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 July 08, 2020. 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. 08 Jul 2020.

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 2020 Jul 08]. 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 July 08, 2020. 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. 08 Jul 2020.

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 2020 Jul 08]. 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 Louisville

3. Lewis, Robert K., 1977-. Inflammatory cell tumor necrosis factor signaling modulates post-infarction left ventricular remodeling.

Degree: PhD, 2010, University of Louisville

URL: 10.18297/etd/820 ; https://ir.library.louisville.edu/etd/820

► The fundamental question of the exact nature of the role played by TNF in the failing myocardium remains one of contention. Many preclinical studies have… (more)

▼ The fundamental question of the exact nature of the role played by TNF in the failing myocardium remains one of contention. Many preclinical studies have demonstrated beneficial effects with TNF antagonism and recently the dichotomous role played by the two TNF receptors in chronic ischemic injury has come to light. The failing heart has also been determined to have low levels of inflammatory cell infiltration. As these cells are known to be potent producers of inflammatory cytokines, we hypothesized that inflammatory cell localized TNF receptors play an important role in the progression of LV remodeling following ischemic injury. To isolate the in vivo effects of inflammatory cell TNF receptors, we generated chimeric mice. Wild-type (WT, C57BLl6) mice underwent radiation-induced bone marrow (BM) ablation followed by reconstitution with BM from WT mice (WTc control, n=30), TNFR 1-/- mice (R1-/-c, n = 30) or TNFR2 -/- mice (R2-/-c, n = 30). Six weeks later, WTc, R1-/-c, and R2-/-c mice were subjected to coronary ligation to induce heart failure (HF) or sham operation. Our results demonstrated that compared to WTc sham, 4 weeks after surgery, WTc HF hearts exhibited significantly (p < O.OS): 1) increased LV size (EDV 96.7 ±. 13.7 vs. 26.6 ± 8.2 IJL) and dysfunction (LVEF 2S.S ± 7.S vs. 69.8 ± 4.S%); 2) greater hypertrophy (LV/tibia length [TL] 3.91 ± 0.S3 vs. 2.9 ± 0.4, -4-fold greater atrial natriuretic factor [ANF] mRNA); 3) increased fibrosis (16.10 ± 8.16% vs. 1.4 ± 0.4%) and connective tissue growth factor (CTGF) mRNA expression, and 4) increased (-2-fold) mRNA levels of TNF, interleukin (IL)-1j3, and IL-6. WTc HF mice also had markedly reduced survival (60% vs. 100%) and increased blood levels of activated F4/80+/CD11 b+ monocytes vs. WTc sham mice. In contrast, compared to WTc HF, R1-1-c HF mice exhibited significantly (p < O.OS): 1) improved survival (80%), 2) less LV dilatation and improved LVEF (42.9 ± 4.2%), 3) less cardiac hypertrophy (LVITL 3.14 ± 0.2) and ANF mRNA expression, 4) less cardiac fibrosis (S.48 ± 2.26%) and CTGF mRNA expression, and S) less cardiac TNF and IL-1j3 mRNA expression. Also, compared to WTc HF, R2-/-c HF mice exhibited significantly (p < O.OS) greater circulating F4/80+/CD11 b+ monocytes (1S.32 ± 4.41 vs. 12.1 ±1.24%), and greater cardiac fibrosis (21.92 ±.10.81%). Also noted was an increase, although not significant, in EDV and ESV. In parallel in vitro studies, the contribution of inflammatory cell TNFR1 and TNFR2 (Le., macrophage-derived) to cardiac contractile dysfunction was investigated. Macrophages isolated from WT mice with HF 4 week postinfarction, when co-cultured with na"lve cardiomyocytes induced contractile dysfunction and myocyte reactive oxygen species (ROS) generation in a juxtacrine but not paracrine maner (p<O.001). Interestingly the effect on contractile dysfunction was diminished with the loss of TNFR1 in the HF macrophages but remained unchanged upon loss of TNFR2. Of note, ROS production in these groups followed a similar pattern in that loss of TNFR1 resulted… Advisors/Committee Members: Prabhu, Sumanth D..

Subjects/Keywords: TNF; Heart failure

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

APA (6^th Edition):

Lewis, Robert K., 1. (2010). Inflammatory cell tumor necrosis factor signaling modulates post-infarction left ventricular remodeling. (Doctoral Dissertation). University of Louisville. Retrieved from 10.18297/etd/820 ; https://ir.library.louisville.edu/etd/820

Chicago Manual of Style (16^th Edition):

Lewis, Robert K., 1977-. “Inflammatory cell tumor necrosis factor signaling modulates post-infarction left ventricular remodeling.” 2010. Doctoral Dissertation, University of Louisville. Accessed July 08, 2020. 10.18297/etd/820 ; https://ir.library.louisville.edu/etd/820.

MLA Handbook (7^th Edition):

Lewis, Robert K., 1977-. “Inflammatory cell tumor necrosis factor signaling modulates post-infarction left ventricular remodeling.” 2010. Web. 08 Jul 2020.

Vancouver:

Lewis, Robert K. 1. Inflammatory cell tumor necrosis factor signaling modulates post-infarction left ventricular remodeling. [Internet] [Doctoral dissertation]. University of Louisville; 2010. [cited 2020 Jul 08]. Available from: 10.18297/etd/820 ; https://ir.library.louisville.edu/etd/820.

