大学. Retrieved from http://hdl.handle.net/2237/16803

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):

Moriya, Takashi; Kitamori, Kazuya; Naito, Hisao; Yanagiba, Yukie; Ito, Yuki; Yamagishi, Nozomi; Tamada, Hazuki; Jia, Xiaofang; Tsuchikura, Satoru; Ikeda, Katsumi; Yamori, Yukio. “Simultaneous changes in high-fat and high-cholesterol diet-induced steatohepatitis and severe fibrosis and those underlying molecular mechanisms in novel SHRSP5/Dmcr rat.” 2018. Thesis, Nagoya University / 名古屋大学. Accessed January 26, 2021. http://hdl.handle.net/2237/16803.

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

MLA Handbook (7^th Edition):

Moriya, Takashi; Kitamori, Kazuya; Naito, Hisao; Yanagiba, Yukie; Ito, Yuki; Yamagishi, Nozomi; Tamada, Hazuki; Jia, Xiaofang; Tsuchikura, Satoru; Ikeda, Katsumi; Yamori, Yukio. “Simultaneous changes in high-fat and high-cholesterol diet-induced steatohepatitis and severe fibrosis and those underlying molecular mechanisms in novel SHRSP5/Dmcr rat.” 2018. Web. 26 Jan 2021.

Vancouver:

Moriya, Takashi; Kitamori, Kazuya; Naito, Hisao; Yanagiba, Yukie; Ito, Yuki; Yamagishi, Nozomi; Tamada, Hazuki; Jia, Xiaofang; Tsuchikura, Satoru; Ikeda, Katsumi; Yamori Y. Simultaneous changes in high-fat and high-cholesterol diet-induced steatohepatitis and severe fibrosis and those underlying molecular mechanisms in novel SHRSP5/Dmcr rat. [Internet] [Thesis]. Nagoya University / 名古屋大学; 2018. [cited 2021 Jan 26]. Available from: http://hdl.handle.net/2237/16803.

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

Council of Science Editors:

Moriya, Takashi; Kitamori, Kazuya; Naito, Hisao; Yanagiba, Yukie; Ito, Yuki; Yamagishi, Nozomi; Tamada, Hazuki; Jia, Xiaofang; Tsuchikura, Satoru; Ikeda, Katsumi; Yamori Y. Simultaneous changes in high-fat and high-cholesterol diet-induced steatohepatitis and severe fibrosis and those underlying molecular mechanisms in novel SHRSP5/Dmcr rat. [Thesis]. Nagoya University / 名古屋大学; 2018. Available from: http://hdl.handle.net/2237/16803

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

26. Teixeira, Chantelle Simões Leite. TNF-alfa e metabolismo do adipócito.

Degree: 2015, RCAAP

URL: https://www.rcaap.pt/detail.jsp?id=oai:comum.rcaap.pt:10400.26/10984

►

Dissertação para obtenção do grau de Mestre no Instituto Superior de Ciências da Saúde Egas Moniz

A prevalência da obesidade tem vindo a aumentar ao… (more)

Subjects/Keywords: Obesidade; Tecido adiposo; TNF-α; Adipócito

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APA (6^th Edition):

Teixeira, C. S. L. (2015). TNF-alfa e metabolismo do adipócito. (Thesis). RCAAP. Retrieved from https://www.rcaap.pt/detail.jsp?id=oai:comum.rcaap.pt:10400.26/10984

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):

Teixeira, Chantelle Simões Leite. “TNF-alfa e metabolismo do adipócito.” 2015. Thesis, RCAAP. Accessed January 26, 2021. https://www.rcaap.pt/detail.jsp?id=oai:comum.rcaap.pt:10400.26/10984.

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

MLA Handbook (7^th Edition):

Teixeira, Chantelle Simões Leite. “TNF-alfa e metabolismo do adipócito.” 2015. Web. 26 Jan 2021.

Vancouver:

Teixeira CSL. TNF-alfa e metabolismo do adipócito. [Internet] [Thesis]. RCAAP; 2015. [cited 2021 Jan 26]. Available from: https://www.rcaap.pt/detail.jsp?id=oai:comum.rcaap.pt:10400.26/10984.

