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Shelton, Heath W., and Russell W. Brown. "INHIBITION OF TNF-ALPHA DECREASES MICROGLIA ACTIVATION IN RATS NEONATALLY TREATED WITH POLY I:C." Digital Commons @ East Tennessee State University, 2018. https://dc.etsu.edu/asrf/2018/schedule/166.
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Introduction: Current medical treatment for individuals diagnosed with schizophrenia (SCHZ) primarily relies on the inhibition of the dopamine D2 receptor that has been shown to be supersensitive in these patients. Treatment occurs through the use of antipsychotic medication which leads to a number of debilitating dose-dependent side effects, such as weight gain, agranulocytosis, and seizures. Patients diagnosed with SCHZ have also been shown to have increased inflammation in their central nervous system (CNS), particularly within specific brain regions such as the prefrontal cortex and hippocampus. This is in large part due to the interaction between a pro-inflammatory cytokine called tumor necrosis factor-alpha (TNFa) and microglia, which are resident CNS defense cells. TNFa is a cell-signaling protein, regulates a variety of immune cells, and is involved in the acute phase reaction of inflammation. Upon activation by TNFa secretion, microglial cells switch from being anti-inflammatory (M2) to pro-inflammatory (M1), thereby resulting in neuroinflammation as well as synaptic loss and neuronal death. In this project, we hypothesized oral administration through the diet of a novel TNFa modulator (PD2024) developed by P2D Biosciences, Inc. (Cincinnati, OH) would significantly reduce microglia activation in rats neonatally treated with Polyinosinic:polycytidylic acid (poly I:C). Methods and Results: To test our hypothesis, four groups (Neonatal Poly I:C/TNFa, Neonatal Poly I:C/Control, Neonatal Saline/TNFa, and Neonatal Saline/Control) were intraperitoneally injected with either poly I:C or saline during postnatal days (P)5-7. Poly I:C is an immunostimulant that mimics neonatal infection in humans, which also has been found to be a factor for the development of SCHZ later in life. Between days (P)30-(P)60, the Neonatal Poly I:C/TNFa and Neonatal Saline/TNFa groups were orally administered PD2024 through the diet. After (P)60, brain tissue was evaluated by immunohistochemistry (IHC) and confocal microscopy. Immunohistochemistry was used to label microglial cells in the prefrontal cortex and hippocampus with a green fluorescent dye attached to Iba1, a protein that specifically binds to these cells. Upon completion of IHC, tissue was evaluated using a confocal microscope and then analyzed with NIH ImageJ software. Analysis parameters included cell count, sampled cell body fluorescence, and overall image fluorescence. The results obtained showed a significant decrease in microglia activation for the Poly I:C/TNFa group when compared to the Poly I:C/Control group, as well as similarities in activation levels with the Saline/Control group. These results were demonstrated in both sampled cell body fluorescence and overall image fluorescence measurements. Conclusion: This data supports the hypothesis that PD2024 is successful in reducing microglia activation through the modulation of TNFa. Therefore, treatment with a TNFa modulator such as PD2024 alongside of current antipsychotic medication could mediate neuroinflammation and reduce the dose-dependent side effects. This approach could be a promising therapeutic treatment option for those diagnosed with schizophrenia, as well as potentially for other neurocognitive and behavioral disorders.
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Paschalinou, Eleni. "Nachweis von Punktmutationen im TNF-alpha- und INF-gamma-Promotor bei Patienten nach allogener Stammzelltransplantation oder Knochenmarktransplantation." [S.l. : s.n.], 2008.
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Romanatto, Talita. "Ação do fator de necrose tumoral alfa (TNF-'alfa') no hipotalamo : efeitos sobre expressão proteica, ingestão alimentar e consumo de 'O IND.2'/produção de 'CO IND.2'." [s.n.], 2006. http://repositorio.unicamp.br/jspui/handle/REPOSIP/310369.