Council of Science Editors:

Lewis, Robert K. 1. Inflammatory cell tumor necrosis factor signaling modulates post-infarction left ventricular remodeling. [Doctoral Dissertation]. University of Louisville; 2010. Available from: 10.18297/etd/820 ; https://ir.library.louisville.edu/etd/820

University of Illinois – Chicago

4. 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 July 08, 2020. 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. 08 Jul 2020.

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 2020 Jul 08]. 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 Toledo Health Science Campus

5. Saunders, Rudel Anton. Characterization of the Anti-Obesity and Anti-Adipogenic Effects of the Limonoid Prieurianin.

Degree: PhD, College of Medicine, 2010, University of Toledo Health Science Campus

URL: http://rave.ohiolink.edu/etdc/view?acc_num=mco1271698805

► Phospholipid transfer protein (PLTP) is critically important for reverse cholesteroltransport (RCT), and its expression level and activity increase when mice are fed a highfat… (more)

Subjects/Keywords: Biology; PLTP; NFkB; TNF; Prieurianin

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

APA (6^th Edition):

Saunders, R. A. (2010). Characterization of the Anti-Obesity and Anti-Adipogenic Effects of the Limonoid Prieurianin. (Doctoral Dissertation). University of Toledo Health Science Campus. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=mco1271698805

Chicago Manual of Style (16^th Edition):

Saunders, Rudel Anton. “Characterization of the Anti-Obesity and Anti-Adipogenic Effects of the Limonoid Prieurianin.” 2010. Doctoral Dissertation, University of Toledo Health Science Campus. Accessed July 08, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=mco1271698805.

MLA Handbook (7^th Edition):

Saunders, Rudel Anton. “Characterization of the Anti-Obesity and Anti-Adipogenic Effects of the Limonoid Prieurianin.” 2010. Web. 08 Jul 2020.

Vancouver:

Saunders RA. Characterization of the Anti-Obesity and Anti-Adipogenic Effects of the Limonoid Prieurianin. [Internet] [Doctoral dissertation]. University of Toledo Health Science Campus; 2010. [cited 2020 Jul 08]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=mco1271698805.

Council of Science Editors:

Saunders RA. Characterization of the Anti-Obesity and Anti-Adipogenic Effects of the Limonoid Prieurianin. [Doctoral Dissertation]. University of Toledo Health Science Campus; 2010. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=mco1271698805

University of Alberta

6. 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 July 08, 2020. 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. 08 Jul 2020.

Vancouver:

Srivastava N. NEUTROPHIL SECRETION OF THE PROINFLAMMATORY CYTOKINE TNF VIA RECYCLING ENDOSOMES. [Internet] [Masters thesis]. University of Alberta; 2015. [cited 2020 Jul 08]. 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

7. 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 July 08, 2020. 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. 08 Jul 2020.

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 2020 Jul 08]. 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

University of Rochester

8. 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 July 08, 2020. 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. 08 Jul 2020.

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 2020 Jul 08]. 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

North Carolina State University

9. 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 July 08, 2020. 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. 08 Jul 2020.

Vancouver:

Harris VG. The intracellular targeting of cPLA2. [Internet] [Thesis]. North Carolina State University; 2002. [cited 2020 Jul 08]. 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

10. 조, 영숙. 악관절 질환에게서 추출한 관절낭액의 proinflammatory cytokine의 농도변화.

Degree: 2009, Ajou University

URL: http://repository.ajou.ac.kr/handle/201003/1782 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000010066

►

"cytokine은 신호 전달 단백의 하나로 이 분자들은 호르몬처럼 세포 간 정보 전달에 광범위하게 이용된다. TNF-α는 염증과 관련되어 급성 반응을 나타내며 IL-6은 특정 미생물 물질에 반응하여… (more)

▼

"cytokine은 신호 전달 단백의 하나로 이 분자들은 호르몬처럼 세포 간 정보 전달에 광범위하게 이용된다. TNF-α는 염증과 관련되어 급성 반응을 나타내며 IL-6은 특정 미생물 물질에 반응하여 분비되어 proinflammatory cytokine으로 작용한다. 대개 이들의 level이 높은 경우는 악관절 질환의 증상과 큰 연관이 있다고 알려져 있다. 이들은 관절과 관련된 골 및 연골의 파괴를 촉진하여 악관절 질환과 관련하여 동통과 관절잡음 또는 개구량의 감소 등과 같은 임상적 증상과 징후를 나타내므로 악관절 질환 중 관절 내장증과 골관절염등과 주로 연관이 있다고 알려져 있다. 본 연구의 목적은 관절낭액 내의 TNF-α와 IL-6의 분석을 통하여 두 물질의 농도와 동통 발생, 개구제한, 악관절 잡음 등의 임상 증상과의 상관 관계를 규명하는데 있다. 연구 재료는 5명의 정상인을 대조군으로, 아주대학 병원 치과에 동통과 개구제한을 주소로 내원하여 악관절 질환으로 진단된 환자 중 악관절 세척술의 적응증이 되는 24명을 실험군으로 하여 세척술 시 추출된 관절낭액을 이용하였다."

