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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 (6th 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 (16th Edition):
藤原, 範雄. “腫瘍壊死因子産生阻害剤の合成と構造活性相関および薬理作用に関する研究 : Synthesis, pharmacological evaluation and SAR study of novel tumor necrosis factor-alpha inhibitors; シュヨウ エシ インシ サンセイ ソガイザイ ノ ゴウセイ ト コウゾウ カッセイ ソウカン オヨビ ヤクリ サヨウ ニ カンスル ケンキュウ.” Thesis, Nara Institute of Science and Technology / 奈良先端科学技術大学院大学. Accessed January 26, 2021.
http://hdl.handle.net/10061/5235.
Note: this citation may be lacking information needed for this citation format:
No year of publication.
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
藤原, 範雄. “腫瘍壊死因子産生阻害剤の合成と構造活性相関および薬理作用に関する研究 : Synthesis, pharmacological evaluation and SAR study of novel tumor necrosis factor-alpha inhibitors; シュヨウ エシ インシ サンセイ ソガイザイ ノ ゴウセイ ト コウゾウ カッセイ ソウカン オヨビ ヤクリ サヨウ ニ カンスル ケンキュウ.” Web. 26 Jan 2021.
Note: this citation may be lacking information needed for this citation format:
No year of publication.
Vancouver:
藤原 . 腫瘍壊死因子産生阻害剤の合成と構造活性相関および薬理作用に関する研究 : Synthesis, pharmacological evaluation and SAR study of novel tumor necrosis factor-alpha inhibitors; シュヨウ エシ インシ サンセイ ソガイザイ ノ ゴウセイ ト コウゾウ カッセイ ソウカン オヨビ ヤクリ サヨウ ニ カンスル ケンキュウ. [Internet] [Thesis]. Nara Institute of Science and Technology / 奈良先端科学技術大学院大学; [cited 2021 Jan 26].
Available from: http://hdl.handle.net/10061/5235.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
No year of publication.
Council of Science Editors:
藤原 . 腫瘍壊死因子産生阻害剤の合成と構造活性相関および薬理作用に関する研究 : Synthesis, pharmacological evaluation and SAR study of novel tumor necrosis factor-alpha inhibitors; シュヨウ エシ インシ サンセイ ソガイザイ ノ ゴウセイ ト コウゾウ カッセイ ソウカン オヨビ ヤクリ サヨウ ニ カンスル ケンキュウ. [Thesis]. Nara Institute of Science and Technology / 奈良先端科学技術大学院大学; Available from: http://hdl.handle.net/10061/5235
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
No year of publication.
2.
Sousa, Cláudia Emanuele Carvalho de.
Caracterização do eixo imune-pineal: mecanismo de ação do controle da função pineal pela citocina pró-inflamatória TNF.
Degree: Mestrado, Fisiologia Geral, 2011, University of São Paulo
URL: http://www.teses.usp.br/teses/disponiveis/41/41135/tde-27042011-131503/
;
► O TNF atua diretamente sobre a pineal inibindo a via biossintética da melatonina. De forma semelhante o LPS, potente ativador da resposta imune inata, tem…
(more)
▼ O TNF atua diretamente sobre a pineal inibindo a via biossintética da melatonina. De forma semelhante o LPS, potente ativador da resposta imune inata, tem efeito inibitório sobre a produção de melatonina e seu precursor. A supressão da síntese noturna de melatonina é admitida de forma a permitir a montagem da resposta inflamatória, tanto durante o dia como à noite. Dados do grupo tem demonstrado que o NFKB é um fator constitutivamente expresso na glândula pineal e que o ritmo diário de translocação pode ser determinante para o início da síntese de melatonina. A inibição de sua ativação potencia a síntese de melatonina enquanto que fatores que classicamente promovem a sua ativação inibem esta produção. Nesta dissertação, verificamos as moléculas envolvidas no reconhecimento e na de sinalização desta citocina na pineal. Demonstramos que a pineal está apta a responder ao TNF, células gliais da pineal e as células secretoras, os pinealócitos, expressam constitutivamente o receptor TNF-R1. O TNF promove a translocação nuclear dos dímeros p50/p50 e p50/RelA do NFKB em glândulas pineais em cultura. Confirmamos a ativação desta via em pinealócitos pela análise da proteína inibitória IKB. Vimos que a ativação desse fator é essencial para expressão da iNOS e a produção de NO induzida por TNF em pinealócitos isolados. Além disso, mostramos que o TNF promove a redução da expressão do receptor TNF-R1 na membrana de pinealócitos. Em resumo, mostramos neste trabalho que a pineal está instrumentalizada a responder ao TNF, e que os pinealócitos são alvos diretos para o seu reconhecimento. Confirmamos a relevância do fator NFKB na resposta da pineal em situações de injúria, ampliando o conceito de que a pineal está apta a detectar moléculas do processo inflamatório.
TNF acts directly on the pineal gland by inhibiting the biosynthesis of melatonin. Similarly, LPS, a potent activator of the innate immune response has an inhibitory effect on the production of melatonin and its precursor. The suppression of nocturnal melatonin synthesis is admitted to allow the full mounting of the inflammatory response both during the day and night. Data from our laboratory have shown that the NFKB is constitutively expressed in the pineal gland and that the daily rate of translocation can be determinant for the onset of melatonin synthesis. Inhibition of their activation potentiates melatonin synthesis whereas factors that promote its activation classically inhibit this production. In this dissertation we find the molecules involved in recognition and signaling of this cytokine in the pineal. We demonstrated that the pineal is responsive to TNF, the pineal glial cells and secretory cells, the pinealocytes, constitutively express the TNF-R1. TNF promotes nuclear translocation of p50/RelA and p50/p50 NFKB dimers in the pineal glands in culture. We confirmed the activation of this pathway in pinealocytes by analyzing the inhibitory protein IKB. We have seen that the activation of this factor is essential for iNOS expression and NO production induced by…
Advisors/Committee Members: Markus, Regina Pekelmann.
Subjects/Keywords: Glândula pineal; NFKB; NFKB; Pineal gland; TNF; TNF; TNF-R1; TNF-R1
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th 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 (16th Edition):
Sousa, Cláudia Emanuele Carvalho de. “Caracterização do eixo imune-pineal: mecanismo de ação do controle da função pineal pela citocina pró-inflamatória TNF.” 2011. Masters Thesis, University of São Paulo. Accessed January 26, 2021.
http://www.teses.usp.br/teses/disponiveis/41/41135/tde-27042011-131503/ ;.
MLA Handbook (7th Edition):
Sousa, Cláudia Emanuele Carvalho de. “Caracterização do eixo imune-pineal: mecanismo de ação do controle da função pineal pela citocina pró-inflamatória TNF.” 2011. Web. 26 Jan 2021.
Vancouver:
Sousa CECd. Caracterização do eixo imune-pineal: mecanismo de ação do controle da função pineal pela citocina pró-inflamatória TNF. [Internet] [Masters thesis]. University of São Paulo; 2011. [cited 2021 Jan 26].
Available from: http://www.teses.usp.br/teses/disponiveis/41/41135/tde-27042011-131503/ ;.
Council of Science Editors:
Sousa CECd. Caracterização do eixo imune-pineal: mecanismo de ação do controle da função pineal pela citocina pró-inflamatória TNF. [Masters Thesis]. University of São Paulo; 2011. Available from: http://www.teses.usp.br/teses/disponiveis/41/41135/tde-27042011-131503/ ;

University of Illinois – Chicago
3.
Lee, Wan-Ju.
Utilization and Risk of Serious Infection Associated with TNF-α Inhibitors in Children and Young Adults.
Degree: 2016, University of Illinois – Chicago
URL: http://hdl.handle.net/10027/21614
► This dissertation examined use of tumor necrosis factor-alpha inhibitors (TNFI) and risk of TNFI-associated serious infection compared to oral immunosuppressants in children and young adults…
(more)
▼ This dissertation examined use of tumor necrosis factor-alpha inhibitors (TNFI) and risk of TNFI-associated serious infection compared to oral immunosuppressants in children and young adults with juvenile idiopathic arthritis (JIA)/rheumatoid arthritis (RA) and inflammatory bowel disease (IBD). Four retrospective cohort studies were conducted using the Truven Health MarketScan Research Database (2009-2013). TNFI treatment patterns, early TNFI therapy rates, and time to TNFI initiation were examined in incident JIA/RA and IBD cohorts. Serious infections were defined as those requiring hospitalization. Cox proportional hazard models were used to estimate the risk of serious infection associated with TNFIs in JIA and IBD cohorts. High-dimensional propensity score models were used to control for potential confounding. In two studies examining treatment patterns, 18.6% of the incident JIA/RA cohort initiated TNFIs, and etanercept was most commonly used, while in the incident IBD cohort, 27.6% initiated TNFIs, and infliximab was most commonly used. In both cohorts, time from new diagnosis to first TNFI prescription was shorter in more recent years. Specifically, early TNFI therapy increased over time in the IBD cohort. In a third study, 2,495 JIA patients were followed for 1,810 person-years. Serious infection rates were 2.7/100 person-years for TNFIs and 1.28/100 person-years for disease-modifying antirheumatic drugs (DMARD). TNFI monotherapy posed a 2.7-fold increase in risk of serious infection compared to DMARDs alone. In the fourth study, 10,838 IBD patients were followed for 9,849 person-years. Serious infection rates were 5.25/100 person-years for TNFIs and 3.59/100 person-years for immunomodulators (methotrexate and thiopurines). New use of TNFI monotherapy was associated with a 1.36-fold higher risk of serious infection compared to immunomodulator initiation. The risk of serious infection differed by individual TNFIs and route of administration. This dissertation characterized the utilization of TNFIs and indicated that a more aggressive treatment approach has emerged for children and young adults with JIA/RA and IBD despite an FDA warning about TNFI-associated serious infections. However, study findings support the warning for children with JIA and IBD. This dissertation provides insights into how TNFIs are being used and informs decision-making about use of these drugs–particularly regarding balancing the benefits and risks of TNFIs.
Advisors/Committee Members: Schumock, Glen T (advisor), Lee, Todd A (committee member), Calip, Gregory S (committee member), Suda, Katie J (committee member), Briars, Leslie (committee member), Schumock, Glen T (chair).
Subjects/Keywords: TNF inhibitors; infections
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th 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 (16th Edition):
Lee, Wan-Ju. “Utilization and Risk of Serious Infection Associated with TNF-α Inhibitors in Children and Young Adults.” 2016. Thesis, University of Illinois – Chicago. Accessed January 26, 2021.
http://hdl.handle.net/10027/21614.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Lee, Wan-Ju. “Utilization and Risk of Serious Infection Associated with TNF-α Inhibitors in Children and Young Adults.” 2016. Web. 26 Jan 2021.
Vancouver:
Lee W. Utilization and Risk of Serious Infection Associated with TNF-α Inhibitors in Children and Young Adults. [Internet] [Thesis]. University of Illinois – Chicago; 2016. [cited 2021 Jan 26].
Available from: http://hdl.handle.net/10027/21614.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Lee W. Utilization and Risk of Serious Infection Associated with TNF-α Inhibitors in Children and Young Adults. [Thesis]. University of Illinois – Chicago; 2016. Available from: http://hdl.handle.net/10027/21614
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Rochester
4.
Chen, Tony (1981 - ).
The Role of interstitial fluid flow as a mediator of
matrix anisotropy and as a protective mechanism against
inflammation in cartilage tissue engineering.
Degree: PhD, 2011, University of Rochester
URL: http://hdl.handle.net/1802/14143
► Injuries to articular cartilage are debilitating and typically require surgical intervention due to the tissue’s inability to self-repair. Current surgical options for focal cartilage defects…
(more)
▼ Injuries to articular cartilage are debilitating
and typically require surgical intervention due to the tissue’s
inability to self-repair. Current surgical options for focal
cartilage defects are successful only in treating the associated
symptoms, but produce inconsistent clinical outcomes in the long
term, and are implicated in degenerative joint changes years later.
As an alternative, functional tissue engineering may soon offer
translational approaches for cartilage repair by producing
implantable artificial tissues that recapitulate the composition,
structure, and function of the native tissue. While current tissue
engineering bioreactors that introduce various physiologically
inspired mechanical stimuli are able to reproduce the mechanical
properties of native cartilage, recreating the tissue’s structural
and compositional anisotropy, which might influence the integration
of the implanted tissue with the surrounding cartilage, has to date
remained elusive. Furthermore, the fate of the engineered construct
during the inflammatory phase that ensues upon implantation in the
joint has been less studied, as most of the literature focuses on
developing engineered cartilage in idealized culture conditions in
vitro, and for the most part neglects the interplay between
inflammation and repair mechanobiology.
This
dissertation sets to recreate aspects of the characteristic zonal
anisotropy of articular cartilage using custom-designed bioreactors
based on Couette and Poiseuille flow with the hypothesis that
interstitial fluid flow can influence matrix synthesis and the
alignment of collagen fibers. Using in situ hybridization and
immunohistochemistry, tissue engineered cartilage (TEC) hydrogels
that were cultured in a novel bioreactor that simulates rotational
Couette flow demonstrated an increase in aggrecan and type II
collagen mRNA expression and protein synthesis near the surface of
the hydrogel exposed to the flow, compared to deeper regions within
the hydrogel and control hydrogels not stimulated by Couette flow.
Furthermore, the alignment of the collagen fibers in the
superficial layer of the bioreactor-cultured TEC hydrogels was
significantly enhanced compared to controls. When quantified using
Fast Fourier Transform (FFT) algorithms, the collagen alignment in
the surface region of the bioreactor-cultured TEC hydrogels was
remarkably similar to the alignment pattern of collagen in the
superficial zone of native articular cartilage.