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Orientador: Licio Augusto VellosoDissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciencias Medicas
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Resumo: A insulina e a leptina induzem uma potente resposta anorexigênica e termogênica atuando sobre neurônios do hipotálamo. Evidências recentes sugerem que a resistência à ação desses hormônios deve participar dos mecanismos centrais que favorecem o desenvolvimento da obesidade e sua associação com o diabetes mellitus. O consumo de dieta rica em gordura induz a expressão de proteínas pró-inflamatórias em hipotálamo de ratos, inclusive da citocina TNF-a. O presente estudo avaliou o efeito de diferentes doses intracerebroventriculares (ICV) de TNF-a sobre a ativação da via de sinalização da insulina, a ingestão alimentar e o consumo de O2/produção de CO2. Ratos Wistar, machos de oito semanas, foram canulados por via ICV e tratados com diferentes doses de TNF-a, insulina ou salina. A dose mais alta de TNF-a promoveu uma redução de 20% na ingestão alimentar de 12 horas, sendo esta redução inferior àquela produzida pela insulina. Na mesma dose, a citocina promoveu um aumento da temperatura corporal e do quociente respiratório. O TNF-a induziu a ativação de elementos da via pró-inflamatória no hipotálamo, como JNK, p38 e NF?B, o que resultou na transcrição de genes de resposta rápida e indução de proteínas da família SOCS. Com relação à via molecular da insulina, o TNF-a não induziu a ativação de substratos proximais e intermediários, no entanto, mesmo a dose mais baixa foi capaz de ativar elementos distais da via, como ERK e FOXO-1. Cocluindo, o TNF-a exerce um potente efeito anorexigênico e pró-termogênico no hipotálamo de ratos através de mecanismos independentes da ativação de proteínas proximais da via de sinalização da insulina. ERK e FOXO-1, que participam como intermediários em várias outras vias de sinalização, incluindo a via da insulina, são ativados pelo TNF-a no hipotálamo e podem estar envolvidas no efeito anorexigênico e pró-termogênico do TNF-a nesse órgão
Abstrasct: Insulin and leptin induce potent anorexigenic and pro-thermogenic responses in specialized neurons of the hypothalamus. Recent evidence suggest that resistance to the action of these hormones play a role in the mechanisms that favor the development of obesity and its common association with type 2 diabetes mellitus. The consumption of a fat-rich diet induces molecular and functional resistance to leptin and insulin in the hypothalamus, which is accompanied by the expression of pro-inflammatory proteins including the cytokine TNF-a. The present study has evaluated the effect of different doses of intracerebroventricular (ICV) TNF-a upon the activation of insulin signal transduction, food ingestion, and the consumption of O2/ production of CO2. For that, eight weeks old male Wistar rats were ICV cannulated and treated with saline, insulin or TNF-a. High dose TNF-a ?promotes a reduction of 20 % of 12 h food intake, which is an inhibitory effect marginally inferior than the one produced by insulin. In addition, TNF-a increases body temperature and respiratory quotient, effects not reproduced by insulin. TNF-a is also capable of activating canonical pro-inflammatory signal in the hypothalamus, inducing JNK, p38, and NF?B, which results in the transcription of early responsive genes and induction of proteins of the SOCS family. Finally, TNF-a does not activate signal transduction through early and intermediary elements of the insulin signaling pathway such as IRS-2 and Akt, however, TNF-a, even at low doses, is capable of activating late elements of the insulin signaling pathway such as ERK and FOXO-1. In conclusion, TNF-a exerts potent anorexigenic and pro-thermogenic effects in the hypothalamus through mechanisms independent of the activation of proteins that participate in early and intermediary steps of the insulin signaling pathway. ERK and FOXO-1, which act as late signal transducers for several signaling pathways, including insulin, are activated by TNF-a in the hypothalamus and may participate in the anorexigenic/pro-thermogenic effects of TNF-a in this organ
Mestrado
Medicina Experimental
Mestre em Fisiopatologia Médica
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MARTINS, Norielem de Jesus. "Educa??o escolar ind?gena Guarani no Estado do Rio de Janeiro: tens?es e desafios na conquista de direitos." Universidade Federal Rural do Rio de Janeiro, 2016. https://tede.ufrrj.br/jspui/handle/jspui/1422.