"국문요약 ⅰ 차례 ⅱ 표 차례 ⅲ Ⅰ. 서론 1 Ⅱ. 연구대상 및 방법 4 A. 환자와 임상적 평가 기준 4 B. 실험 방법 5 1. 악관절 낭액의 추출과 수집 5 2. 분석 방법 5 3. 자료 분석 6 Ⅲ. 결과 7 A. 정상군과 비정상군의 비교 9 B. 비정상군 내의 급성 환자와 만성 환자의 수치 비교 10 C. 비정상군 중 개구제한이 있는 사람과 정상군과의 수치 비교 11 D. 비정상군 중 개구제한이 있는 경우 만성과 급성 환자의 수치 비교 12 E. 비정상군 중 술전에 관절잡음이 있는 사람과 정상군 비교 13 F. 비정상군 중 관절잡음이 있는 사람의 만성과 급성의 수치 비교 14 Ⅳ. 총괄 및 고찰 15 Ⅴ. 결론 19 참고문헌 20 ABSTRACT 27"

Master

Advisors/Committee Members: 200524355, 조, 영숙.

Subjects/Keywords: 악관절장애; TNF-a; IL-6

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

APA (6^th Edition):

조, �. (2009). 악관절 질환에게서 추출한 관절낭액의 proinflammatory cytokine의 농도변화. (Thesis). Ajou University. Retrieved from http://repository.ajou.ac.kr/handle/201003/1782 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000010066

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):

조, 영숙. “악관절 질환에게서 추출한 관절낭액의 proinflammatory cytokine의 농도변화.” 2009. Thesis, Ajou University. Accessed July 08, 2020. http://repository.ajou.ac.kr/handle/201003/1782 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000010066.

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

MLA Handbook (7^th Edition):

조, 영숙. “악관절 질환에게서 추출한 관절낭액의 proinflammatory cytokine의 농도변화.” 2009. Web. 08 Jul 2020.

Vancouver:

조 �. 악관절 질환에게서 추출한 관절낭액의 proinflammatory cytokine의 농도변화. [Internet] [Thesis]. Ajou University; 2009. [cited 2020 Jul 08]. Available from: http://repository.ajou.ac.kr/handle/201003/1782 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000010066.

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

Council of Science Editors:

조 �. 악관절 질환에게서 추출한 관절낭액의 proinflammatory cytokine의 농도변화. [Thesis]. Ajou University; 2009. Available from: http://repository.ajou.ac.kr/handle/201003/1782 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000010066

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

University of Debrecen

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

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 July 08, 2020. 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. 08 Jul 2020.

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 2020 Jul 08]. 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

12. 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 (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 July 08, 2020. 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. 08 Jul 2020.

Vancouver:

Hajdu DZ. Az antipszichotikumok makrofágok funkcionális aktivitására gyakorolt hatása . [Internet] [Thesis]. University of Debrecen; 2014. [cited 2020 Jul 08]. 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

13. 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/ ;

►

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)

▼

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 July 08, 2020. 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. 08 Jul 2020.

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 2020 Jul 08]. 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/ ;

14. 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 July 08, 2020. 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. 08 Jul 2020.

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 2020 Jul 08]. 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

15. 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 July 08, 2020. 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. 08 Jul 2020.

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 2020 Jul 08]. 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

16. 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 July 08, 2020. 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. 08 Jul 2020.

Vancouver:

Γεωργιάδου �. Μελέτη των υποδοχέων του TNFα στα κύτταρα Kupffer και στο ηπατοκυτταρικό καρκίνωμα. [Internet] [Thesis]. University of Crete (UOC); Πανεπιστήμιο Κρήτης; 2011. [cited 2020 Jul 08]. 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

Louisiana State University

17. Wang, Yanning. TNF-alpha inhibition of adiponectin expression by targeting PPAR-gamma and C/EBP in adipocytes.

Degree: MS, Human Ecology, 2009, Louisiana State University

URL: etd-07012009-181133 ; https://digitalcommons.lsu.edu/gradschool_theses/3684

► Chronic inflammation is involved in the adipose tissue dysfunction through regulation of endocrine and storage function of adipocytes. As a representative proinflammatory cytokine, TNF-α was… (more)

Subjects/Keywords: C/EBP; PPAR-gamma; TNF-alpha; Adiponectin

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

APA (6^th Edition):

Wang, Y. (2009). TNF-alpha inhibition of adiponectin expression by targeting PPAR-gamma and C/EBP in adipocytes. (Masters Thesis). Louisiana State University. Retrieved from etd-07012009-181133 ; https://digitalcommons.lsu.edu/gradschool_theses/3684

Chicago Manual of Style (16^th Edition):

Wang, Yanning. “TNF-alpha inhibition of adiponectin expression by targeting PPAR-gamma and C/EBP in adipocytes.” 2009. Masters Thesis, Louisiana State University. Accessed July 08, 2020. etd-07012009-181133 ; https://digitalcommons.lsu.edu/gradschool_theses/3684.

MLA Handbook (7^th Edition):

Wang, Yanning. “TNF-alpha inhibition of adiponectin expression by targeting PPAR-gamma and C/EBP in adipocytes.” 2009. Web. 08 Jul 2020.

Vancouver:

Wang Y. TNF-alpha inhibition of adiponectin expression by targeting PPAR-gamma and C/EBP in adipocytes. [Internet] [Masters thesis]. Louisiana State University; 2009. [cited 2020 Jul 08]. Available from: etd-07012009-181133 ; https://digitalcommons.lsu.edu/gradschool_theses/3684.