To
formally test the hypothesis that the aforementioned effects of
Couette flow are related to interstitial flow fields, the
interstitial flow velocity profiles within TEC hydrogels were
experimentally measured as a function of flow rate through a
parallel plate (Poiseuille flow) bioreactor using a flow
visualization technique based on Fluorescence Recovery After
Photobleaching (FRAP). Experimental measurements of the fluid
velocity profile over a range of flow rates demonstrated that
Poiseuille flow induced measurable interstitial flow fields near
the flow-exposed surface of…
Subjects/Keywords: Collagen alignment; Chondrocyte; TNF-&alpha
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th 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 (16th Edition):
Chen, Tony (1981 - ). “The Role of interstitial fluid flow as a mediator of
matrix anisotropy and as a protective mechanism against
inflammation in cartilage tissue engineering.” 2011. Doctoral Dissertation, University of Rochester. Accessed January 26, 2021.
http://hdl.handle.net/1802/14143.
MLA Handbook (7th Edition):
Chen, Tony (1981 - ). “The Role of interstitial fluid flow as a mediator of
matrix anisotropy and as a protective mechanism against
inflammation in cartilage tissue engineering.” 2011. Web. 26 Jan 2021.
Vancouver:
Chen T(-). The Role of interstitial fluid flow as a mediator of
matrix anisotropy and as a protective mechanism against
inflammation in cartilage tissue engineering. [Internet] [Doctoral dissertation]. University of Rochester; 2011. [cited 2021 Jan 26].
Available from: http://hdl.handle.net/1802/14143.
Council of Science Editors:
Chen T(-). The Role of interstitial fluid flow as a mediator of
matrix anisotropy and as a protective mechanism against
inflammation in cartilage tissue engineering. [Doctoral Dissertation]. University of Rochester; 2011. Available from: http://hdl.handle.net/1802/14143

University of Alberta
5.
Srivastava, Nutan.
NEUTROPHIL SECRETION OF THE PROINFLAMMATORY CYTOKINE TNF VIA
RECYCLING ENDOSOMES.
Degree: MS, Department of Medicine, 2015, University of Alberta
URL: https://era.library.ualberta.ca/files/mp48sg31c
► Neutrophils are highly abundant innate immune cells that are important in immediate responses to injury and infection, and secrete the proinflammatory cytokine tumor necrosis factor…
(more)
▼ 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
(TNF). Inflammatory cytokines have many potent effects and their
excess or deficiency may have many clinical consequences. However,
cytokine trafficking and secretion in neutrophils has not been well
characterized. Recycling endosomes (REs) are specialized secretory
compartments that perform multiple functions including trafficking
of cytokines to cell surfaces, although these are not characterized
in neutrophils. Our objective is to identify trafficking components
in neutrophils that may contribute to cytokine secretion. This
study presents data that shows that LPS induced 30-40% TNF
secretion from stored sources, with the remainder newly
synthesized. We also found that neutrophils possess REs as
determined by transferrin uptake and VAMP-3 labeling. TNF also
colocalized with REs, primary and secondary granules as well as
early and late endosomes, suggesting multiple sites of TNF storage
and trafficking in neutrophils. TNF colocalized with VAMP-3 around
periphery of cells after 1 h stimulation with LPS, suggesting
TLR4-induced TNF trafficking via REs. The present study provides
evidence that movement of TNF+VAMP-3+ vesicles towards the cell
periphery in response to LPS. This suggests that neutrophils
utilize REs for trafficking of TNF to the cell surface in response
to TLR4 signaling. These findings contribute to our understanding
of how neutrophils package, transport, and release
cytokines.
Subjects/Keywords: Neutrophil; Recycling endosomes; TNF-alpha
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th 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 (16th Edition):
Srivastava, Nutan. “NEUTROPHIL SECRETION OF THE PROINFLAMMATORY CYTOKINE TNF VIA
RECYCLING ENDOSOMES.” 2015. Masters Thesis, University of Alberta. Accessed January 26, 2021.
https://era.library.ualberta.ca/files/mp48sg31c.
MLA Handbook (7th Edition):
Srivastava, Nutan. “NEUTROPHIL SECRETION OF THE PROINFLAMMATORY CYTOKINE TNF VIA
RECYCLING ENDOSOMES.” 2015. Web. 26 Jan 2021.
Vancouver:
Srivastava N. NEUTROPHIL SECRETION OF THE PROINFLAMMATORY CYTOKINE TNF VIA
RECYCLING ENDOSOMES. [Internet] [Masters thesis]. University of Alberta; 2015. [cited 2021 Jan 26].
Available from: https://era.library.ualberta.ca/files/mp48sg31c.
Council of Science Editors:
Srivastava N. NEUTROPHIL SECRETION OF THE PROINFLAMMATORY CYTOKINE TNF VIA
RECYCLING ENDOSOMES. [Masters Thesis]. University of Alberta; 2015. Available from: https://era.library.ualberta.ca/files/mp48sg31c

Universidade do Rio Grande do Sul
6.
Jardim, Fernanda Rafaela.
Ação da adenosina extracelular sobre uma linhagem de célula estrelada hepática tratada com TNF-[alfa] : papel do receptor A2B.
Degree: 2008, Universidade do Rio Grande do Sul
URL: http://hdl.handle.net/10183/14831
► Fibrose hepática é caracterizada pelo acúmulo de matriz extracelular fibrótica, cuja presença danifica as funções do fígado. Células estreladas hepáticas (HSCs) participam ativamente deste processo,…
(more)
▼ Fibrose hepática é caracterizada pelo acúmulo de matriz extracelular fibrótica, cuja presença danifica as funções do fígado. Células estreladas hepáticas (HSCs) participam ativamente deste processo, modificando seu fenótipo quiescente, rico em lipídios no citoplasma, para o fenótipo ativado, em resposta ao insulto fibrogênico. A regressão do processo fibrótico pode, inclusive, estar relacionada com a apoptose das HSCs e também com sua reversão fenotípica, do estado ativado ao estado quiescente. Adenosina tem papel hepatoprotetor bem conhecido e medeia várias ações antiinflamatórias em diferentes tipos celulares e condições patológicas.
TNF-α é uma citocina pró-inflamatória com importantes funções no início e perpetuação do processo fibrogênico. Tendo em vista o papel antiinflamatório da adenosina, este trabalho investigou, em linhagem de HSC em cultura - GRX -, as ações desse nucleosídeo em presença ou ausência dos sinais inflamatórios que acompanham o tratamento com
TNF- α. Assim, foram analisados os efeitos da adenosina extracelular na síntese lipídica, avaliando a reversão fenotípica da GRX, e a apoptose em resposta à adenosina e/ou
TNF-α. Além disso, a regulação dos níveis de adenosina extracelular, bem como a presença dos receptores de adenosina foram investigadas. O efeito de adenosina e/ou
TNF-α sobre a produção de óxido nítrico (NO) e atividade e expressão de gelatinases (MMP-9 e -2), ambos importantes mediadores na fibrose hepática, também foram alvo deste estudo. Nossos resultados mostram a presença do receptor de adenosina A2B (A2BR), e a regulação dos níveis extracelulares de adenosina por
TNF-α, através do aumento da atividade ecto-adenosina deaminase. Além disso, demontramos que adenosina extracelular não modifica a síntese de lipídios nas células GRX. Os dados ainda indicam que adenosina, em presença ou ausência de
TNF-α, não resulta em apoptose, e que esta citocina também não induz à formação de corpos apoptóticos nas células tratadas. O estudo mostra que a produção de NO foi aumentada com
TNF-α, com potencialização deste efeito na presença de adenosina, provavelmente mediado pelo A2BR e não por inosina, produto da hidrólise de adenosina. Com relação às gelatinases, o tratamento com adenosina diminui a atividade de MMP-9 tanto em ausência, quanto em presença de
TNF-α, revertendo a ação da citocina, a níveis de controle, com o envolvimento do receptor A2BR mediando os efeitos do nucleosídeo. No entanto, a expressão da MMP-9 não foi afetada pelo tratamento com adenosina, porém, o nucleosídeo diminui os efeitos de
TNF-α sobre a expressão da gelatinase. Com relação à MMP-2, ambos tratamentos com adenosina e com
TNF-α, bem como o tratamento com adenosina, em presença da citocina, diminuem a atividade da gelatinase, sem efeitos aditivos. A expressão do mRNA de MMP-2 aumentou em resposta aos tratamentos com adenosina e
TNF-α, isolados ou em associação, indicando a presença de mecanismo pós-transcricional de regulação para MMP-2. Este trabalho mostra, claramente, que adenosina extracelular e
TNF-α estão…
Advisors/Committee Members: Bernard, Elena Aida.
Subjects/Keywords: Adenosina; TNF-alfa; Cirrose hepática
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th 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 (16th Edition):
Jardim, Fernanda Rafaela. “Ação da adenosina extracelular sobre uma linhagem de célula estrelada hepática tratada com TNF-[alfa] : papel do receptor A2B.” 2008. Thesis, Universidade do Rio Grande do Sul. Accessed January 26, 2021.
http://hdl.handle.net/10183/14831.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Jardim, Fernanda Rafaela. “Ação da adenosina extracelular sobre uma linhagem de célula estrelada hepática tratada com TNF-[alfa] : papel do receptor A2B.” 2008. Web. 26 Jan 2021.
Vancouver:
Jardim FR. Ação da adenosina extracelular sobre uma linhagem de célula estrelada hepática tratada com TNF-[alfa] : papel do receptor A2B. [Internet] [Thesis]. Universidade do Rio Grande do Sul; 2008. [cited 2021 Jan 26].
Available from: http://hdl.handle.net/10183/14831.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Jardim FR. Ação da adenosina extracelular sobre uma linhagem de célula estrelada hepática tratada com TNF-[alfa] : papel do receptor A2B. [Thesis]. Universidade do Rio Grande do Sul; 2008. Available from: http://hdl.handle.net/10183/14831
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Vanderbilt University
7.
Ardestani, Shidrokh.
New insights into tumor necrosis factor-alpha in cancer: distinct isoforms exert opposing effects on tumor associated myeloid cells and tumorigenesis.
Degree: PhD, Pathology, 2013, Vanderbilt University
URL: http://hdl.handle.net/1803/13448
► TNF-α, produced by most malignant cells, orchestrates the interplay between malignant cells and myeloid cells, which have been linked to tumor growth and metastasis. Although…
(more)
▼ TNF-α, produced by most malignant cells, orchestrates the interplay between malignant cells and myeloid cells, which have been linked to tumor growth and metastasis. Although
TNF-α can exist as one of two isoforms, a 26-kDa membrane tethered form (mTNF-α) or a soluble 17-kDa cytokine (sTNF-α), the vast majority of published studies have only investigated the biological effects of the soluble form. We demonstrate for the first time that membrane and soluble isoforms have diametrically opposing effects on both tumor growth and myeloid content. Mouse lung and melanoma tumor lines expressing mTNF-α, generated small tumors devoid of monocytes versus respective control lines or lines expressing sTNF-α. The lack of myeloid cells was due to a direct effect of mTNF-α on myeloid survival via induction of cell necrosis by increasing reactive oxygen species. Using cultured RAW 264.7 monocytic cell line and L929 fibroblasts we showed that mTNF-α increased reactive oxygen species (ROS)-mediated cytotoxicity, independent of caspase-3 activity. Although
TNF-α receptors (TNFR) on target cells were required for this effect, we observed that mTNF-α-induced cell death could be mediated through both TNFR-1 and the death domain-lacking TNFR-2. ROS generation and cytotoxicity were inhibited by a mitochondrial respiratory chain inhibitor but not by an inhibitor of NADPH oxidase. Furthermore, mTNF-α mediated cytotoxicity was independent of RIP-1, a serine/threonine kinase which serves as a main adaptor protein of sTNF-α induced programmed necrosis, but rather depended on ceramide signaling pathways. Furthermore, we found that human none-small-cells lung carcinomas (NSCLCs) expressed varying levels of both soluble and membrane
TNF-α. Analysis of publicly accessible NSCLC microarray database showed that gene expression patterns favoring mTNF-α were predictive of improved lung cancer survival.
Advisors/Committee Members: Sarki Abdulkadir (committee member), Jin Chen (committee member), Ambra Pozzi (committee member), Bill Valentine (Committee Chair).
Subjects/Keywords: ROS; Myeloid cells; TNF-alpha
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Ardestani, S. (2013). New insights into tumor necrosis factor-alpha in cancer: distinct isoforms exert opposing effects on tumor associated myeloid cells and tumorigenesis. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/13448
Chicago Manual of Style (16th Edition):
Ardestani, Shidrokh. “New insights into tumor necrosis factor-alpha in cancer: distinct isoforms exert opposing effects on tumor associated myeloid cells and tumorigenesis.” 2013. Doctoral Dissertation, Vanderbilt University. Accessed January 26, 2021.
http://hdl.handle.net/1803/13448.
MLA Handbook (7th Edition):
Ardestani, Shidrokh. “New insights into tumor necrosis factor-alpha in cancer: distinct isoforms exert opposing effects on tumor associated myeloid cells and tumorigenesis.” 2013. Web. 26 Jan 2021.
Vancouver:
Ardestani S. New insights into tumor necrosis factor-alpha in cancer: distinct isoforms exert opposing effects on tumor associated myeloid cells and tumorigenesis. [Internet] [Doctoral dissertation]. Vanderbilt University; 2013. [cited 2021 Jan 26].
Available from: http://hdl.handle.net/1803/13448.