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La comprensi?n de la educaci?n como una pr?ctica cultural que se impone a los pueblos ind?genas, podemos reflexionar sobre nuestra ignorancia o negligencia de formas de educar a estas personas, lo que implica propias proceso de la civilizaci?n, los idiomas, las diversas concepciones del territorio y pertenencia. Las pol?ticas p?blicas para la educaci?n ind?gena en Brasil son recientes, y aunque se han conseguido muchos derechos en la educaci?n en los ?ltimos decenios, algunos no actualizan completamente. A pesar de la especificidad de los principios, la diferencia, la interculturalidad y el biling?ismo que apoyan la educaci?n ind?gena tambi?n identific? una fuerte influencia colonial en las pol?ticas p?blicas de Educaci?n Nacional, el di?logo y dificulta la implementaci?n de los derechos ind?genas. A pesar de estos callejones sin salida, las nuevas pol?ticas han ido constituyendo en una perspectiva intercultural, respetando la territorialidad ind?gena. En el estado de R?o de Janeiro, esta pol?tica comienza a tomar forma a partir de la acci?n de colaboraci?n entre el Estado, los municipios y el gobierno federal. Por lo tanto, el objetivo de esta investigaci?n es analizar la situaci?n de las pol?ticas p?blicas actuales de la educaci?n ind?gena guaran? en el Estado de R?o de Janeiro, la identificaci?n de las posibles formas de garantizar el derecho a la educaci?n con miras a la acci?n colaborativa. Para su realizaci?n, nos centramos en el enfoque cualitativo, observaci?n participante y las entrevistas realizadas en el periodo 2014-2015. Nuestro campo de estudio son las pol?ticas p?blicas para la educaci?n ind?gena en R?o de Janeiro llevadas a cabo por el Gobierno del Estado, los municipios donde est?n ubicados los pueblos guaran?es y universidades p?blicas. El an?lisis de los acuerdos de cooperaci?n entre las entidades federales de la pol?tica de los territorios Etnoeducacionais, nos dimos cuenta de la necesidad de invertir en un plan de acci?n que responda a las particularidades de cada pueblo y que permite una mayor autonom?a que el actual modelo de gesti?n, lo que permite la ejecuci?n de las garant?as los derechos alcanzados.
Compreendendo a educa??o escolar como uma pr?tica cultural que se imp?s aos povos ind?genas, podemos refletir sobre o nosso desconhecimento ou neglig?ncia sobre as formas de educar destes povos, que envolvem processos civilizat?rios pr?prios, linguagens, concep??es diversificadas de territ?rio e pertencimento. As pol?ticas p?blicas de Educa??o Escolar Ind?gena no Brasil s?o recentes, e embora muitos direitos tenham sido conquistados no campo educacional, ao longo das ?ltimas d?cadas, alguns n?o se efetivam plenamente. Apesar dos princ?pios da especificidade, diferen?a, interculturalidade e bilinguismo que fundamentam a Educa??o Escolar Ind?gena, identificamos, ainda, uma forte influ?ncia colonial nas pol?ticas p?blicas da Educa??o Nacional, dificultando o di?logo e a implementa??o de direitos ind?genas. Apesar destes impasses, novas pol?ticas v?m se constituindo em uma perspectiva intercultural, respeitando as territorialidades ind?genas. No Estado do Rio de Janeiro, esta pol?tica come?a a se estruturar a partir da a??o colaborativa entre Estado, Munic?pios e Governo Federal. Sendo assim, o objetivo desta pesquisa ? analisar a situa??o das atuais pol?ticas p?blicas de educa??o escolar ind?gena Guarani no Estado do Rio de Janeiro, identificando caminhos poss?veis para a garantia do direito ? educa??o, na perspectiva da a??o colaborativa. Para sua realiza??o, privilegiamos a abordagem qualitativa, a observa??o participante e entrevistas efetuadas no per?odo de 2014-2015. Nosso campo de estudo s?o as pol?ticas p?blicas para a Educa??o Escolar Ind?gena no Rio de Janeiro, realizadas pelo Governo Estadual, Munic?pios onde est?o localizadas as aldeias Guarani e Universidades P?blicas. Analisando o regime colabora??o entre entes federados a partir da pol?tica dos Territ?rios Etnoeducacionais, percebemos que ? necess?rio investir em um plano de a??o que contemple as especificidades de cada aldeia e que possibilite maior autonomia que a do modelo de gest?o atual, possibilitando a garantia de efetiva??o dos direitos conquistados.
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Shelton, Heath W., W. Drew Gill, Prasad Gabbita, and Russell W. Brown. "The Effect of Two Novel Anti-Inflammatory Drugs on Sensorimotor Gating and Microglial Activation in the Poly I:C Rodent Model of Schizophrenia." Digital Commons @ East Tennessee State University, 2019. https://dc.etsu.edu/asrf/2019/schedule/160.