Council of Science Editors:

Wang Y. TNF-alpha inhibition of adiponectin expression by targeting PPAR-gamma and C/EBP in adipocytes. [Masters Thesis]. Louisiana State University; 2009. Available from: etd-07012009-181133 ; https://digitalcommons.lsu.edu/gradschool_theses/3684

Temple University

18. 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

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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 July 08, 2020. 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. 08 Jul 2020.

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 2020 Jul 08]. 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

19. 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 July 08, 2020. 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. 08 Jul 2020.

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 2020 Jul 08]. 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

University of Rochester

20. Janelsins, Michelle Christine; Bowers, William J. Inflammation in Alzheimer’s disease : implicating tumor necrosis factor-alpha as a key mediator of disease pathogenesis.

Degree: PhD, 2009, University of Rochester

URL: http://hdl.handle.net/1802/6616

► Alzheimer’s disease (AD) is a complex neurodegenerative disorder that progressively impairs intellectual and emotional functioning in afflicted individuals. The disease is characterized pathologically by a… (more)

▼ Alzheimer’s disease (AD) is a complex neurodegenerative disorder that progressively impairs intellectual and emotional functioning in afflicted individuals. The disease is characterized pathologically by a temporal and spatial advancement of amyloid-beta (Aβ) deposition, neurofibrillary tangle formation, synaptic degeneration, and neuronal loss. Inflammatory processes have been implicated in initiating and/or propagating AD-associated pathology within the brain, as inflammatory cytokine expression and other markers of inflammation are pronounced in individuals with AD pathology. We utilized the 3xTg-AD mouse model (which harbors pathological features similar to human AD) to first identify inflammatory molecule(s) present in the brain prior to overt classical pathologies. We observed a significant 14.8-fold and 10.8-fold up-regulation in transcript levels of the proinflammatory cytokine, tumor necrosis factor-alpha (TNF-α), and chemokine, monocyte chemoattractant protein-1 (MCP-1), respectively, specifically within the entorhinal cortex of these mice but not age-matched controls. Interestingly, correlative increases in numbers of F4/80-positive microglia/macrophage cells were regionally enhanced with respect to TNF-α and MCP-1 expression within the entorhinal cortex. Both microglia and neurons were found to express TNF-α transcripts. To further define the role of neuronally derived TNF-α in early AD pathogenesis, a recombinant adeno-associated virus (rAAV) vector expressing TNF-α was constructed and stereotactically delivered to “pre-pathologic” 3xTg-AD mice and non-transgenic (Non-Tg) control mice. Neuronal over-expression of TNF-α for 4 months hastened intracellular Aβ accumulation in 3xTg-AD mice with concomitant enhancement in microglial staining intensities. Following chronic neuronal expression of TNF-α in 3xTg-AD and Non-Tg mice for 10 months, significant transcriptional enhancement of TNF receptor II (TNFRII) and Jun-related genes with coincident neuronal death specifically within the brains of 3xTg-AD mice was observed. This indicates that chronic TNF-α expression alone is insufficiently neurotoxic, but that a pathologic interaction exists between TNF-α and the AD-related transgene products expressed by neurons in the 3xTg-AD mouse brain. These studies provide in vivo evidence for chronic neuronal TNF-α expression as a key mediator in perpetuating AD-related inflammatory events, and ultimately, neuronal death.

Subjects/Keywords: AD mouse model; Neuroinflammation; Alzheimer's TNF-α

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

APA (6^th Edition):

Janelsins, Michelle Christine; Bowers, W. J. (2009). Inflammation in Alzheimer’s disease : implicating tumor necrosis factor-alpha as a key mediator of disease pathogenesis. (Doctoral Dissertation). University of Rochester. Retrieved from http://hdl.handle.net/1802/6616

Chicago Manual of Style (16^th Edition):

Janelsins, Michelle Christine; Bowers, William J. “Inflammation in Alzheimer’s disease : implicating tumor necrosis factor-alpha as a key mediator of disease pathogenesis.” 2009. Doctoral Dissertation, University of Rochester. Accessed July 08, 2020. http://hdl.handle.net/1802/6616.

MLA Handbook (7^th Edition):

Janelsins, Michelle Christine; Bowers, William J. “Inflammation in Alzheimer’s disease : implicating tumor necrosis factor-alpha as a key mediator of disease pathogenesis.” 2009. Web. 08 Jul 2020.

Vancouver:

Janelsins, Michelle Christine; Bowers WJ. Inflammation in Alzheimer’s disease : implicating tumor necrosis factor-alpha as a key mediator of disease pathogenesis. [Internet] [Doctoral dissertation]. University of Rochester; 2009. [cited 2020 Jul 08]. Available from: http://hdl.handle.net/1802/6616.

Council of Science Editors:

Janelsins, Michelle Christine; Bowers WJ. Inflammation in Alzheimer’s disease : implicating tumor necrosis factor-alpha as a key mediator of disease pathogenesis. [Doctoral Dissertation]. University of Rochester; 2009. Available from: http://hdl.handle.net/1802/6616

Boston University

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

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 July 08, 2020. 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. 08 Jul 2020.