Council of Science Editors:
Ardestani S. New insights into tumor necrosis factor-alpha in cancer: distinct isoforms exert opposing effects on tumor associated myeloid cells and tumorigenesis. [Doctoral Dissertation]. Vanderbilt University; 2013. Available from: http://hdl.handle.net/1803/13448

North Carolina State University
8.
Harris, Virginia Gail.
The intracellular targeting of cPLA2.
Degree: MS, Microbiology, 2002, North Carolina State University
URL: http://www.lib.ncsu.edu/resolver/1840.16/1243
► Tumor necrosis factor-α (TNF) is an inflammatory cytokine that can induce apoptosis in virus-infected cells, susceptible tumor cells, and cells whose transcriptional or translational processes…
(more)
▼ Tumor necrosis factor-α (
TNF) is an inflammatory cytokine that can induce apoptosis in virus-infected cells, susceptible tumor cells, and cells whose transcriptional or translational processes have been disrupted. The apoptotic pathway that is activated by
TNF is dependent on the activity of the enzyme cytosolic phospholipase A2 (cPLA2). This enzyme cleaves arachidonic acid from membrane phospholipid, which in turn causes mitochondrial dysfunction leading to cell death. The goal of this research project was to identify the specific intracellular membrane to which cPLA2 binds during
TNF-induced apoptosis. The membrane site for cPLA2 interaction during apoptosis would be a possible target for anti-apoptotic drug development. Three methods were tested in an attempt to identify the membrane location, including; immunofluorescence, biochemical fractionation, and GC/MS. Our results with immunofluorescence suggested that cPLA2 translocates to the nuclear membrane during apoptosis. The identity of the nuclear membrane was confirmed by staining with an antibody to the nuclear pore complex. In addition, cPLA2 staining was noted within the nucleus, perhaps indicating an interaction with chromatin, and small areas of punctate staining were noted in the perinuclear region. Biochemical fractionation indicated that the association of cPLA2 with the nuclear membrane was calcium-dependent since this association could not be stabilized in the absence of calcium. GC/MS, which was used in an attempt to find amputated phospholipids remaining in membranes as a result of cPLA2 activity, instead revealed higher levels of arachidonic acid suggesting that cells may increase the synthesis or repair of arachidonic acid containing membranes following the activation of cPLA2. Finally, our results revealed several novel, lower molecular weight forms of cPLA2 that were associated with nuclei in a calcium-independent fashion. Taken together these results suggest that it will be important to understand the mechanisms controlling the association of cPLA2 with nuclei.
Advisors/Committee Members: Scott Laster, Committee Member (advisor), Amy Grunden, Committee Member (advisor), Geraldine Luginbuhl, Committee Member (advisor).
Subjects/Keywords: cPLA2; TNF
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th 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 (16th Edition):
Harris, Virginia Gail. “The intracellular targeting of cPLA2.” 2002. Thesis, North Carolina State University. Accessed January 26, 2021.
http://www.lib.ncsu.edu/resolver/1840.16/1243.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Harris, Virginia Gail. “The intracellular targeting of cPLA2.” 2002. Web. 26 Jan 2021.
Vancouver:
Harris VG. The intracellular targeting of cPLA2. [Internet] [Thesis]. North Carolina State University; 2002. [cited 2021 Jan 26].
Available from: http://www.lib.ncsu.edu/resolver/1840.16/1243.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Harris VG. The intracellular targeting of cPLA2. [Thesis]. North Carolina State University; 2002. Available from: http://www.lib.ncsu.edu/resolver/1840.16/1243
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Debrecen
9.
Nemes, Olívia.
Tumor nekrózis faktor-alfa (TNF-α) szerepe
.
Degree: DE – Természettudományi és Technológiai Kar – Biológiai és Ökológiai Intézet, University of Debrecen
URL: http://hdl.handle.net/2437/211769
► A TNF-α egy gyulladást keltő citokin, amelynek kettő formája ismert, egy szolubilis és egy membrán kötött. Részt vesznek a fertőzés és a daganatok elleni védekezésben,…
(more)
▼ 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, a sejtek túlélésének szabályozásában, illetve a homeosztázis fenntartásában is. Apoptózist indukál, gátolja a daganatos sejtek szaporodását és befolyásolja számos gyulladási mediátor termelődését.
Advisors/Committee Members: Szondy, Zsuzsanna (advisor).
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 (6th 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 (16th Edition):
Nemes, Olívia. “Tumor nekrózis faktor-alfa (TNF-α) szerepe
.” Thesis, University of Debrecen. Accessed January 26, 2021.
http://hdl.handle.net/2437/211769.
Note: this citation may be lacking information needed for this citation format:
No year of publication.
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Nemes, Olívia. “Tumor nekrózis faktor-alfa (TNF-α) szerepe
.” Web. 26 Jan 2021.
Note: this citation may be lacking information needed for this citation format:
No year of publication.
Vancouver:
Nemes O. Tumor nekrózis faktor-alfa (TNF-α) szerepe
. [Internet] [Thesis]. University of Debrecen; [cited 2021 Jan 26].
Available from: http://hdl.handle.net/2437/211769.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
No year of publication.
Council of Science Editors:
Nemes O. Tumor nekrózis faktor-alfa (TNF-α) szerepe
. [Thesis]. University of Debrecen; Available from: http://hdl.handle.net/2437/211769
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
No year of publication.

University of Debrecen
10.
Hajdu, Dorottya Zsuzsanna.
Az antipszichotikumok makrofágok funkcionális aktivitására gyakorolt hatása
.
Degree: DE – Természettudományi és Technológiai Kar – Biológiai és Ökológiai Intézet, 2014, University of Debrecen
URL: http://hdl.handle.net/2437/191161
► Célom volt az atípusos antipszichotikumok hatásának vizsgálata humán monocita-makrofág differenciálódásra. Kísérleteim során használt gyógyszerek a Quetiapin, Aripiprasol, Ziprasidon, Risperidon, Clozapin és Olanzapin, a Haloperidol antipszichotikumok…
(more)
▼ 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 voltak. Vizsgáltam, hogy ezek a gyógyszerek befolyásolják-e a makrofágok fagocitózis képességét, citokin expresszióját és szuperoxid termelését. A monocitákat humán vérből izoláltam mágneses szeparálással, majd makrofág kolónia-stimuláló faktort (M-CSF) tartalmazó tápoldatban differenciáltattam, naponta ismétlődő, a klinikumban alkalmazott szérum koncentrációnak megfelelő antipszichotikum kezelés mellett. A fagocitózis képesség vizsgálatára humán vérből izolált apoptótikus neutrofil granulocitákkal végzett, áramlási citometriás meghatározáson alapuló fagocitózis mérést alkalmaztam. A makrofágok
TNF-α szekrécióját, LPS stimulust követően szendvics ELISA módszerrel határoztam meg. A makrofágok PMA indukált szuperoxid termelését L-012 kemilumineszcenciás próba jelenlétében vizsgáltam. Eredményeim azt mutatják, hogy az in vivo kezelési koncentrációk mellett, az Olanzapin, Haloperidol és a Risperidon szignifikánsan csökkentette a makrofágok fagocitózis képességét apoptótikus neutrofilek iránt. Az LPS stimulust követően, a makrofág által szekretált
TNF-α mennyiségét a gyógyszeres kezelés a legtöbb esetben csökkentette. Ugyanakkor a Haloperidol kivételével az antipszichotikumok fokozták a makrofágok PMA indukált szuperoxid termelését.
Advisors/Committee Members: Balajthy, Zoltán (advisor).
Subjects/Keywords: monocita;
differenciálódás;
TNF-alfa
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th 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 (16th Edition):
Hajdu, Dorottya Zsuzsanna. “Az antipszichotikumok makrofágok funkcionális aktivitására gyakorolt hatása
.” 2014. Thesis, University of Debrecen. Accessed January 26, 2021.
http://hdl.handle.net/2437/191161.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Hajdu, Dorottya Zsuzsanna. “Az antipszichotikumok makrofágok funkcionális aktivitására gyakorolt hatása
.” 2014. Web. 26 Jan 2021.
Vancouver:
Hajdu DZ. Az antipszichotikumok makrofágok funkcionális aktivitására gyakorolt hatása
. [Internet] [Thesis]. University of Debrecen; 2014. [cited 2021 Jan 26].
Available from: http://hdl.handle.net/2437/191161.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Hajdu DZ. Az antipszichotikumok makrofágok funkcionális aktivitására gyakorolt hatása
. [Thesis]. University of Debrecen; 2014. Available from: http://hdl.handle.net/2437/191161
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
11.
Silva, Mariana Machado da.
Polimorfismo da região do fator de necrose tumoral (TNF) na síndrome da lipodistrofia associada à terapia anti-retroviral em portadores do HIV-1.
Degree: Mestrado, Enfermagem Fundamental, 2008, University of São Paulo
URL: http://www.teses.usp.br/teses/disponiveis/22/22132/tde-27052008-144002/
;
► 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 (6th 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 (16th Edition):
Silva, Mariana Machado da. “Polimorfismo da região do fator de necrose tumoral (TNF) na síndrome da lipodistrofia associada à terapia anti-retroviral em portadores do HIV-1.” 2008. Masters Thesis, University of São Paulo. Accessed January 26, 2021.
http://www.teses.usp.br/teses/disponiveis/22/22132/tde-27052008-144002/ ;.
MLA Handbook (7th Edition):
Silva, Mariana Machado da. “Polimorfismo da região do fator de necrose tumoral (TNF) na síndrome da lipodistrofia associada à terapia anti-retroviral em portadores do HIV-1.” 2008. Web. 26 Jan 2021.
Vancouver:
Silva MMd. Polimorfismo da região do fator de necrose tumoral (TNF) na síndrome da lipodistrofia associada à terapia anti-retroviral em portadores do HIV-1. [Internet] [Masters thesis]. University of São Paulo; 2008. [cited 2021 Jan 26].
Available from: http://www.teses.usp.br/teses/disponiveis/22/22132/tde-27052008-144002/ ;.
Council of Science Editors:
Silva MMd. Polimorfismo da região do fator de necrose tumoral (TNF) na síndrome da lipodistrofia associada à terapia anti-retroviral em portadores do HIV-1. [Masters Thesis]. University of São Paulo; 2008. Available from: http://www.teses.usp.br/teses/disponiveis/22/22132/tde-27052008-144002/ ;
12.
Kouris, Anargyros.
Ψωρίαση: διερεύνηση μεταβολών των Τ-λεμφοκυττάρων στην ανοσολογική διαταραχή των ασθενών με ψωρίαση.
Degree: 2014, National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ)
URL: http://hdl.handle.net/10442/hedi/42257
► 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)
▼ 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 (6th 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 (16th Edition):
Kouris, Anargyros. “Ψωρίαση: διερεύνηση μεταβολών των Τ-λεμφοκυττάρων στην ανοσολογική διαταραχή των ασθενών με ψωρίαση.” 2014. Thesis, National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ). Accessed January 26, 2021.
http://hdl.handle.net/10442/hedi/42257.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Kouris, Anargyros. “Ψωρίαση: διερεύνηση μεταβολών των Τ-λεμφοκυττάρων στην ανοσολογική διαταραχή των ασθενών με ψωρίαση.” 2014. Web. 26 Jan 2021.
Vancouver:
Kouris A. Ψωρίαση: διερεύνηση μεταβολών των Τ-λεμφοκυττάρων στην ανοσολογική διαταραχή των ασθενών με ψωρίαση. [Internet] [Thesis]. National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ); 2014. [cited 2021 Jan 26].
Available from: http://hdl.handle.net/10442/hedi/42257.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Kouris A. Ψωρίαση: διερεύνηση μεταβολών των Τ-λεμφοκυττάρων στην ανοσολογική διαταραχή των ασθενών με ψωρίαση. [Thesis]. National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ); 2014. Available from: http://hdl.handle.net/10442/hedi/42257
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Univerzitet u Beogradu
13.
Ilić, Branislav B., 1981-.
Ispitivanje polimorfizama gena za metilentetrahidrofolat
reduktazu, glutation transferazu, faktor nekroze tumora alfa i
njegove receptore u epitelnim tumorima usne duplje.
Degree: Stomatološki fakultet, 2016, Univerzitet u Beogradu
URL: https://fedorabg.bg.ac.rs/fedora/get/o:13271/bdef:Content/get
► oralna hirurgija - onkogenetika / oral surgery - oncogenetic
Uvod: Odontogeni keratocistični tumor (OKT) i oralni planocelularni karcinom (OPK) pripadaju grupi oralnih epitelnih tumora. Iako…
(more)
▼ 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 (6th 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 (16th Edition):
Ilić, Branislav B., 1981-. “Ispitivanje polimorfizama gena za metilentetrahidrofolat
reduktazu, glutation transferazu, faktor nekroze tumora alfa i
njegove receptore u epitelnim tumorima usne duplje.” 2016. Thesis, Univerzitet u Beogradu. Accessed January 26, 2021.
https://fedorabg.bg.ac.rs/fedora/get/o:13271/bdef:Content/get.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Ilić, Branislav B., 1981-. “Ispitivanje polimorfizama gena za metilentetrahidrofolat
reduktazu, glutation transferazu, faktor nekroze tumora alfa i
njegove receptore u epitelnim tumorima usne duplje.” 2016. Web. 26 Jan 2021.
Vancouver:
Ilić, Branislav B. 1. Ispitivanje polimorfizama gena za metilentetrahidrofolat
reduktazu, glutation transferazu, faktor nekroze tumora alfa i
njegove receptore u epitelnim tumorima usne duplje. [Internet] [Thesis]. Univerzitet u Beogradu; 2016. [cited 2021 Jan 26].