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

Council of Science Editors:

Teixeira CSL. TNF-alfa e metabolismo do adipócito. [Thesis]. RCAAP; 2015. Available from: https://www.rcaap.pt/detail.jsp?id=oai:comum.rcaap.pt:10400.26/10984

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

27. Bumdelger, Batmunkh. Induction of Timp1 in Smooth Muscle Cells during Development of Abdominal Aortic Aneurysms : 腹部大動脈瘤形成における、平滑筋細胞でのTimp1遺伝子誘導.

Degree: 博士(医学), 2014, Hiroshima University / 広島大学

URL: http://ir.lib.hiroshima-u.ac.jp/00036323

► Abdominal aortic aneurysm (AAA) is known to develop mainly by the increased diameter of aorta through metalloproteinases (MMPs). Although activities of MMPs are tightly regulated… (more)

Subjects/Keywords: Abdominal aortic aneurysm; Mmp9; Timp1; TNF-α

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APA (6^th Edition):

Bumdelger, B. (2014). Induction of Timp1 in Smooth Muscle Cells during Development of Abdominal Aortic Aneurysms : 腹部大動脈瘤形成における、平滑筋細胞でのTimp1遺伝子誘導. (Thesis). Hiroshima University / 広島大学. Retrieved from http://ir.lib.hiroshima-u.ac.jp/00036323

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):

Bumdelger, Batmunkh. “Induction of Timp1 in Smooth Muscle Cells during Development of Abdominal Aortic Aneurysms : 腹部大動脈瘤形成における、平滑筋細胞でのTimp1遺伝子誘導.” 2014. Thesis, Hiroshima University / 広島大学. Accessed January 26, 2021. http://ir.lib.hiroshima-u.ac.jp/00036323.

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

MLA Handbook (7^th Edition):

Bumdelger, Batmunkh. “Induction of Timp1 in Smooth Muscle Cells during Development of Abdominal Aortic Aneurysms : 腹部大動脈瘤形成における、平滑筋細胞でのTimp1遺伝子誘導.” 2014. Web. 26 Jan 2021.

Vancouver:

Bumdelger B. Induction of Timp1 in Smooth Muscle Cells during Development of Abdominal Aortic Aneurysms : 腹部大動脈瘤形成における、平滑筋細胞でのTimp1遺伝子誘導. [Internet] [Thesis]. Hiroshima University / 広島大学; 2014. [cited 2021 Jan 26]. Available from: http://ir.lib.hiroshima-u.ac.jp/00036323.

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

Council of Science Editors:

Bumdelger B. Induction of Timp1 in Smooth Muscle Cells during Development of Abdominal Aortic Aneurysms : 腹部大動脈瘤形成における、平滑筋細胞でのTimp1遺伝子誘導. [Thesis]. Hiroshima University / 広島大学; 2014. Available from: http://ir.lib.hiroshima-u.ac.jp/00036323

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

Univerzitet u Beogradu

28. Poluga, Jasmina L., 1963-. Odnos koncentracije proinflamatornih citokina u serumu i kliničkih, parazitoloških i hematoloških promena u toku importovane malarije.

Degree: Medicinski fakultet, 2013, Univerzitet u Beogradu

URL: https://fedorabg.bg.ac.rs/fedora/get/o:5550/bdef:Content/get

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Infektivne bolesti - malarija / Infectious diseases - malaria

REZIME: Malarija je multisistemska, potencijalno letalna bolest uzrokovana parazitima roda Plasmodium. Dokazano je da kod malarije… (more)

Subjects/Keywords: malaria; cytokines; parasitemia; thrombocytopenia; TNF- ; IL-6

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

APA (6^th Edition):

Poluga, Jasmina L., 1. (2013). Odnos koncentracije proinflamatornih citokina u serumu i kliničkih, parazitoloških i hematoloških promena u toku importovane malarije. (Thesis). Univerzitet u Beogradu. Retrieved from https://fedorabg.bg.ac.rs/fedora/get/o:5550/bdef:Content/get

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):

Poluga, Jasmina L., 1963-. “Odnos koncentracije proinflamatornih citokina u serumu i kliničkih, parazitoloških i hematoloških promena u toku importovane malarije.” 2013. Thesis, Univerzitet u Beogradu. Accessed January 26, 2021. https://fedorabg.bg.ac.rs/fedora/get/o:5550/bdef:Content/get.