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 2020 Jul 08]. 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

Universidade Nova

22. 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 July 08, 2020. 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. 08 Jul 2020.

Vancouver:

Raposeiro RMM. Osteoclast activity in ankylosing spondylitis patients before and after TNF-blocking therapy. [Internet] [Thesis]. Universidade Nova; 2014. [cited 2020 Jul 08]. 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

23. 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 July 08, 2020. 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. 08 Jul 2020.

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 2020 Jul 08]. 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

24. Bazin, Thomas. Microbiote intestinal et inflammation : prédiction de la réponse aux anti-TNFα dans les maladies inflammatoires chroniques et modulation de la croissance bactérienne in vitro en réponse au TNFα : Gut microbiota and inflammation : prediction of anti-TNFα response in chronic inflammatory diseases and modulation of bacterial growth in vitro in response to TNFα.

Degree: Docteur es, Microbiologie-immunologie, 2018, Bordeaux

URL: http://www.theses.fr/2018BORD0285

►

L’interface hôte/microbiote intestinal est un système d’interactions complexes dont le déséquilibre est associé au développement des maladies inflammatoires chroniques. Les traitements anti-TNFα sont très efficaces… (more)

▼

L’interface hôte/microbiote intestinal est un système d’interactions complexes dont le déséquilibre est associé au développement des maladies inflammatoires chroniques. Les traitements anti-TNFα sont très efficaces dans ces maladies, mais seulement chez certains patients. L’objectif de ce travail était de rechercher un lien entre composition du microbiote intestinal et réponse aux traitements anti-TNFα dans deux types de maladies inflammatoires chroniques, les spondyloarthrites et les maladies inflammatoires chroniques de l’intestin. Nous avons retrouvé des variations de la composition du microbiote intestinal après traitement par anti-TNFα chez des patients atteints de spondyloarthrite et avons identifié un nœud taxonomique prédictif de la réponse thérapeutique à trois mois. Ce nœud taxonomique, l’ordre des Burkholderiales, étant ainsi un biomarqueur potentiellement utilisable en pratique clinique, nous avons déposé une demande de brevet européen, qui est en cours d’instruction. Ce travail a été poursuivi par un nouveau protocole de recherche clinique incluant des patients atteints de spondyloarthrites mais aussi de maladies inflammatoires chroniques intestinales. Ce protocole est financé par le CHU de Bordeaux dans le cadre de l’Appel d’Offre Interne. Il permettra de valider les hypothèses de notre premier travail, en réalisant notamment des PCR quantitatives utilisant des amorces spécifiques de l’ordre des Burkholderiales. Nous avons de plus retrouvé in vitro pour la première fois à notre connaissance une modulation de la croissance bactérienne chez Bacteroides fragilis en réponse au TNFα humain.

The host/gut microbiota interface is a system of complex interactions whose imbalance is associated with the development of chronic inflammatory diseases. Anti-TNFα treatments are very effective in these diseases, but only in some patients. The purpose of this work was to find a link between the composition of the intestinal microbiota and clinical response to anti-TNFα treatments in two types of chronic inflammatory diseases, spondyloarthritis and inflammatory bowel disease. We found variations in the composition of the intestinal microbiota after treatment with anti-TNFα in patients with spondyloarthritis and identified a taxonomic node predictive of the therapeutic response at 3 months. This taxonomic node, the Burkholderiales order, being a biomarker potentially usable in clinical practice, we have filed a European patent application, which is currently under investigation. This work was continued by a new clinical research protocol including patients with spondyloarthritis but also with inflammatory bowel diseases. This protocol is funded by the Bordeaux University Hospital as part of the internal call for tenders. It will validate the hypotheses of our first work, notably by performing quantitative PCRs using specific primers targeting the order of Burkholderiales. In vitro, we have also found for the first time, to our knowledge, a modulation of bacterial growth in Bacteroides fragilis in response to human TNFα.

Advisors/Committee Members: Schaeverbeke, Thierry (thesis director).

Subjects/Keywords: Microbiote intestinal; Maladies inflammatoire chronique intestinale; Spondyloarthrite; Inflammation; Anti TNF-Alpha; TNF-Alpha; Intestinal microbiota; Inflammatory bowel disease; Spondyloarthritis; Inflammation; TNF-Alpha inhibitor; TNF-Alpha

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

APA (6^th Edition):

Bazin, T. (2018). Microbiote intestinal et inflammation : prédiction de la réponse aux anti-TNFα dans les maladies inflammatoires chroniques et modulation de la croissance bactérienne in vitro en réponse au TNFα : Gut microbiota and inflammation : prediction of anti-TNFα response in chronic inflammatory diseases and modulation of bacterial growth in vitro in response to TNFα. (Doctoral Dissertation). Bordeaux. Retrieved from http://www.theses.fr/2018BORD0285

Chicago Manual of Style (16^th Edition):

Bazin, Thomas. “Microbiote intestinal et inflammation : prédiction de la réponse aux anti-TNFα dans les maladies inflammatoires chroniques et modulation de la croissance bactérienne in vitro en réponse au TNFα : Gut microbiota and inflammation : prediction of anti-TNFα response in chronic inflammatory diseases and modulation of bacterial growth in vitro in response to TNFα.” 2018. Doctoral Dissertation, Bordeaux. Accessed July 08, 2020. http://www.theses.fr/2018BORD0285.