Available from: https://fedorabg.bg.ac.rs/fedora/get/o:13271/bdef:Content/get.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Ilić, Branislav B. 1. Ispitivanje polimorfizama gena za metilentetrahidrofolat
reduktazu, glutation transferazu, faktor nekroze tumora alfa i
njegove receptore u epitelnim tumorima usne duplje. [Thesis]. Univerzitet u Beogradu; 2016. Available from: https://fedorabg.bg.ac.rs/fedora/get/o:13271/bdef:Content/get
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
14.
Γεωργιάδου, Μαρία.
Μελέτη των υποδοχέων του TNFα στα κύτταρα Kupffer και στο ηπατοκυτταρικό καρκίνωμα.
Degree: 2011, University of Crete (UOC); Πανεπιστήμιο Κρήτης
URL: http://hdl.handle.net/10442/hedi/26069
► Tumor necrosis factor (TNF), a pleiotropic cytokine involved in a broad spectrum of inflammatory and immune responses, exerts its biological effects by engaging two distinct…
(more)
▼ Tumor necrosis factor (TNF), a pleiotropic cytokine involved in a broad spectrum of inflammatory and immune responses, exerts its biological effects by engaging two distinct cell surface receptors, the 55-kD TNFR1 and the 75-kD TNFR2. Both TNF Receptors (TNFRs) have the ability to mediate cell death via various mechanisms. TNFR1 stimulation may also result in inhibition of apoptosis through induction of the transcription factor NF-kappaB, specifically the heterodimer p50/p65. In response to TNF, p65 undergoes several post-translational modifications, including phosphorylation on serines 536 and 468, and translocates to the nucleus, where it typically mediates expression of many pro-survival genes. Depending on the cell type and the stimulus involved, NF-kappaB may also have a proapoptotic function. TNF in liver is mainly produced by Kupffer cells (KC), the resident liver macrophages, and has a pivotal role in hepatic homeostasis and pathophysiology, since it holds the capacity to induce both hepatocyte cell death and proliferation. KC have been demonstrated to be implicated in the defence against the development of hepatic metastases from various extrahepatic tumors, but on the other hand, they may also be detrimental in the development of liver cancer. Hepatocellular carcinoma (HCC), the main histological type of liver cancer, is a major cause of morbidity and mortality worldwide. Because of its innate resistance to the conventional treatment regiments, the investigation of new therapeutic agents is required. A large number of clinical and experimental data indicate that Octreotide, a potent synthetic somatostatin analogue with antiproliferative, antisecretory and immunomodulatory properties, may be a promising anti-cancer therapeutic agent. Octreotide has been reported to prolong survival in approximately 40% of patients with unresectable hepatocellular carcinoma. Although the favourable findings have been disputed, these negative studies have been criticized for the selection of the participating patients. Previous work in our laboratory has demonstrated that Octreotide has a direct antiproliferative effect on human hepatoma cells HepG2 and modulates the expression of pro- or antifibrotic agents, inflammatory mediators, chemokines and apoptosis related proteins in rat KC. To further explore the mechanisms by which Octreotide exerts its antineoplastic actions, we evaluated its influence, at the clinically feasible concentration of 10-8 Μ, on TNFRs expression, NF-kappaB activation and apoptotic response of KC and HepG2/Hep3B human hepatoma cells to TNF. Rat KC were isolated by centrifugal elutriation. TNFR1 and TNFR2 expression was studied by RT-PCR, quantitative PCR, Western Blot and immunofluorescence. TNF mRNA expression in KC was also assessed by semiquantitative PCR. Intracellular localization of NF-kappaB in HepG2/Hep3B was detected by immunofluorescent analysis and a cell-based ELISA assay was used to quantitate total and active (phosphorylated at serine 536 and serine 468) p65. Apoptosis was examined by a…
Subjects/Keywords: Ηπατοκυτταρικό καρκίνωμα; Οκτρεοτίδη; Υποδοχείς TNF; Απόπτωση; Hepatocellular carcinoma; Kupffer cells; Octreotide; TNF; TNF receptors; p65; Apoptosis
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Record Details
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th 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 (16th Edition):
Γεωργιάδου, Μαρία. “Μελέτη των υποδοχέων του TNFα στα κύτταρα Kupffer και στο ηπατοκυτταρικό καρκίνωμα.” 2011. Thesis, University of Crete (UOC); Πανεπιστήμιο Κρήτης. Accessed January 26, 2021.
http://hdl.handle.net/10442/hedi/26069.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Γεωργιάδου, Μαρία. “Μελέτη των υποδοχέων του TNFα στα κύτταρα Kupffer και στο ηπατοκυτταρικό καρκίνωμα.” 2011. Web. 26 Jan 2021.
Vancouver:
Γεωργιάδου . Μελέτη των υποδοχέων του TNFα στα κύτταρα Kupffer και στο ηπατοκυτταρικό καρκίνωμα. [Internet] [Thesis]. University of Crete (UOC); Πανεπιστήμιο Κρήτης; 2011. [cited 2021 Jan 26].
Available from: http://hdl.handle.net/10442/hedi/26069.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Γεωργιάδου . Μελέτη των υποδοχέων του TNFα στα κύτταρα Kupffer και στο ηπατοκυτταρικό καρκίνωμα. [Thesis]. University of Crete (UOC); Πανεπιστήμιο Κρήτης; 2011. Available from: http://hdl.handle.net/10442/hedi/26069
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Rochester
15.
Fahrenthold, Berkeley Kristyn.
Assessment of the Involvement of Intrinsic and Extrinsic
Cell Death Pathways in Retinal Ganglion Cell Death after
Excitotoxic Injury.
Degree: PhD, 2017, University of Rochester
URL: http://hdl.handle.net/1802/32924
► Excitotoxicity leads to disruption of the intracellular environment and activation of cytotoxic cascades that cause neuronal death. Multiple cell types, including both neurons and glia,…
(more)
▼ Excitotoxicity leads to disruption of the
intracellular environment and activation of
cytotoxic cascades
that cause neuronal death. Multiple cell types, including both
neurons
and glia, are affected by excitotoxic insult. In the
mammalian retina, cells that die following
this insult are retinal
ganglion (RGCs) and amacrine cells. Both intrinsic and extrinsic
signals have been hypothesized to activate injury response and cell
death pathways that
ultimately result in RGC death. Here, I test
the importance of a TNF-dependent extrinsic
apoptotic pathway and
JNK signaling, an intrinsic cell death pathway shown to result in
RGC apoptosis after diverse insults, in excitotoxicity induced RGC
death. Tumor necrosis
factor (TNF), through BID-dependent
signaling, is known to be a key extrinsic mediator
of neuronal
degeneration. TNF released by Müller glial cells has also been
suggested to be
important in RGC death after an excitotoxic
injury. To critically test the importance of TNF
in RGC death
after excitotoxic injury, the excitotoxin N-methyl-D-aspartate
(NMDA) was
intravitreally injected into mice deficient in TNF.
Absence of Tnf did not confer short- or
long-term protection to
RGCs. Further suggesting that TNF mediated extrinsic cell death
pathways are not required for excitotoxic RGC death, Bid deficiency
did not protect RGCs
nor did it prevent cytochrome c release.
Thus, a key extrinsic pathway that has been
implicated in RGC
death was found to not be necessary for RGC death after
excitotoxic
injury. Intrinsic cell signaling pathways have also
been implicated in excitotoxic neuronal
death. JNK signaling is
known to be a critical mediator of NMDA-induced cell death in
other neuronal cell types. JNK signaling is also known to be
critical for RGC death after a
variety injuries and is activated
in RGCs after excitotoxic injury. To test the importance of
JNK
signaling in RGC death after an excitotoxic insult, mice deficient
in various JNK
isoforms were used. Despite known expression in
RGCs, involvement in excitotoxic injury
in other neurons, and a
prominent role in mediating RGC death after other insults,
attenuating JNK signaling did not prevent RGC death after
excitotoxic insult. Collectively,
these results indicate that the
cell death pathways that orchestrate RGC death after diverse
pathological insults are not analogous. Future studies aimed at
using a combinatorial
approach to target multiple cell death
pathways simultaneously will be needed to shed light
on the
mechanisms that lead to RGC death after an excitotoxic
insult.
Subjects/Keywords: Retina; Excitotoxicity; NMDA; TNF; JNK; CHOP
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Fahrenthold, B. K. (2017). Assessment of the Involvement of Intrinsic and Extrinsic
Cell Death Pathways in Retinal Ganglion Cell Death after
Excitotoxic Injury. (Doctoral Dissertation). University of Rochester. Retrieved from http://hdl.handle.net/1802/32924
Chicago Manual of Style (16th Edition):
Fahrenthold, Berkeley Kristyn. “Assessment of the Involvement of Intrinsic and Extrinsic
Cell Death Pathways in Retinal Ganglion Cell Death after
Excitotoxic Injury.” 2017. Doctoral Dissertation, University of Rochester. Accessed January 26, 2021.
http://hdl.handle.net/1802/32924.
MLA Handbook (7th Edition):
Fahrenthold, Berkeley Kristyn. “Assessment of the Involvement of Intrinsic and Extrinsic
Cell Death Pathways in Retinal Ganglion Cell Death after
Excitotoxic Injury.” 2017. Web. 26 Jan 2021.
Vancouver:
Fahrenthold BK. Assessment of the Involvement of Intrinsic and Extrinsic
Cell Death Pathways in Retinal Ganglion Cell Death after
Excitotoxic Injury. [Internet] [Doctoral dissertation]. University of Rochester; 2017. [cited 2021 Jan 26].
Available from: http://hdl.handle.net/1802/32924.
Council of Science Editors:
Fahrenthold BK. Assessment of the Involvement of Intrinsic and Extrinsic
Cell Death Pathways in Retinal Ganglion Cell Death after
Excitotoxic Injury. [Doctoral Dissertation]. University of Rochester; 2017. Available from: http://hdl.handle.net/1802/32924
16.
Izadi, Hooman.
Innate immune responses to B. burgdorferi mediated by JNK1 and the cochaperone, methylation controlled DNAJ (MCJ).
Degree: PhD, Animal Biotechnology & Biomedical Sciences, 2011, U of Massachusetts : PhD
URL: https://scholarworks.umass.edu/open_access_dissertations/360
► The infections agent of Lyme disease, Borrelia Burgdorferi is a complex microorganism with a highly diverse genome. One of the most remarkable aspects of…
(more)
▼ The infections agent of Lyme disease, Borrelia Burgdorferi is a complex microorganism with a highly diverse genome. One of the most remarkable aspects of the
B. burgdorferi genome is the large number of sequences encoding predicted or known lipoproteins, including outer-surface proteins. The
B. burgdorferi genome encodes no recognizable toxins. Instead, this extracellular pathogen causes pathology by migration through tissues, adhesion to host cells, and evasion of immune clearance. Inflammation elicited by infection with
B. burgdorferi depends on the ability of the spirochete to survive in the mammalian host, as well as the immune response that arises upon the interaction of the bacterium with phagocytic, T and other cell types. Innate immune responses are critical in recognition and clearance of pathogens, and also play an important role in the outcome of adaptive immune responses. The regulation of innate immune responses to pathogens occurs through the interaction of Toll-like receptors (TLRs) with pathogen-associated molecular patterns (PAMPs) and the activation of several signaling pathways whose contribution to the overall innate immune response to pathogens is poorly understood. In this study we demonstrate a mechanism of control of murine macrophage responses mediated by TLR1/2 heterodimers through c-Jun N-terminal kinase 1 (JNK1) activity. JNK also controls tumor necrosis factor production and TLR-mediated macrophage responses to
B. burgdorferi. We also show that the proximal promoter region of the human tlr1 gene contains an AP-1 binding site that is subjected to regulation by the kinase and binds two complexes that involve the JNK substrates c-Jun, JunD, and ATF-2. These results demonstrate that JNK1 regulates the response to TLR1/2 ligands and suggest a positive feedback loop that may serve to increase the innate immune response to the spirochete. MCJ is a newly identified member of the DnaJ protein family of cochaperones that contains unique features different than the normally described DnaJ proteins. However, there is little known about its function and the role it plays in different cells and systems. It has been previously shown that MCJ is required for the repression of the ABCB1 drug transporter expression in breast cancer cells, and that this repression is mediated through the control of c-Jun protein stability. We were therefore interested in determining the role that MCJ plays in macrophages in response to
B. burgdorferi antigens. We now provide evidence that MCJ controls inflammatory responses of macrophages through the regulation of c-Jun protein stability, and the expression and release of the inflammatory cytokine
TNF through the regulation of the expression of
TNF converting enzyme (TACE) inhibitor tissue inhibitor of metalloproteinase 3 (TIMP-3).
Advisors/Committee Members: Juan Anguita, Barbara A. Osborne, Wilmore Webley.
Subjects/Keywords: JNK1; MCJ; TLR; TNF; Animal Sciences; Biotechnology
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APA ·
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Vancouver ·
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to Zotero / EndNote / Reference
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APA (6th Edition):
Izadi, H. (2011). Innate immune responses to B. burgdorferi mediated by JNK1 and the cochaperone, methylation controlled DNAJ (MCJ). (Doctoral Dissertation). U of Massachusetts : PhD. Retrieved from https://scholarworks.umass.edu/open_access_dissertations/360
Chicago Manual of Style (16th Edition):
Izadi, Hooman. “Innate immune responses to B. burgdorferi mediated by JNK1 and the cochaperone, methylation controlled DNAJ (MCJ).” 2011. Doctoral Dissertation, U of Massachusetts : PhD. Accessed January 26, 2021.
https://scholarworks.umass.edu/open_access_dissertations/360.
MLA Handbook (7th Edition):
Izadi, Hooman. “Innate immune responses to B. burgdorferi mediated by JNK1 and the cochaperone, methylation controlled DNAJ (MCJ).” 2011. Web. 26 Jan 2021.