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

MLA Handbook (7^th Edition):

Poluga, Jasmina L., 1963-. “Odnos koncentracije proinflamatornih citokina u serumu i kliničkih, parazitoloških i hematoloških promena u toku importovane malarije.” 2013. Web. 26 Jan 2021.

Vancouver:

Poluga, Jasmina L. 1. Odnos koncentracije proinflamatornih citokina u serumu i kliničkih, parazitoloških i hematoloških promena u toku importovane malarije. [Internet] [Thesis]. Univerzitet u Beogradu; 2013. [cited 2021 Jan 26]. Available from: https://fedorabg.bg.ac.rs/fedora/get/o:5550/bdef:Content/get.

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

Council of Science Editors:

Poluga, Jasmina L. 1. Odnos koncentracije proinflamatornih citokina u serumu i kliničkih, parazitoloških i hematoloških promena u toku importovane malarije. [Thesis]. Univerzitet u Beogradu; 2013. Available from: https://fedorabg.bg.ac.rs/fedora/get/o:5550/bdef:Content/get

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

Univerzitet u Beogradu

29. Vuković-Petrović, Irena, 1988- 21801063. Ekspresija gena i proteina koji regulišu autofagiju u mononuklearnim ćelijama periferne krvi pacijenata sa multiplom sklerozom.

Degree: Medicinski fakultet, 2019, Univerzitet u Beogradu

URL: https://fedorabg.bg.ac.rs/fedora/get/o:19959/bdef:Content/get

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Medicina - Molekularna medicina / Medicine - Molecular medicine

Uvod: Multipla skleroza (MS) je hronična inflamatorna bolest centralnog nervnog sistema (CNS) u kojoj infiltracija limfocitima… (more)

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Medicina - Molekularna medicina / Medicine - Molecular medicine

Uvod: Multipla skleroza (MS) je hronična inflamatorna bolest centralnog nervnog sistema (CNS) u kojoj infiltracija limfocitima dovodi do oštećenja mijelina i aksona. Autofagija, proces kontrolisane auto-digestije koji reguliše homeostazu ćelije, važan je u urođenoj i adaptivnoj imunosti. Uloga autofagije nije do sada detaljno izučavana u različitim populacijama limfocita u MS. Ciljevi istraživanja: Ispitati ekspresiju gena za regulatore autofagije (ATG7, ATG10, ATG5, ATG4B, ATG3, ATG13, ATG8A, ATG14, SQSTM1, BCL2, ULK1, BNIP3, FOXO1, FOXO3, VPS34, BECN1, ATF4) i proinflamatorne citokine (TNF, IFN-γ, IL-17 i GM-CSF), kao i aktivnost autofagije u mononuklearnim ćelijama periferne krvi (MNĆPK) i različitim populacijama limfocita pacijenata sa MS i kontrolnih ispitanika. Pacijenti i metode: Naša studija je uključila novoobolele pacijente sa MS, dijagnostikovane prema McDonald-ovim kriterijumima (2001.), koji u trenutku uzimanja uzorka nisu bili uključeni ni u jedan terapijski protokol. Koristeći kvantitativni PCR u realnom vremenu ispitali smo ekspresiju gena koji regulišu autofagiju i ekspresiju gena za proinflamatorne citokine u MNĆPK i CD3+CD4+ T-limfocitima, CD3+CD4- Tlimfocitima i CD3-CD19+B-limfocitima pacijenata sa MS i kontrola. Takođe smo analizirali aktivnost bazalne autofagije imunoblot metodom u MNĆPK i CD3+CD4- Tlimfocitima ove dve grupe ispitanika. Rezultati: Nivoi iRNK i proteina ATG5, potrebnog za formiranje autofagozoma, bili su povišeni u CD4+ i CD4- T-limfocitima, ali ne i u B-limfocitima i MNĆPK pacijenata sa MS u poređenju sa kontrolnim ispitanicima. Ekspresija ostalih ispitivanih autofagnih gena i aktivnost autofagije nisu se značajno razlikovale u ovim grupama ispitanika. Nivoi ATG5 iRNK u CD4+ T-limfocitima pacijenata sa MS bili su u pozitivnoj korelaciji sa nivoma iRNK za proinflamatorni citokin - faktor nekroze tumora (TNF).Zaključak: Naši rezultati ukazuju da povišena ekspresija ATG5, nezavisno od autofagije, može biti povezana sa proinflamatornom ulogom T-limfocita u MS.