MLA Handbook (7^th Edition):

Bazin, Thomas. “Microbiote intestinal et inflammation : prédiction de la réponse aux anti-TNFα dans les maladies inflammatoires chroniques et modulation de la croissance bactérienne in vitro en réponse au TNFα : Gut microbiota and inflammation : prediction of anti-TNFα response in chronic inflammatory diseases and modulation of bacterial growth in vitro in response to TNFα.” 2018. Web. 08 Jul 2020.

Vancouver:

Bazin T. Microbiote intestinal et inflammation : prédiction de la réponse aux anti-TNFα dans les maladies inflammatoires chroniques et modulation de la croissance bactérienne in vitro en réponse au TNFα : Gut microbiota and inflammation : prediction of anti-TNFα response in chronic inflammatory diseases and modulation of bacterial growth in vitro in response to TNFα. [Internet] [Doctoral dissertation]. Bordeaux; 2018. [cited 2020 Jul 08]. Available from: http://www.theses.fr/2018BORD0285.

Council of Science Editors:

Bazin T. Microbiote intestinal et inflammation : prédiction de la réponse aux anti-TNFα dans les maladies inflammatoires chroniques et modulation de la croissance bactérienne in vitro en réponse au TNFα : Gut microbiota and inflammation : prediction of anti-TNFα response in chronic inflammatory diseases and modulation of bacterial growth in vitro in response to TNFα. [Doctoral Dissertation]. Bordeaux; 2018. Available from: http://www.theses.fr/2018BORD0285

25. 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 July 08, 2020. 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. 08 Jul 2020.

Vancouver:

Teixeira CSL. TNF-alfa e metabolismo do adipócito. [Internet] [Thesis]. RCAAP; 2015. [cited 2020 Jul 08]. 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

University of Oslo

26. Ben Omar, Sakina. Cysteinproteasene legumain og cathepsin B i monocytter/makrofager og i aterosklerotiske plakk.

Degree: 2008, University of Oslo

URL: http://urn.nb.no/URN:NBN:no-21459 ; https://www.duo.uio.no/handle/10852/12236 ; Fulltext https://www.duo.uio.no/bitstream/handle/10852/12236/1/BenOmar_masteroppgave.pdf

► Aterosklerose er en inflammatorisk sykdom der immuncellenes aktivitet er sentral i patogenesen. I blodåreveggen utvikles aterosklerotiske plakk som består av ekstracellulært materiale og lipidrike makrofag-skumceller,… (more)

▼ Aterosklerose er en inflammatorisk sykdom der immuncellenes aktivitet er sentral i patogenesen. I blodåreveggen utvikles aterosklerotiske plakk som består av ekstracellulært materiale og lipidrike makrofag-skumceller, som hovedsakelig dannes ved opptak av oksidert ”low density lipoprotein” (oxLDL). Makrofag-skumceller er hovedkilden til proteaser som fører til destabilisering av plakk ved nedbrytning av ekstracellulær matriks, og plakkets fibrøse kappe. De lysosomale cysteinproteasene legumain og cathepsin B er vist å overuttrykkes i aterosklerotiske plakk. I denne studien ble native THP-1 celler (human monocyttisk cellelinje), eller THP-1 celler differensiert med forbolester (PMA) til makrofager, inkubert med ulike konsentrasjoner av henholdsvis oxLDL, tumornekrosefaktor-α (TNFα), og LXR-ligandene 22-(R/S)-hydroksykolesterol (22R/S) og T0901317, alene eller i kombinasjoner. Enzymaktivitet av legumain og cathepsin B ble målt i cellelysat ved hjelp av spesifikke peptidsubstrater. Eventuell celledød ble analysert ved celleviabilitet (MTS) og LDH-lekkasje til medium. Proteinuttrykket av legumain og cathepsin B i behandlede celler og i aterosklerotiske carotisplakk ble analysert ved hjelp av Western blotting med spesifikke antistoffer. PMA-stimulering av THP-1 celler førte til en kraftig økning i enzymaktivitet av legumain og cathepsin B. Ved inkubering av PMA-stimulerte THP-1 celler med oxLDL, ble det observert en doseavhengig reduksjon av både legumain- og cathepsin B-aktivitet. En tilsvarende effekt ble observert med 22R, men ikke 22S. Det ble også vist at effekten av oxLDL på enzymaktiviteten kunne være en direkte effekt på de lysosomale enzymene. Økende konsentrasjoner av 22R førte i tillegg til celledød i PMA-stimulerte THP-1 celler. TNFα induserte differensiering av native THP-1 celler til adherente celler med økt legumain- og cathepsin B-aktivitet, og overuttrykk av cathepsin B-protein sammenlignet med ikke-adherente celler fra samme cellepopulasjon. Disse resultatene indikerer at det inflammatoriske miljøet i aterosklerotiske plakk kan påvirke uttrykket og aktiviteten av lysosomale proteaser. Western blotting av patologisk plakkmateriale viste signifikant oppregulering av cathepsin B i carotisplakk fra symptomatiske sammenlignet med asymptomatiske pasienter, men legumain ble ikke identifisert i de samme plakkprøvene. Dette tyder på at cathepsin B oppreguleres ved progresjon av aterosklerotiske plakk. Advisors/Committee Members: Harald Thidemann Johansen, Rigmor Solberg og Bente Halvorsen.