Vancouver:
Izadi H. Innate immune responses to B. burgdorferi mediated by JNK1 and the cochaperone, methylation controlled DNAJ (MCJ). [Internet] [Doctoral dissertation]. U of Massachusetts : PhD; 2011. [cited 2021 Jan 26].
Available from: https://scholarworks.umass.edu/open_access_dissertations/360.
Council of Science Editors:
Izadi H. Innate immune responses to B. burgdorferi mediated by JNK1 and the cochaperone, methylation controlled DNAJ (MCJ). [Doctoral Dissertation]. U of Massachusetts : PhD; 2011. Available from: https://scholarworks.umass.edu/open_access_dissertations/360

Temple University
17.
Pozniak, Paul Daniel.
TNF-alpha-Induced Neuroregeneration through an NF-kappaB-dependent Pathway: A New Mechanism Involving EphB2 in the Context of HIV-1 Neuroinflammation.
Degree: PhD, 2016, Temple University
URL: http://digital.library.temple.edu/u?/p245801coll10,386002
► Biomedical Neuroscience
The use of highly active antiretroviral therapy (HAART) has significantly decreased the mortality rate of HIV-1 patients, however the increased survival has led…
(more)
▼ Biomedical Neuroscience
The use of highly active antiretroviral therapy (HAART) has significantly decreased the mortality rate of HIV-1 patients, however the increased survival has led to the development of complications associated with the persistence of the viral infection. Nearly half of HIV-1-infected individuals develop HIV-associated neurocognitive disorders (HAND) as the effects of the chronic infection leads to neuronal injury and synaptic loss in the central nervous system (CNS). The neurotoxicity of HIV-1 has largely been attributed to the inflammation caused by viral replication and the altered signaling of astrocytes, microglia, and macrophages. Although HAART has improved the control of viral replication, the effects from inflammation remain a concern, particularly those of the pro-inflammatory cytokine, tumor necrosis factor alpha (TNF-α). TNF-α has been a therapeutic target for other diseases associated with chronic inflammation, such as rheumatoid arthritis, but emerging evidence has suggested that TNF-α signaling can have a dual role, especially in the CNS, proving the complexity in the modulation of the TNF-α pathway. Although the detrimental effects of TNF-α have been well-characterized, we lack a complete understanding of the beneficial role of TNF-α. TNF-α signaling has largely been considered to be neurotoxic but has been able to regulate neurite outgrowth in the context of neural development. Since TNF-α is upregulated in various neurodegenerative conditions, we considered potential outcomes of TNF-α on neurite outgrowth following injury. Initially, most would assume that TNF-α would prevent neurite outgrowth as apoptosis is a common outcome of TNF-α-induced signaling. If TNF-α signaling strictly prevents neurite outgrowth, anti-TNFα therapies could be considered to reverse this effect. However, upon induced injury, we observed an increase in neurite regrowth following induced injury in human primary fetal neurons, demonstrating a strong need for a deeper understanding of this dual role of TNF-α. Anti-TNF-α therapies have been considered for HIV-1-infected patients to reduce the chronic inflammation, however inhibiting TNF-α signaling could have side-effects that could prevent neuronal recovery from HIV-1 effects. Targeting pathways downstream of TNF-α signaling would be more advantageous to mediate the beneficial role of TNF-α in the CNS. We investigated the transcriptional effects of TNF-α treatment on neurons to uncover a potential pathway to promote neurite outgrowth. One pathway we have discovered to be beneficial in primary human fetal neurons is TNF-α-induced Ephrin B2 upregulation. Ephrin B2 (EphB2) receptors are important mediators of neuronal development and synaptic plasticity, however little has been established in regards to their role in HIV and inflammation, particularly in the CNS. EphB2 can mediate axonal development by providing retractive cues to assist the axon to reach the target, but EphB2 can also promote dendritic branching to improve learning and memory, which would…
Advisors/Committee Members: Khalili, Kamel;, Gordon, Jennifer, Ph.D., Hu, Wenhui, Langford, Dianne, Smith, George M., Wigdahl, Brian;.
Subjects/Keywords: Neurosciences;
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th 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 (16th Edition):
Pozniak, Paul Daniel. “TNF-alpha-Induced Neuroregeneration through an NF-kappaB-dependent Pathway: A New Mechanism Involving EphB2 in the Context of HIV-1 Neuroinflammation.” 2016. Doctoral Dissertation, Temple University. Accessed January 26, 2021.
http://digital.library.temple.edu/u?/p245801coll10,386002.
MLA Handbook (7th Edition):
Pozniak, Paul Daniel. “TNF-alpha-Induced Neuroregeneration through an NF-kappaB-dependent Pathway: A New Mechanism Involving EphB2 in the Context of HIV-1 Neuroinflammation.” 2016. Web. 26 Jan 2021.
Vancouver:
Pozniak PD. TNF-alpha-Induced Neuroregeneration through an NF-kappaB-dependent Pathway: A New Mechanism Involving EphB2 in the Context of HIV-1 Neuroinflammation. [Internet] [Doctoral dissertation]. Temple University; 2016. [cited 2021 Jan 26].
Available from: http://digital.library.temple.edu/u?/p245801coll10,386002.
Council of Science Editors:
Pozniak PD. TNF-alpha-Induced Neuroregeneration through an NF-kappaB-dependent Pathway: A New Mechanism Involving EphB2 in the Context of HIV-1 Neuroinflammation. [Doctoral Dissertation]. Temple University; 2016. Available from: http://digital.library.temple.edu/u?/p245801coll10,386002

Universidade do Rio Grande do Norte
18.
Carvalho, Fabiana Maria Coimbra de.
Efeito anti-inflamatório de proteínas sacietogênicas da semente de tamarindo em modelo experimental de síndrome metabólica
.
Degree: 2016, Universidade do Rio Grande do Norte
URL: http://repositorio.ufrn.br/handle/123456789/21674
► Trypsin inhibitors are studied in a variety of models for their anti-obesity and anti-inflammatory bioactive properties. Our group has previously demonstrated the satietogenic effect of…
(more)
▼ 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 tamarind seed trypsin inhibitors (TTI) in eutrophic mouse models and anti-inflammatory effects of other trypsin inhibitors. In this study, we evaluated TTI effect upon satiety, biochemical and inflammatory parameters in an experimental model of metabolic syndrome (MetS). Three groups of n=5 male Wistar rats with obesity-based MetS received for 10 days one of the following: 1) Cafeteria diet; 2) Cafeteria diet + TTI (25 mg/Kg); 3) Standard diet. TTI reduced food intake in animals with MetS. Nevertheless, weight gain was not different between studied groups. Dyslipidemia parameters were not different with the use of TTI, only the group receiving standard diet showed lower VLDL and triglycerides (TG) (Kruskal-Wallis, p < 0.05). IL-6 production did not differ between groups. Interestingly,
TNF-α was lower in animals receiving TTI. Our results corroborate the satietogenic effect of TTI in a MetS model. Furthermore, we show that TTI used with a cafeteria diet may decrease inflammation regardless of weight loss. This puts TTI as a candidate for studies to test its effectiveness as an adjuvant in MetS treatment.
Advisors/Committee Members: Morais, Ana Heloneida de Araújo (advisor), 02587306418 (advisor), http://lattes.cnpq.br/1233944493334651 (advisor), Maciel, Bruna Leal Lima (advisor), 96256192320 (advisor), http://lattes.cnpq.br/5790541670952158 (advisor).
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 (6th 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 (16th Edition):
Carvalho, Fabiana Maria Coimbra de. “Efeito anti-inflamatório de proteínas sacietogênicas da semente de tamarindo em modelo experimental de síndrome metabólica
.” 2016. Masters Thesis, Universidade do Rio Grande do Norte. Accessed January 26, 2021.
http://repositorio.ufrn.br/handle/123456789/21674.
MLA Handbook (7th Edition):
Carvalho, Fabiana Maria Coimbra de. “Efeito anti-inflamatório de proteínas sacietogênicas da semente de tamarindo em modelo experimental de síndrome metabólica
.” 2016. Web. 26 Jan 2021.
Vancouver:
Carvalho FMCd. Efeito anti-inflamatório de proteínas sacietogênicas da semente de tamarindo em modelo experimental de síndrome metabólica
. [Internet] [Masters thesis]. Universidade do Rio Grande do Norte; 2016. [cited 2021 Jan 26].
Available from: http://repositorio.ufrn.br/handle/123456789/21674.
Council of Science Editors:
Carvalho FMCd. Efeito anti-inflamatório de proteínas sacietogênicas da semente de tamarindo em modelo experimental de síndrome metabólica
. [Masters Thesis]. Universidade do Rio Grande do Norte; 2016. Available from: http://repositorio.ufrn.br/handle/123456789/21674
19.
Papazian, Irini.
Μελέτη του ρόλου του διαλυτού και διαμεμβρανικού TNF κατά την παθολογία του ΚΝΣ.
Degree: 2019, National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ)
URL: http://hdl.handle.net/10442/hedi/45595
► TNF is a member of a large family of cytokines and has multiple roles in the CNS. Regulated TNF production is necessary for successful host…
(more)
▼ TNF is a member of a large family of cytokines and has multiple roles in the CNS. Regulated TNF production is necessary for successful host defense responses against infection and for tissue repair mechanisms. On the other hand, deregulation of TNF production and molecular signaling leads to chronic inflammation and immune activation, which can lead to autoimmunity. Increased TNF levels have been associated with inflammatory autoimmune diseases, including neurodegenerative CNS disorders such as multiple sclerosis (MS). However, while TNF inhibitors are blockbuster drugs for chronic immune diseases in the periphery, such as rheumatoid arthritis, they exacerbate disease in MS patients, induce de novo demyelination in patients treated for other diseases, and even cause MS. These clinical data clearly show that TNF has overall beneficial effects in the CNS. In experimental models for MS, TNF receptor 1 (TNFR1) mediates the detrimental pro- inflammatory effects of soluble TNF (solTNF), whereas TNFR2 and transmembrane TNF (tmTNF) are essential for beneficial effects, mainly in myelin maintenance and repair. This mechanistic framework supports the use of novel selective inhibitors of solTNF and/or TNFR1, or TNFR2 agonists, for safer therapy of chronic inflammatory diseases including those of the CNS. A potential obstacle to such an approach is substantial evidence that TNF has neuroprotective effects against a wide variety of oxidative and excitotoxic stimuli when used to pretreat cultured neurons, and that protection involves both TNFR1 and TNFR2. However, the relevance of these effects for CNS protection in vivo have yet to be proven and is this subject of this thesis. In a separate line of investigation, previous studies in our lab show that, similar to TNF, conditioned medium from MSC has neuroprotective effects against glutamate excitotoxicity when used to pretreat cultured neurons. MSC provide therapeutic effects in experimental CNS disease models and therefore show promise as cell-based therapies for humans. However, their modes of action, and whether TNF is secreted and involved in their neuroprotection, need to be elucidated. To address the questions described above, we used a genetic approach, combining mice with conventionally and conditionally targeted genes for TNF and its receptors, with an in vitro of glutamate excitotoxicity and in vivo models for multiple sclerosis. Glutamate, and specifically NMDA excitotoxicity, was used because it is directly relevant for neuronal death in a wide variety of neurodegenerative disorders including MS. The NMDA, AMPA and kainate receptors belong to the family of ionotropic glutamate receptors and bind glutamate, which is the major excitatory neurotransmitter in the mammalian CNS. Under certain conditions, dysregulated glutamate function can lead to pathology. High levels of glutamate are toxic for neurons and induce so-called excitotoxic death resulting from increased calcium influx into the cell via the NMDA receptors. First the neuroprotective function of TNF against…
Subjects/Keywords: TNF υποδοχείς; TNF; Νευροεκφυλισμός; Νευροπροστασία; Σκλήρυνση κατά πλάκας; Γλουταμινικοί υποδοχείς; Απομυελίνωση απο κουπριζόνη; Πειραματική αυτοάνοση εγκεφαλομυελίτιδα; TNF receptors; TNF; Neurodegeneration; Neuroprotection; Multiple sclerosis; Glutamate receptors; Cuprizone model; Experimental autoimmune encephalomyelitis
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Papazian, I. (2019). Μελέτη του ρόλου του διαλυτού και διαμεμβρανικού TNF κατά την παθολογία του ΚΝΣ. (Thesis). National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ). Retrieved from http://hdl.handle.net/10442/hedi/45595
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Papazian, Irini. “Μελέτη του ρόλου του διαλυτού και διαμεμβρανικού TNF κατά την παθολογία του ΚΝΣ.” 2019. Thesis, National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ). Accessed January 26, 2021.
http://hdl.handle.net/10442/hedi/45595.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Papazian, Irini. “Μελέτη του ρόλου του διαλυτού και διαμεμβρανικού TNF κατά την παθολογία του ΚΝΣ.” 2019. Web. 26 Jan 2021.
Vancouver:
Papazian I. Μελέτη του ρόλου του διαλυτού και διαμεμβρανικού TNF κατά την παθολογία του ΚΝΣ. [Internet] [Thesis]. National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ); 2019. [cited 2021 Jan 26].
Available from: http://hdl.handle.net/10442/hedi/45595.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Papazian I. Μελέτη του ρόλου του διαλυτού και διαμεμβρανικού TNF κατά την παθολογία του ΚΝΣ. [Thesis]. National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ); 2019. Available from: http://hdl.handle.net/10442/hedi/45595
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Vanderbilt University
20.
Hilliard, Valda Catherine.
TNF-alpha converting enzyme-dependent ErbB4 transactivation by TNF promotes colonic epithelial cell survival.