Advisors/Committee Members: Drulović, Jelena, 1960- 12542823.

Subjects/Keywords: multiple sclerosis; T cells; autophagy; ATG5; TNF

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

APA (6^th Edition):

Vuković-Petrović, Irena, 1. 2. (2019). Ekspresija gena i proteina koji regulišu autofagiju u mononuklearnim ćelijama periferne krvi pacijenata sa multiplom sklerozom. (Thesis). Univerzitet u Beogradu. Retrieved from https://fedorabg.bg.ac.rs/fedora/get/o:19959/bdef:Content/get

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):

Vuković-Petrović, Irena, 1988- 21801063. “Ekspresija gena i proteina koji regulišu autofagiju u mononuklearnim ćelijama periferne krvi pacijenata sa multiplom sklerozom.” 2019. Thesis, Univerzitet u Beogradu. Accessed January 26, 2021. https://fedorabg.bg.ac.rs/fedora/get/o:19959/bdef:Content/get.

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

MLA Handbook (7^th Edition):

Vuković-Petrović, Irena, 1988- 21801063. “Ekspresija gena i proteina koji regulišu autofagiju u mononuklearnim ćelijama periferne krvi pacijenata sa multiplom sklerozom.” 2019. Web. 26 Jan 2021.

Vancouver:

Vuković-Petrović, Irena 12. Ekspresija gena i proteina koji regulišu autofagiju u mononuklearnim ćelijama periferne krvi pacijenata sa multiplom sklerozom. [Internet] [Thesis]. Univerzitet u Beogradu; 2019. [cited 2021 Jan 26]. Available from: https://fedorabg.bg.ac.rs/fedora/get/o:19959/bdef:Content/get.

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

Council of Science Editors:

Vuković-Petrović, Irena 12. Ekspresija gena i proteina koji regulišu autofagiju u mononuklearnim ćelijama periferne krvi pacijenata sa multiplom sklerozom. [Thesis]. Univerzitet u Beogradu; 2019. Available from: https://fedorabg.bg.ac.rs/fedora/get/o:19959/bdef:Content/get

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

Harvard University

30. Anderson, Edwin. The Predictive Power of Past Failure: Using Clinically Available Data to Improve Treatment Algorithms.

Degree: ALM, 2018, Harvard University

URL: http://nrs.harvard.edu/urn-3:HUL.InstRepos:42004088

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Pediatric rheumatology is a small but rapidly evolving specialty within the field of immunology that has been revolutionized by development of a new class of… (more)

Subjects/Keywords: pediatric rheumatology; juvenile idiopathic arthritis; anti-TNF

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

APA (6^th Edition):

Anderson, E. (2018). The Predictive Power of Past Failure: Using Clinically Available Data to Improve Treatment Algorithms. (Masters Thesis). Harvard University. Retrieved from http://nrs.harvard.edu/urn-3:HUL.InstRepos:42004088

Chicago Manual of Style (16^th Edition):

Anderson, Edwin. “The Predictive Power of Past Failure: Using Clinically Available Data to Improve Treatment Algorithms.” 2018. Masters Thesis, Harvard University. Accessed January 26, 2021. http://nrs.harvard.edu/urn-3:HUL.InstRepos:42004088.

MLA Handbook (7^th Edition):

Anderson, Edwin. “The Predictive Power of Past Failure: Using Clinically Available Data to Improve Treatment Algorithms.” 2018. Web. 26 Jan 2021.

Vancouver:

Anderson E. The Predictive Power of Past Failure: Using Clinically Available Data to Improve Treatment Algorithms. [Internet] [Masters thesis]. Harvard University; 2018. [cited 2021 Jan 26]. Available from: http://nrs.harvard.edu/urn-3:HUL.InstRepos:42004088.

Council of Science Editors:

Anderson E. The Predictive Power of Past Failure: Using Clinically Available Data to Improve Treatment Algorithms. [Masters Thesis]. Harvard University; 2018. Available from: http://nrs.harvard.edu/urn-3:HUL.InstRepos:42004088

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Open Access Theses and Dissertations