Subjects/Keywords: oksidert LDL OXLDL TNF-aTNFalpha; VDP::568

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APA (6^th Edition):

Ben Omar, S. (2008). Cysteinproteasene legumain og cathepsin B i monocytter/makrofager og i aterosklerotiske plakk. (Thesis). University of Oslo. Retrieved from http://urn.nb.no/URN:NBN:no-21459 ; https://www.duo.uio.no/handle/10852/12236 ; Fulltext https://www.duo.uio.no/bitstream/handle/10852/12236/1/BenOmar_masteroppgave.pdf

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):

Ben Omar, Sakina. “Cysteinproteasene legumain og cathepsin B i monocytter/makrofager og i aterosklerotiske plakk.” 2008. Thesis, University of Oslo. Accessed July 08, 2020. http://urn.nb.no/URN:NBN:no-21459 ; https://www.duo.uio.no/handle/10852/12236 ; Fulltext https://www.duo.uio.no/bitstream/handle/10852/12236/1/BenOmar_masteroppgave.pdf.

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

MLA Handbook (7^th Edition):

Ben Omar, Sakina. “Cysteinproteasene legumain og cathepsin B i monocytter/makrofager og i aterosklerotiske plakk.” 2008. Web. 08 Jul 2020.

Vancouver:

Ben Omar S. Cysteinproteasene legumain og cathepsin B i monocytter/makrofager og i aterosklerotiske plakk. [Internet] [Thesis]. University of Oslo; 2008. [cited 2020 Jul 08]. Available from: http://urn.nb.no/URN:NBN:no-21459 ; https://www.duo.uio.no/handle/10852/12236 ; Fulltext https://www.duo.uio.no/bitstream/handle/10852/12236/1/BenOmar_masteroppgave.pdf.

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

Council of Science Editors:

Ben Omar S. Cysteinproteasene legumain og cathepsin B i monocytter/makrofager og i aterosklerotiske plakk. [Thesis]. University of Oslo; 2008. Available from: http://urn.nb.no/URN:NBN:no-21459 ; https://www.duo.uio.no/handle/10852/12236 ; Fulltext https://www.duo.uio.no/bitstream/handle/10852/12236/1/BenOmar_masteroppgave.pdf

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 July 08, 2020. 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. 08 Jul 2020.

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 2020 Jul 08]. 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

►

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 (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 July 08, 2020. 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. 08 Jul 2020.

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 2020 Jul 08]. 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

Cornell University

29. Aurand, Thomas. Development Of Novel Genetic Circuits For The Detection Of Disease Biomarkers .

Degree: 2016, Cornell University

URL: http://hdl.handle.net/1813/44390

► The US Centers for Disease Control and Prevention (CDC) estimates chronic diseases account for 86% of the annual health care costs in the US. Monitoring… (more)

▼ The US Centers for Disease Control and Prevention (CDC) estimates chronic diseases account for 86% of the annual health care costs in the US. Monitoring and intervention of chronic diseases such as cardiovascular disease, diabetes, and arthritis, are required to decelerate their progression. Some markers of these diseases are secreted into the intestine, providing an alternative monitoring approach. The development of bacteria based environmental sensors, or bioreporters using synthetic biology techniques provides a novel approach to monitor disease biomarkers. In the studies presented here, we developed two novel bioreporter systems using genetic circuits to monitor disease biomarkers. We identified the peptide fragments of the outer membrane protein, OprF of Pseudomonas aeruginosa which bind interferon-[gamma] (IFN-[gamma]) and interact with tumor necrosis factor-[alpha] (TNF-[alpha]). We engineered sensors for IFN-[gamma] and TNF-[alpha] as fusion proteins of OmpA/OprF, expressed in Escherichia coli. The phage shock protein A, pspA promoter was used for the first time to transduce the interaction of the markers with the OmpA/OprF sensor into a quantifiable signal, measured as [beta]-galactosidase activity. This novel detection system for IFN-[gamma] and TNF-[alpha] was capable of detecting these inflammatory markers. Subsequently, the detection systems were tested in an in vitro model of intestinal barrier dysfunction. Direct application of the bioreporter systems to the intestinal "lumen" portion of the model demonstrated strong detection of the cytokines which diffused through the permeable barrier, showing the promise for the potential advancement to use in vivo models. The threshold detection concertation for the bioreporter systems was in the active range observed in stool samples of patients with Inflammatory Bowel Disease. Secondly, we developed a detection system for elevated concentrations of uric acid, which are implicated in gout, a form of arthritis. We used the transcriptional regulator, PucR of the purine catabolism pathway of Bacillus subtilis to develop a synthetic promoter responsive to uric acid, driving the production of GFP. With this novel system we could differentiate between healthy and hyperuricemic concentrations of uric acid observed in the gut. The sensor systems we developed in these studies provide an essential contribution to the development of future diagnostic systems and active therapeutics. Advisors/Committee Members: Ley,Ruth E. (committeeMember), King,Cynthia A. (committeeMember).