Degree: PhD, Cell and Developmental Biology, 2011, Vanderbilt University
URL: http://hdl.handle.net/1803/13315
► Disruption of intestinal epithelial homeostasis, including enhanced apoptosis, is a hallmark of inflammatory bowel disease (IBD). We have shown that tumor necrosis factor (TNF) increases…
(more)
▼ Disruption of intestinal epithelial homeostasis, including enhanced apoptosis, is a hallmark of inflammatory bowel disease (IBD). We have shown that tumor necrosis factor (
TNF) increases the kinase activity of ErbB4, a member of the epidermal growth factor receptor family that is elevated in mucosa of IBD patients and which promotes colon epithelial cell survival. In this study, we tested the hypothesis that
TNF transactivates ErbB4 through
TNF-alpha converting enzyme (TACE)-mediated ligand release, and that this transactivation is necessary to protect colonic epithelial cells from cytokine-induced apoptosis. Using neutralizing antibodies, we show that HB-EGF is required for ErbB4 phosphorylation in response to
TNF. Pharmacological or genetic inhibition of the metalloprotease TACE, which mediates HB-EGF release from cells, blocked
TNF-induced ErbB4 activation. MEK, but not Src or p38, was also required for transactivation. TACE activity and ligand binding were required for ErbB4-mediated anti-apoptotic signaling; while mouse colon epithelial cells expressing ErbB4 were resistant to
TNF-induced apoptosis, TACE inhibition or blockade of ErbB4 ligand binding reversed the survival advantage. We conclude that
TNF transactivates ErbB4 through TACE-dependent HB-EGF release, thus protecting colon epithelial cells from cytokine-induced apoptosis. These findings have important implications for understanding how ErbB4 protects the colon from apoptosis-induced tissue injury in inflammatory conditions such as IBD.
Advisors/Committee Members: D. Brent Polk (committee member), Matthew J. Tyska (committee member), Anna L. Means (committee member), William E. Russell (committee member), Steven K. Hanks (Committee Chair).
Subjects/Keywords: colon; ADAM17; TACE; TNF; ErbB4; apoptosis
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Hilliard, V. C. (2011). TNF-alpha converting enzyme-dependent ErbB4 transactivation by TNF promotes colonic epithelial cell survival. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/13315
Chicago Manual of Style (16th Edition):
Hilliard, Valda Catherine. “TNF-alpha converting enzyme-dependent ErbB4 transactivation by TNF promotes colonic epithelial cell survival.” 2011. Doctoral Dissertation, Vanderbilt University. Accessed January 26, 2021.
http://hdl.handle.net/1803/13315.
MLA Handbook (7th Edition):
Hilliard, Valda Catherine. “TNF-alpha converting enzyme-dependent ErbB4 transactivation by TNF promotes colonic epithelial cell survival.” 2011. Web. 26 Jan 2021.
Vancouver:
Hilliard VC. TNF-alpha converting enzyme-dependent ErbB4 transactivation by TNF promotes colonic epithelial cell survival. [Internet] [Doctoral dissertation]. Vanderbilt University; 2011. [cited 2021 Jan 26].
Available from: http://hdl.handle.net/1803/13315.
Council of Science Editors:
Hilliard VC. TNF-alpha converting enzyme-dependent ErbB4 transactivation by TNF promotes colonic epithelial cell survival. [Doctoral Dissertation]. Vanderbilt University; 2011. Available from: http://hdl.handle.net/1803/13315

University of Saskatchewan
21.
Brymer, Kyle Jordan 1991-.
Examining the Antidepressant Potential of TNF-alpha and Reelin on Associated Behavioural and Neurobiological Markers in a Preclinical Model of Depression.
Degree: 2019, University of Saskatchewan
URL: http://hdl.handle.net/10388/12264
► Depression is a debilitating psychiatric disorder affecting approximately 10% of the world’s population. Cognitive dysfunction is an often ignored aspect of depression, and predicts patient…
(more)
▼ Depression is a debilitating psychiatric disorder affecting approximately 10% of the world’s population. Cognitive dysfunction is an often ignored aspect of depression, and predicts patient response to antidepressants. While several classes of antidepressants have been developed for the treatment of depression, over one-third of patients do not respond to conventional antidepressants, and all currently available antidepressants require weeks of continuous administration to achieve therapeutic effects. The delay in the onset of therapeutic effects from the time of taking antidepressants can put patients at risk for suicide. Therefore, there is a need in the literature to develop and identify novel antidepressants that do not work on conventional targets and that have fast-acting properties.
The primary goals of this dissertation were to investigate the pattern of cognitive impairments following CORT treatment and to examine the antidepressant potential of
TNF-α receptor inhibition and reelin. To begin, in Chapter 2, I examined the effect of repeated CORT injections on depression-like behaviour using the forced swim test, the object-location, object-in-place, and object-recognition memory tests, and sensorimotor gating using prepulse inhibition. These data suggested that CORT increases depression-like behaviour while simultaneously impairing hippocampal and prefrontal cortex-dependent memory and sensorimotor gating. In Chapter 3, I examined the effects of the
TNF-α inhibitor etanercept on CORT induced depression-like behaviour, cognition, and markers of synaptic plasticity through post-mortem analysis of brain tissue. I found that CORT increased depression-like behaviour on the forced swim test and impaired object memory. CORT also impaired several post-mortem markers of hippocampal plasticity, and etanercept restored these measures back to control levels.
In Chapter 4 I examined the antidepressant potential of intrahippocampal reelin infusions and its effects on cognition and markers of synaptic plasticity. I found CORT treatment increased depression-like behaviour on the forced swim test and impaired object memory. Reelin treatment restored both of these measures back to control levels within one day. CORT also decreased markers of hippocampal plasticity, and reelin restored these measures back to control levels. Finally, in Chapter 5, I examined the contribution of AMPA signaling to the antidepressant effects of reelin. I found that infusion of the AMPA antagonist CNQX blocked reelin’s antidepressant effects on the forced swim test, without altering CORT’s pattern of changes on markers of hippocampal plasticity. The results of this dissertation reveal novel compounds with antidepressant properties that warrant further investigation into their potential use in humans
Advisors/Committee Members: Kalynchuk, Lisa E, Caruncho, Hector J, Paterson, Phyllis, Cummings, Jorden, Hunter, Paulette.
Subjects/Keywords: Stress; Depression; Reelin; TNF; Neurogenesis; Glutamate
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Brymer, K. J. 1. (2019). Examining the Antidepressant Potential of TNF-alpha and Reelin on Associated Behavioural and Neurobiological Markers in a Preclinical Model of Depression. (Thesis). University of Saskatchewan. Retrieved from http://hdl.handle.net/10388/12264
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Brymer, Kyle Jordan 1991-. “Examining the Antidepressant Potential of TNF-alpha and Reelin on Associated Behavioural and Neurobiological Markers in a Preclinical Model of Depression.” 2019. Thesis, University of Saskatchewan. Accessed January 26, 2021.
http://hdl.handle.net/10388/12264.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Brymer, Kyle Jordan 1991-. “Examining the Antidepressant Potential of TNF-alpha and Reelin on Associated Behavioural and Neurobiological Markers in a Preclinical Model of Depression.” 2019. Web. 26 Jan 2021.
Vancouver:
Brymer KJ1. Examining the Antidepressant Potential of TNF-alpha and Reelin on Associated Behavioural and Neurobiological Markers in a Preclinical Model of Depression. [Internet] [Thesis]. University of Saskatchewan; 2019. [cited 2021 Jan 26].
Available from: http://hdl.handle.net/10388/12264.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Brymer KJ1. Examining the Antidepressant Potential of TNF-alpha and Reelin on Associated Behavioural and Neurobiological Markers in a Preclinical Model of Depression. [Thesis]. University of Saskatchewan; 2019. Available from: http://hdl.handle.net/10388/12264
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Boston University
22.
Bhambhani, Vijeta.
Micro-RNA mediated regulation of a cytokine factor: TNF-alpha: an exploration of gene expression control in proliferating and quiescent cells.
Degree: MS, Medical Sciences, 2015, Boston University
URL: http://hdl.handle.net/2144/16241
► Two types mechanisms that control gene expression involve cis-regulatory factors and trans-regulatory factors. Cis-acting regulatory RNAs include targeted messenger RNA (mRNA) specificity and AU-rich elements…
(more)
▼ 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 (AREs). AU-rich mRNAs are a subcategory of mRNAs that have AREs in their 3'-Untranslated Regions (UTRs). These ARE-genes have been observed to correlate with rapid mRNA decay patterns. They comprise approximately 12% of all transcripts and are known to encode for a group of proteins that have involvement in the inflammatory response. Trans-acting regulatory mechanisms are micro RNAs (miRNAs) in eukaryotes, and small RNAs (sRNA) in prokaryotes. Misregulation of these mechanisms can lead to many disease states if rapid mRNA decay does not occur, leading to tumorigenesis, and eventually, different types of cancer. In this project, the TNF-α ARE was studied in both serum-positive and quiescent G0 conditions in order to analyze whether the translation of the gene differed in any respect due to the binding of a known miRNA called miR-130a. Additionally, both serum-positive and one-day serum-starved quiescent G0 conditions were analyzed for eIF5B and FXR1 levels to analyze whether there was a correlation between the two proteins.
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 (6th 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 (16th Edition):
Bhambhani, Vijeta. “Micro-RNA mediated regulation of a cytokine factor: TNF-alpha: an exploration of gene expression control in proliferating and quiescent cells.” 2015. Masters Thesis, Boston University. Accessed January 26, 2021.
http://hdl.handle.net/2144/16241.
MLA Handbook (7th Edition):
Bhambhani, Vijeta. “Micro-RNA mediated regulation of a cytokine factor: TNF-alpha: an exploration of gene expression control in proliferating and quiescent cells.” 2015. Web. 26 Jan 2021.
Vancouver:
Bhambhani V. Micro-RNA mediated regulation of a cytokine factor: TNF-alpha: an exploration of gene expression control in proliferating and quiescent cells. [Internet] [Masters thesis]. Boston University; 2015. [cited 2021 Jan 26].
Available from: http://hdl.handle.net/2144/16241.
Council of Science Editors:
Bhambhani V. Micro-RNA mediated regulation of a cytokine factor: TNF-alpha: an exploration of gene expression control in proliferating and quiescent cells. [Masters Thesis]. Boston University; 2015. Available from: http://hdl.handle.net/2144/16241

University of Toronto
23.
Wong, Aaron.
Dissecting The Role Of TNFα In Kawasaki Disease: Alteration Of Cell Fate By TNFα After Superantigen Activation.
Degree: 2011, University of Toronto
URL: http://hdl.handle.net/1807/31634
► Kawasaki disease (KD) is an acute inflammatory disease characterized by persistent inflammation of the coronary arteries. KD is characterized by the release of cytokines such…
(more)
▼ Kawasaki disease (KD) is an acute inflammatory disease characterized by persistent inflammation of the coronary arteries. KD is characterized by the release of cytokines such as tumor necrosis factor alpha (TNFα) and is thought to be initiated by a superantigen (SAg). The Lactobacillus casei cell wall extract model of KD demonstrates a critical requirement for TNFα and its receptor during pathogenesis, although the precise effect of TNFα is unknown. A persistent T cell infiltrate in the coronary artery disagrees with established fates of SAg activated cells, which undergo apoptosis. In this work, TNFα was found to promote the survival of SAg-reactive T cells. The results demonstrate that TNFα regulates B7.2 molecule expression on antigen presenting cells, and that TNFα indirectly promotes the survival of SEB-stimulated T cells by driving costimulation. These observations demonstrate how TNFα prevents T cell apoptosis and lend support to KD therapies which target TNFα and B7.
MAST
Advisors/Committee Members: Yeung, Rae S. M., Immunology.
Subjects/Keywords: Kawasaki Disease; TNF; Superantigen; apoptosis; 0982; 0379
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Wong, A. (2011). Dissecting The Role Of TNFα In Kawasaki Disease: Alteration Of Cell Fate By TNFα After Superantigen Activation. (Masters Thesis). University of Toronto. Retrieved from http://hdl.handle.net/1807/31634
Chicago Manual of Style (16th Edition):
Wong, Aaron. “Dissecting The Role Of TNFα In Kawasaki Disease: Alteration Of Cell Fate By TNFα After Superantigen Activation.” 2011. Masters Thesis, University of Toronto. Accessed January 26, 2021.
http://hdl.handle.net/1807/31634.
MLA Handbook (7th Edition):
Wong, Aaron. “Dissecting The Role Of TNFα In Kawasaki Disease: Alteration Of Cell Fate By TNFα After Superantigen Activation.” 2011. Web. 26 Jan 2021.
Vancouver:
Wong A. Dissecting The Role Of TNFα In Kawasaki Disease: Alteration Of Cell Fate By TNFα After Superantigen Activation. [Internet] [Masters thesis]. University of Toronto; 2011. [cited 2021 Jan 26].
Available from: http://hdl.handle.net/1807/31634.
Council of Science Editors:
Wong A. Dissecting The Role Of TNFα In Kawasaki Disease: Alteration Of Cell Fate By TNFα After Superantigen Activation. [Masters Thesis]. University of Toronto; 2011. Available from: http://hdl.handle.net/1807/31634

Universidade Nova
24.
Raposeiro, Rita Maria Mendes.
Osteoclast activity in ankylosing spondylitis patients before and after TNF-blocking therapy.
Degree: 2014, Universidade Nova
URL: http://www.rcaap.pt/detail.jsp?id=oai:run.unl.pt:10362/13804
► Ankylosing spondylitis (AS) is a chronic inflammatory rheumatic disease of the axial skeleton. The major outcome of this disease is defined by new bone formation,…
(more)
▼ 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, commonly observed in the ligaments of the intervertebral joints, that can lead to the formation of bony spurs, known as syndesmophytes.
Previous studies have shown that serum levels of
TNF, IL-6 and IL-17 are increased in AS patients and may be implicated in the development of secondary osteoporosis, since these cytokines are able to induce osteoclast (OC) differentiation and, therefore, bone resorption.
In this work we aimed to assess the effects of
TNF-blocking therapy in the systemic inflammatory environment of AS patients with active disease as well as in OC differentiation and activity. To accomplish this objective, we cultured circulating monocytes from AS patients, before and after therapy, under osteoclastogenic conditions and we performed two functional assays (TRAP staining and resorption pit assay) and analyzed the expression of osteoclast specific genes.
We have shown that AS patients with active disease have increased levels of pro-inflammatory cytokines when compared with healthy subjects. We also found that IL-17, TGF-β and osteoprotegerin are decreased after
TNF-blocking therapy. Interestingly, we also observed that after
TNF-blocking therapy the expression of some genes is favoring osteoclastogenesis and that differentiated OCs have increased resorption activity.
These results suggest that in active AS there may be an uncoupling between inflammation and OC activity that is reset by
TNF-blocking therapy.
Advisors/Committee Members: Lopes, Joana, Perpétuo, Inês.
Subjects/Keywords: Ankylosing spondylitis; Inflammation; Osteoclastogenesis; TNF-blocking therapy
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APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th 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 (16th Edition):
Raposeiro, Rita Maria Mendes. “Osteoclast activity in ankylosing spondylitis patients before and after TNF-blocking therapy.” 2014. Thesis, Universidade Nova. Accessed January 26, 2021.
http://www.rcaap.pt/detail.jsp?id=oai:run.unl.pt:10362/13804.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Raposeiro, Rita Maria Mendes. “Osteoclast activity in ankylosing spondylitis patients before and after TNF-blocking therapy.” 2014. Web. 26 Jan 2021.
Vancouver:
Raposeiro RMM. Osteoclast activity in ankylosing spondylitis patients before and after TNF-blocking therapy. [Internet] [Thesis]. Universidade Nova; 2014. [cited 2021 Jan 26].
Available from: http://www.rcaap.pt/detail.jsp?id=oai:run.unl.pt:10362/13804.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Raposeiro RMM. Osteoclast activity in ankylosing spondylitis patients before and after TNF-blocking therapy. [Thesis]. Universidade Nova; 2014. Available from: http://www.rcaap.pt/detail.jsp?id=oai:run.unl.pt:10362/13804
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
25.
Moriya, Takashi; Kitamori, Kazuya; Naito, Hisao; Yanagiba, Yukie; Ito, Yuki; Yamagishi, Nozomi; Tamada, Hazuki; Jia, Xiaofang; Tsuchikura, Satoru; Ikeda, Katsumi; Yamori, Yukio.
Simultaneous changes in high-fat and high-cholesterol diet-induced steatohepatitis and severe fibrosis and those underlying molecular mechanisms in novel SHRSP5/Dmcr rat.
Degree: 2018, Nagoya University / 名古屋大学
URL: http://hdl.handle.net/2237/16803
► Objectives: The aim of this study was to identify the molecular mechanisms underlying high-fat and high-cholesterol (HFC) diet-induced steatohepatitis and associated liver fibrosis progression in…
(more)
▼ Objectives: The aim of this study was to identify the molecular mechanisms underlying high-fat and high-cholesterol (HFC) diet-induced steatohepatitis and associated liver fibrosis progression in a novel stroke-prone, spontaneously hypertensive 5/Dmcr (SHRSP5/Dmcr) rat model. Methods: SHRSP5/Dmcr rats were given the control or HFC-diet for 2, 8, and 16 weeks. Plasma and hepatic gene expression of key molecules involved in fatty acid oxidation, inflammation, oxidative stress, and fibrosis were subsequently analyzed. Results: Rats fed the HFC-diet showed increased plasma tumor necrosis factor-α (TNF-α) and hepatic p50/p65 signals, but reduced hepatic Cu2+/Zn2+-superoxide dismutase across the treatment period and reduced plasma total adiponectin at 8 weeks. In HFC-diet-fed rats, transforming growth factor-β1 (TGF-β1) was elevated prior to the appearance of obvious liver fibrosis pathology at 2 weeks, followed by elevations in platelet-derived growth factor-B (PDGF-B) and α-smooth muscle actin (α-SMA), corresponding to evident liver fibrosis, at 8 weeks and by α1 type I collagen production at 16 weeks. The HFC-diet increased hepatic total cholesterol accumulation, although hepatic triglyceride declined by 0.3-fold from 2 to 16 weeks due to reduced hepatic triglyceride synthesis, as suggested by the diacylglycerol acyltransferase 1 and 2 measurements. Conclusions: TNF-α and p50/p65 molecular signals appeared to be major factors for HFC-diet-induced hepatic inflammation and oxidative stress facilitating liver disease progression. While the up-regulation of TGF-β1 prior to the appearance of any evident liver fibrosis could be an early signal for progressive liver fibrosis, elevated PDGF-B and α-SMA levels signified evident liver fibrosis at 8 weeks, and subsequent increased α1 type I collagen production and reduced triglyceride synthesis indicated extensive liver fibrosis at 16 weeks in this novel SHRSP5/Dmcr model.
名古屋大学博士学位論文 学位の種類 : 博士(医学)(課程) 学位授与年月日:平成24年4月27日 森谷隆氏の博士論文として提出された
First published online: 2012-03-10
Subjects/Keywords: Steatohepatitis; Inflammation; TNF-α; NF-κb; Fibrosis
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th 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 (16th Edition):
Moriya, Takashi; Kitamori, Kazuya; Naito, Hisao; Yanagiba, Yukie; Ito, Yuki; Yamagishi, Nozomi; Tamada, Hazuki; Jia, Xiaofang; Tsuchikura, Satoru; Ikeda, Katsumi; Yamori, Yukio. “Simultaneous changes in high-fat and high-cholesterol diet-induced steatohepatitis and severe fibrosis and those underlying molecular mechanisms in novel SHRSP5/Dmcr rat.” 2018. Thesis, Nagoya University / 名古屋大学. Accessed January 26, 2021.
http://hdl.handle.net/2237/16803.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Moriya, Takashi; Kitamori, Kazuya; Naito, Hisao; Yanagiba, Yukie; Ito, Yuki; Yamagishi, Nozomi; Tamada, Hazuki; Jia, Xiaofang; Tsuchikura, Satoru; Ikeda, Katsumi; Yamori, Yukio. “Simultaneous changes in high-fat and high-cholesterol diet-induced steatohepatitis and severe fibrosis and those underlying molecular mechanisms in novel SHRSP5/Dmcr rat.” 2018. Web. 26 Jan 2021.
Vancouver:
Moriya, Takashi; Kitamori, Kazuya; Naito, Hisao; Yanagiba, Yukie; Ito, Yuki; Yamagishi, Nozomi; Tamada, Hazuki; Jia, Xiaofang; Tsuchikura, Satoru; Ikeda, Katsumi; Yamori Y. Simultaneous changes in high-fat and high-cholesterol diet-induced steatohepatitis and severe fibrosis and those underlying molecular mechanisms in novel SHRSP5/Dmcr rat. [Internet] [Thesis]. Nagoya University / 名古屋大学; 2018. [cited 2021 Jan 26].
Available from: http://hdl.handle.net/2237/16803.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Moriya, Takashi; Kitamori, Kazuya; Naito, Hisao; Yanagiba, Yukie; Ito, Yuki; Yamagishi, Nozomi; Tamada, Hazuki; Jia, Xiaofang; Tsuchikura, Satoru; Ikeda, Katsumi; Yamori Y. Simultaneous changes in high-fat and high-cholesterol diet-induced steatohepatitis and severe fibrosis and those underlying molecular mechanisms in novel SHRSP5/Dmcr rat. [Thesis]. Nagoya University / 名古屋大学; 2018. Available from: http://hdl.handle.net/2237/16803
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
26.
Teixeira, Chantelle Simões Leite.
TNF-alfa e metabolismo do adipócito.
Degree: 2015, RCAAP
URL: https://www.rcaap.pt/detail.jsp?id=oai:comum.rcaap.pt:10400.26/10984
► Dissertação para obtenção do grau de Mestre no Instituto Superior de Ciências da Saúde Egas Moniz
A prevalência da obesidade tem vindo a aumentar ao…
(more)
▼ 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 longo dos anos influenciando a qualidade de vida da população, tornando-a mais suscetível ao desenvolvimento de outras patologias como as doenças cardiovasculares e a diabetes. A obesidade é resultante do aumento progressivo do tamanho do tecido adiposo em consequência de maior volume e número de adipócitos, levando a uma crescente síntetese de adipocinas e aumento de células imunitárias que caracteriza a obesidade como uma doença inflamatória crónica. O tecido adiposo deixou de ser considerado apenas como um órgão de armazenamento de lípidos, passando a ser considerado um órgão com função endócrina e desempenhando um papel bastante importante na homeostase do organismo. O tecido adiposo de um indivíduo obeso é caracterizado por um perfil de citocinas pró-inflamatórias como o factor de necrose tumoral-alfa (TNF-α). O TNF-α é uma citocina que possui propriedades pró-inflamatórias, exercendo múltiplas funções biológicas em diferentes tecidos. Em particular, no tecido adiposo, aparenta regular ou interferir no metabolismo do adipócito através de diversos processos. Esta citocina pró-inflamatória tende a desempenhar, entre outros, um papel na redução dos adipócitos. Neste trabalho apresenta-se uma revisão bibliográfica de modo a contribuir para a elucidação dos principais mecanismos associados ao processo inflamatório do tecido adiposo na obesidade, com enfoque particular no TNF-α e no metabolismo do adipócito.
Advisors/Committee Members: Mesquita, Maria Fernanda de.
Subjects/Keywords: Obesidade; Tecido adiposo; TNF-α; Adipócito
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th 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 (16th Edition):
Teixeira, Chantelle Simões Leite. “TNF-alfa e metabolismo do adipócito.” 2015. Thesis, RCAAP. Accessed January 26, 2021.
https://www.rcaap.pt/detail.jsp?id=oai:comum.rcaap.pt:10400.26/10984.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Teixeira, Chantelle Simões Leite. “TNF-alfa e metabolismo do adipócito.” 2015. Web. 26 Jan 2021.
Vancouver:
Teixeira CSL. TNF-alfa e metabolismo do adipócito. [Internet] [Thesis]. RCAAP; 2015. [cited 2021 Jan 26].
Available from: https://www.rcaap.pt/detail.jsp?id=oai:comum.rcaap.pt:10400.26/10984.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Teixeira CSL. TNF-alfa e metabolismo do adipócito. [Thesis]. RCAAP; 2015. Available from: https://www.rcaap.pt/detail.jsp?id=oai:comum.rcaap.pt:10400.26/10984
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
27.
Bumdelger, Batmunkh.
Induction of Timp1 in Smooth Muscle Cells during Development of Abdominal Aortic Aneurysms : 腹部大動脈瘤形成における、平滑筋細胞でのTimp1遺伝子誘導.
Degree: 博士(医学), 2014, Hiroshima University / 広島大学
URL: http://ir.lib.hiroshima-u.ac.jp/00036323
► Abdominal aortic aneurysm (AAA) is known to develop mainly by the increased diameter of aorta through metalloproteinases (MMPs). Although activities of MMPs are tightly regulated…
(more)
▼ 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 by the presence of tissue inhibitor of MMPs (TIMPs) and imbalances between MMPs and TIMPs may serve to fragility of arterial wall, little is known about TIMPs behavior in aneurysmal formation. Here, we utilized a murine experimental AAA model, and found that by immunohistochemical analysis, Timp1 as and Timp1 mRNA levels was also revealed in aortic tissue in AAA by RT-PCR. In cultured vascular smooth muscle cells (SMCs), Tumor Necrosis Factor (TNF)-α significantly activated both Mmp9 and Timp1 expression, and they were blocked by Jun kinase inhibitor (SP600125) in a dose-dependent manner. Interestingly, a proteasome inhibitor (MG132), which is known as an agent for inhibition of the nuclear factor-kappa B (NF-kB), significantly inhibited the TNF-α-induced expression of Timp1, whereas MG132, which also works as an activator of c-Jun/AP-1 pathway, strongly increased Mmp9. Taken together, inflammatory cytokines, including TNF-α, may simultaneously induce MMPs and TIMPs for the remodeling of the medial layer, leading to the increased diameter of the aorta, the aneurysm.
Subjects/Keywords: Abdominal aortic aneurysm; Mmp9; Timp1; TNF-α
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th 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 (16th Edition):
Bumdelger, Batmunkh. “Induction of Timp1 in Smooth Muscle Cells during Development of Abdominal Aortic Aneurysms : 腹部大動脈瘤形成における、平滑筋細胞でのTimp1遺伝子誘導.” 2014. Thesis, Hiroshima University / 広島大学. Accessed January 26, 2021.
http://ir.lib.hiroshima-u.ac.jp/00036323.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Bumdelger, Batmunkh. “Induction of Timp1 in Smooth Muscle Cells during Development of Abdominal Aortic Aneurysms : 腹部大動脈瘤形成における、平滑筋細胞でのTimp1遺伝子誘導.” 2014. Web. 26 Jan 2021.
Vancouver:
Bumdelger B. Induction of Timp1 in Smooth Muscle Cells during Development of Abdominal Aortic Aneurysms : 腹部大動脈瘤形成における、平滑筋細胞でのTimp1遺伝子誘導. [Internet] [Thesis]. Hiroshima University / 広島大学; 2014. [cited 2021 Jan 26].