Subjects/Keywords: Synthetic Biology; IFN-gamma; TNF-alpha

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

APA (6^th Edition):

Aurand, T. (2016). Development Of Novel Genetic Circuits For The Detection Of Disease Biomarkers . (Thesis). Cornell University. Retrieved from http://hdl.handle.net/1813/44390

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):

Aurand, Thomas. “Development Of Novel Genetic Circuits For The Detection Of Disease Biomarkers .” 2016. Thesis, Cornell University. Accessed July 08, 2020. http://hdl.handle.net/1813/44390.

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

MLA Handbook (7^th Edition):

Aurand, Thomas. “Development Of Novel Genetic Circuits For The Detection Of Disease Biomarkers .” 2016. Web. 08 Jul 2020.

Vancouver:

Aurand T. Development Of Novel Genetic Circuits For The Detection Of Disease Biomarkers . [Internet] [Thesis]. Cornell University; 2016. [cited 2020 Jul 08]. Available from: http://hdl.handle.net/1813/44390.

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

Council of Science Editors:

Aurand T. Development Of Novel Genetic Circuits For The Detection Of Disease Biomarkers . [Thesis]. Cornell University; 2016. Available from: http://hdl.handle.net/1813/44390

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

30. Galenkamp, Koen M.O. Priming neuroblastoma for cisplatin and etoposide drug therapy: Role of NF-κB in TNFα-induced expression of Fas.

Degree: Departament de Bioquímica i Biologia Molecular, 2015, Universitat Autònoma de Barcelona

URL: http://hdl.handle.net/10803/326455

► Neuroblastoma (NB) is a pediatric solid tumor that accounts for ~15% of all cancer-related deaths in infants. High-risk NBs are hallmarked by a high degree… (more)

▼ Neuroblastoma (NB) is a pediatric solid tumor that accounts for ~15% of all cancer-related deaths in infants. High-risk NBs are hallmarked by a high degree of heterogeneity and aggressiveness, which results in poor patient outcome. Despite the improvement of standard therapies in the last twenty years, five-year survival rates are still below 50%, which impels the development of new treatment strategies for this condition. Activation of death receptors (DRs) has been proposed as an alternative to standard chemo- and radio-therapies for various types of cancer. In NB, this approach has been largely disregarded, possibly due to the silencing of caspase-8 in 50-70% of the cases. Nevertheless, a significant group of NB patients could benefit from treatment that induces cell death through DR activation. Characterization of DR signaling (especially Fas and TNFR1) and their regulation in NB has been limitedly studied, but is a prerequisite for assessing their therapeutic relevance. Given that the cytokine TNFα has been described to induce Fas expression in various types of cancer, we addressed whether TNFα and FasL co-treatment could be a valid therapeutic strategy in NB. For the purpose of the study, TNFR1- and Fas-mediated signaling and cell death induction was characterized in a set of eight clinically representative NB cell lines. TNFα treatment was shown to induce Fas expression through NF-κB-mediated transcription of FAS and primed for FasL-induced cell death. Moreover, TNFα treatment enhanced the cytotoxic effects caused by DNA-damaging agents (i.e. cisplatin and etoposide) through caspase-8 activation. Further characterization revealed that the high degree of heterogeneity between NBs is also visible at the levels of Fas expression and modulation thereof by TNFα. TNFα-mediated priming for FasL-, cisplatin-, and etoposide-induced cell death was only observed for NBs that induced TNFα-mediated Fas expression. In conclusion, our findings reveal that TNFα primes NB for FasL-induced cell death through the NF-κB-mediated induction of Fas expression. Moreover, TNFα pre-treatment enhanced cisplatin- and etoposide-induced cell death. These findings unveil a novel mechanism that could improve the efficacy of treatment regimens currently used for the eradication of NB tumors. Advisors/Committee Members: [email protected] (authoremail), true (authoremailshow), Comella Carnicé, Joan X. (director), true (authorsendemail).

Subjects/Keywords: Neuroblastoma; Fas; TNF; Ciències Experimentals; 577

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APA (6^th Edition):

Galenkamp, K. M. O. (2015). Priming neuroblastoma for cisplatin and etoposide drug therapy: Role of NF-κB in TNFα-induced expression of Fas. (Thesis). Universitat Autònoma de Barcelona. Retrieved from http://hdl.handle.net/10803/326455

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):

Galenkamp, Koen M O. “Priming neuroblastoma for cisplatin and etoposide drug therapy: Role of NF-κB in TNFα-induced expression of Fas.” 2015. Thesis, Universitat Autònoma de Barcelona. Accessed July 08, 2020. http://hdl.handle.net/10803/326455.

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

MLA Handbook (7^th Edition):

Galenkamp, Koen M O. “Priming neuroblastoma for cisplatin and etoposide drug therapy: Role of NF-κB in TNFα-induced expression of Fas.” 2015. Web. 08 Jul 2020.

Vancouver:

Galenkamp KMO. Priming neuroblastoma for cisplatin and etoposide drug therapy: Role of NF-κB in TNFα-induced expression of Fas. [Internet] [Thesis]. Universitat Autònoma de Barcelona; 2015. [cited 2020 Jul 08]. Available from: http://hdl.handle.net/10803/326455.

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

Council of Science Editors:

Galenkamp KMO. Priming neuroblastoma for cisplatin and etoposide drug therapy: Role of NF-κB in TNFα-induced expression of Fas. [Thesis]. Universitat Autònoma de Barcelona; 2015. Available from: http://hdl.handle.net/10803/326455

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

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Open Access Theses and Dissertations