Available from: http://ir.lib.hiroshima-u.ac.jp/00036323.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Bumdelger B. Induction of Timp1 in Smooth Muscle Cells during Development of Abdominal Aortic Aneurysms : 腹部大動脈瘤形成における、平滑筋細胞でのTimp1遺伝子誘導. [Thesis]. Hiroshima University / 広島大学; 2014. Available from: http://ir.lib.hiroshima-u.ac.jp/00036323
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Univerzitet u Beogradu
28.
Poluga, Jasmina L., 1963-.
Odnos koncentracije proinflamatornih citokina u serumu i
kliničkih, parazitoloških i hematoloških promena u toku importovane
malarije.
Degree: Medicinski fakultet, 2013, Univerzitet u Beogradu
URL: https://fedorabg.bg.ac.rs/fedora/get/o:5550/bdef:Content/get
► Infektivne bolesti - malarija / Infectious diseases - malaria
REZIME: Malarija je multisistemska, potencijalno letalna bolest uzrokovana parazitima roda Plasmodium. Dokazano je da kod malarije…
(more)
▼ Infektivne bolesti - malarija / Infectious diseases
- malaria
REZIME: Malarija je multisistemska, potencijalno
letalna bolest uzrokovana parazitima roda Plasmodium. Dokazano je
da kod malarije oslobadanje proinflamatornih citokina produkuje
sistemski, inflamatorni odgovor i da su njihove koncentracije
povecane, posebno kod teških formi. Smatra se da su citokini
odgovorni za pojavu temperature, povracanja, proliva, mialgija,
trombocitopenije, imunospupresije, koagulopatije i neuroloških
manifestacija. U Klinici za infektivne i tropske bolesti u periodu
2000- 2010. godine je leceno 103 bolesnika sa importovanom
malarijom. U ukupnom uzorku bolesnika odredivani su najznacajniji
klinicki i laboratorijski parametri, sa posebnim osvrtom na stepen
parazitemije.U prospektivnom delu istraživanja koje je ukljucivalo
34 bolesnika uzeti su citokini: TNF- i IL-6. Najvažniji cilj
disertacije je da se odredi nivo citokina TNF- i IL-6 u dve faze:
pre i posle terapije, i ustanovi njihova korelacija sa klinickim,
parazitološkim i hematološkim parametrima. Prema kriterijumima SZO
za teške forme malarije formirana je grupa od 22 bolesnika i
odredivane su njihove najucestalije komplikacije, kao i razlike u
odnosu na ukupan uzorak bolesnika. Ustanovljeno je da su u prvoj
fazi povišeni nivoi citokina TNF- i IL-6, i da postoji njihova jaka
medusobna korelacija, kao i korelacija sa stepenom parazitemije,
povišenim vrednostima d-dimera i laktata, leukopenijom i
trombocitopenijom. Sem toga, utvrdeno je da je znacajno veci broj
bolesnika imao falciparum malariju, parazitemiju manju od 5%, da
nije uzimao hemoprofilaksu, a trombocitopenija je bila najcešca
laboratorijska abnormalnost. Bolesnici sa hiperparazitemijom imali
su znacajno vece vrednosti bilirubina i cešcu pojavu neuroloških
komplikacija, dok su kod teških formi malarije ustanovljene
znacajno više vrednosti TNF- i niže vrednosti
trombocita.
Advisors/Committee Members: Pavlović, Milorad, 1948-.
Subjects/Keywords: malaria; cytokines; parasitemia; thrombocytopenia; TNF-
; IL-6
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th 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 (16th Edition):
Poluga, Jasmina L., 1963-. “Odnos koncentracije proinflamatornih citokina u serumu i
kliničkih, parazitoloških i hematoloških promena u toku importovane
malarije.” 2013. Thesis, Univerzitet u Beogradu. Accessed January 26, 2021.
https://fedorabg.bg.ac.rs/fedora/get/o:5550/bdef:Content/get.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Poluga, Jasmina L., 1963-. “Odnos koncentracije proinflamatornih citokina u serumu i
kliničkih, parazitoloških i hematoloških promena u toku importovane
malarije.” 2013. Web. 26 Jan 2021.
Vancouver:
Poluga, Jasmina L. 1. Odnos koncentracije proinflamatornih citokina u serumu i
kliničkih, parazitoloških i hematoloških promena u toku importovane
malarije. [Internet] [Thesis]. Univerzitet u Beogradu; 2013. [cited 2021 Jan 26].
Available from: https://fedorabg.bg.ac.rs/fedora/get/o:5550/bdef:Content/get.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Poluga, Jasmina L. 1. Odnos koncentracije proinflamatornih citokina u serumu i
kliničkih, parazitoloških i hematoloških promena u toku importovane
malarije. [Thesis]. Univerzitet u Beogradu; 2013. Available from: https://fedorabg.bg.ac.rs/fedora/get/o:5550/bdef:Content/get
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Univerzitet u Beogradu
29.
Vuković-Petrović, Irena, 1988- 21801063.
Ekspresija gena i proteina koji regulišu autofagiju u
mononuklearnim ćelijama periferne krvi pacijenata sa multiplom
sklerozom.
Degree: Medicinski fakultet, 2019, Univerzitet u Beogradu
URL: https://fedorabg.bg.ac.rs/fedora/get/o:19959/bdef:Content/get
► Medicina - Molekularna medicina / Medicine - Molecular medicine
Uvod: Multipla skleroza (MS) je hronična inflamatorna bolest centralnog nervnog sistema (CNS) u kojoj infiltracija limfocitima…
(more)
▼ Medicina - Molekularna medicina / Medicine -
Molecular medicine
Uvod: Multipla skleroza (MS) je hronična
inflamatorna bolest centralnog nervnog sistema (CNS) u kojoj
infiltracija limfocitima dovodi do oštećenja mijelina i aksona.
Autofagija, proces kontrolisane auto-digestije koji reguliše
homeostazu ćelije, važan je u urođenoj i adaptivnoj imunosti. Uloga
autofagije nije do sada detaljno izučavana u različitim
populacijama limfocita u MS. Ciljevi istraživanja: Ispitati
ekspresiju gena za regulatore autofagije (ATG7, ATG10, ATG5, ATG4B,
ATG3, ATG13, ATG8A, ATG14, SQSTM1, BCL2, ULK1, BNIP3, FOXO1, FOXO3,
VPS34, BECN1, ATF4) i proinflamatorne citokine (TNF, IFN-γ, IL-17 i
GM-CSF), kao i aktivnost autofagije u mononuklearnim ćelijama
periferne krvi (MNĆPK) i različitim populacijama limfocita
pacijenata sa MS i kontrolnih ispitanika. Pacijenti i metode: Naša
studija je uključila novoobolele pacijente sa MS, dijagnostikovane
prema McDonald-ovim kriterijumima (2001.), koji u trenutku uzimanja
uzorka nisu bili uključeni ni u jedan terapijski protokol.
Koristeći kvantitativni PCR u realnom vremenu ispitali smo
ekspresiju gena koji regulišu autofagiju i ekspresiju gena za
proinflamatorne citokine u MNĆPK i CD3+CD4+ T-limfocitima, CD3+CD4-
Tlimfocitima i CD3-CD19+B-limfocitima pacijenata sa MS i kontrola.
Takođe smo analizirali aktivnost bazalne autofagije imunoblot
metodom u MNĆPK i CD3+CD4- Tlimfocitima ove dve grupe ispitanika.
Rezultati: Nivoi iRNK i proteina ATG5, potrebnog za formiranje
autofagozoma, bili su povišeni u CD4+ i CD4- T-limfocitima, ali ne
i u B-limfocitima i MNĆPK pacijenata sa MS u poređenju sa
kontrolnim ispitanicima. Ekspresija ostalih ispitivanih autofagnih
gena i aktivnost autofagije nisu se značajno razlikovale u ovim
grupama ispitanika. Nivoi ATG5 iRNK u CD4+ T-limfocitima pacijenata
sa MS bili su u pozitivnoj korelaciji sa nivoma iRNK za
proinflamatorni citokin - faktor nekroze tumora (TNF).Zaključak:
Naši rezultati ukazuju da povišena ekspresija ATG5, nezavisno od
autofagije, može biti povezana sa proinflamatornom ulogom
T-limfocita u MS.
Advisors/Committee Members: Drulović, Jelena, 1960- 12542823.
Subjects/Keywords: multiple sclerosis; T cells; autophagy; ATG5;
TNF
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APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
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APA (6th Edition):
Vuković-Petrović, Irena, 1. 2. (2019). Ekspresija gena i proteina koji regulišu autofagiju u
mononuklearnim ćelijama periferne krvi pacijenata sa multiplom
sklerozom. (Thesis). Univerzitet u Beogradu. Retrieved from https://fedorabg.bg.ac.rs/fedora/get/o:19959/bdef:Content/get
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Vuković-Petrović, Irena, 1988- 21801063. “Ekspresija gena i proteina koji regulišu autofagiju u
mononuklearnim ćelijama periferne krvi pacijenata sa multiplom
sklerozom.” 2019. Thesis, Univerzitet u Beogradu. Accessed January 26, 2021.
https://fedorabg.bg.ac.rs/fedora/get/o:19959/bdef:Content/get.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Vuković-Petrović, Irena, 1988- 21801063. “Ekspresija gena i proteina koji regulišu autofagiju u
mononuklearnim ćelijama periferne krvi pacijenata sa multiplom
sklerozom.” 2019. Web. 26 Jan 2021.
Vancouver:
Vuković-Petrović, Irena 12. Ekspresija gena i proteina koji regulišu autofagiju u
mononuklearnim ćelijama periferne krvi pacijenata sa multiplom
sklerozom. [Internet] [Thesis]. Univerzitet u Beogradu; 2019. [cited 2021 Jan 26].
Available from: https://fedorabg.bg.ac.rs/fedora/get/o:19959/bdef:Content/get.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Vuković-Petrović, Irena 12. Ekspresija gena i proteina koji regulišu autofagiju u
mononuklearnim ćelijama periferne krvi pacijenata sa multiplom
sklerozom. [Thesis]. Univerzitet u Beogradu; 2019. Available from: https://fedorabg.bg.ac.rs/fedora/get/o:19959/bdef:Content/get
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Harvard University
30.
Anderson, Edwin.
The Predictive Power of Past Failure: Using Clinically Available Data to Improve Treatment Algorithms.
Degree: ALM, 2018, Harvard University
URL: http://nrs.harvard.edu/urn-3:HUL.InstRepos:42004088
► Pediatric rheumatology is a small but rapidly evolving specialty within the field of immunology that has been revolutionized by development of a new class of…
(more)
▼ Pediatric rheumatology is a small but rapidly evolving specialty within the field of immunology that has been revolutionized by development of a new class of drugs called biologics. Treatment with these specialized agents results in clinical remission for 60-70% of juvenile idiopathic arthritis patients. The aim of this investigation is to determine if patient characteristics prior to an anti-TNF biologic’s initiation or data from the first three months of response can serve as predictors of the medication’s efficacy. This is a retrospective case-control study conducted on a local population of polyarticular JIA patients treated at Boston Children’s Hospital Rheumatology Program. I reviewed the records of 150 pediatric patients, each being treated with an anti-TNF agent as their first line biologic. Fifty patients discontinued treatment within their first year of prescription while the remaining 100 served as controls. As a secondary analysis, patients were stratified as either responders or nonresponders based on their documented reasons for switching off their first line anti-TNF, regardless of case/control status. Younger age at anti-TNF initiation, reduction in neutrophil count and reduction in JADAS10 score at 3 months showed significant predictive power in determining if a patient is likely to switch off their first line anti-TNF within the first year of treatment. Rheumatoid factor positivity and 3 month reduction in WBC showed significant predictive power in determining if an anti-TNF biologic was discontinued due to clinical ineffectiveness. This study demonstrates the value of mining existing patient medical records to guide future research and contribute to more personalized, effective treatment selection.
Biology
Advisors/Committee Members: Morris, James (committee member), Son, MaryBeth (committee member).
Subjects/Keywords: pediatric rheumatology; juvenile idiopathic arthritis; anti-TNF
Record Details
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Record Details
Similar Records
Cite
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Anderson, E. (2018). The Predictive Power of Past Failure: Using Clinically Available Data to Improve Treatment Algorithms. (Masters Thesis). Harvard University. Retrieved from http://nrs.harvard.edu/urn-3:HUL.InstRepos:42004088
Chicago Manual of Style (16th Edition):
Anderson, Edwin. “The Predictive Power of Past Failure: Using Clinically Available Data to Improve Treatment Algorithms.” 2018. Masters Thesis, Harvard University. Accessed January 26, 2021.
http://nrs.harvard.edu/urn-3:HUL.InstRepos:42004088.
MLA Handbook (7th Edition):
Anderson, Edwin. “The Predictive Power of Past Failure: Using Clinically Available Data to Improve Treatment Algorithms.” 2018. Web. 26 Jan 2021.
Vancouver:
Anderson E. The Predictive Power of Past Failure: Using Clinically Available Data to Improve Treatment Algorithms. [Internet] [Masters thesis]. Harvard University; 2018. [cited 2021 Jan 26].
Available from: http://nrs.harvard.edu/urn-3:HUL.InstRepos:42004088.
Council of Science Editors:
Anderson E. The Predictive Power of Past Failure: Using Clinically Available Data to Improve Treatment Algorithms. [Masters Thesis]. Harvard University; 2018. Available from: http://nrs.harvard.edu/urn-3:HUL.InstRepos:42004088
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