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Antipsychotic medications remain the first line of treatment for individuals diagnosed with schizophrenia (SCZ). However, antipsychotic treatment is often not compliant due to dysregulation of both the central (CNS) and autonomic (ANS) nervous systems, resulting in debilitating dose-dependent side effects. Recent work suggests a new approach for treatment of SCZ that could potentially lower treatment doses and reduce side effects. Increased neuroinflammation has been shown in patients diagnosed with SCZ, particularly within the prefrontal cortex (PFC) and hippocampal (HPC) regions of the brain. Tumor necrosis factor-alpha (TNFa) is one of the key pro-inflammatory cytokines observed to be secreted during the inflammatory response. When TNFa is chronically secreted, resident CNS microglia become pro-inflammatory and toxic to the local environment. Microglial activation alongside of dopamine dysregulation thereby results in both the behavioral and neuroinflammatory aspects of SCZ. In this study, we hypothesized dietary administration of two different novel TNFamodulators (PD2024 – Experiment 1 and PD340 – Experiment 2) developed by our collaborators from P2D Bioscience, Inc. (Cincinnati, OH) would alleviate auditory sensorimotor gating deficits and reduce microglial cell activation caused by neonatal polyinosinic:polycytidylic acid (Poly I:C) treatment in rats, which is a validated rodent model of SCZ. Four groups (Experiment 1: Poly IC/PD2024, Poly IC/Control, Saline/PD2024, Saline/Control and Experiment 2: Poly IC/PD340, Poly IC/Control, Saline/PD340, Saline/Control) were intraperitoneally administered either Poly I:C (2 mg/kg) or saline (0.9% NaCl) from postnatal days 5-7. From P30-67, animals were placed on the experimental diet containing either low (10 mg/kg) or high (30 mg/kg) doses of either PD2024 or PD340, whereas the control animals remained on a normal diet. Prepulse inhibition (PPI) was used to test for auditory sensorimotor gating (behavioral abnormalities) in both adolescence (P44-46) and in adulthood (P60-66). At P67, immunohistochemistry (IHC) and confocal microscopy were used to evaluate and examine microglial cell activation using the Iba1-GFP antibody (neuroinflammatory abnormalities) in the PFC and HPC. Results revealed auditory sensorimotor gating deficits in Poly IC/Controls were alleviated in both adolescence and adulthood with either PD2024 or PD340. It was also found that both TNFa modulators significantly reduced microglial activation in the HPC, but not the PFC. The data supports our hypothesis that dietary administration of PD2024 or PD340 alleviates behavioral deficits and decreases neuroinflammation generated from the Poly I:C rodent model of SCZ. Therefore, an approach with a TNFa modulator alongside of current antipsychotic medications could treat both the behavioral and neuroinflammatory aspects of SCZ.
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Spratte, Julia [Verfasser]. "Heparine modulieren humane endometriale Stromazellen im Hinblick auf deren Differenzierung und Reaktionsverhalten gegenüber TNF-α und INF-γ / Julia Hehui Spratte." Greifswald : Universitätsbibliothek Greifswald, 2013. http://d-nb.info/1033246271/34.
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Roehe, Nara Simone. "A ind?stria automobil?stica e a pol?tica econ?mica do governo Geisel: tens?o em uma parceria hist?rica (1974 - 1978)." Pontif?cia Universidade Cat?lica do Rio Grande do Sul, 2011. http://tede2.pucrs.br/tede2/handle/tede/2393.
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Previous issue date: 2011-03-31O estabelecimento da ind?stria automobil?stica multinacional deu-se na d?cada de 1950, n?o somente atrav?s do esfor?o, mas tamb?m da disposi??o e da estrat?gia do Estado brasileiro. Seguindo o modelo desenvolvimentista, a cria??o do GEIA, em 1956, destacou-se como sendo a primeira legisla??o espec?fica para o setor automotivo que estabeleceu as regras, assim como a concess?o de est?mulos e desest?mulos para a instala??o e atua??o daquela ind?stria no pa?s. No entanto, com as implica??es pol?ticas posteriormente ocorridas, o GEIA foi desmembrado e sua atua??o, como instrumento legal, levada ? inexpressividade. Por outro lado, ap?s sua matura??o no pa?s hospedeiro, entre os anos de 1968 e 1973, a ind?stria automobil?stica se apresentou como um dos segmentos l?deres e principais pilares da expans?o econ?mica brasileira, contribuindo de forma significativa para o crescimento do PIB nacional, cuja varia??o percentual no per?odo consagrou o milagre econ?mico. Mas, frente ? exaust?o do crescimento interno acelerado e ? crise internacional do petr?leo, a partir de 1974, o governo Geisel adotou medidas restritivas preconizando a busca do saneamento econ?mico. Estas diretrizes do Estado, ao serem aplicadas, promoveram diverg?ncias entre os interesses corporativos daquele setor da ind?stria e os interesses nacionais do Brasil. Nesse sentido, depois de um momento de grande expans?o e desregulamenta??o, o ajustamento da ind?stria automobil?stica as novas pol?ticas econ?micas conflitaram o governo com aquele segmento que ? considerado o motor da industrializa??o brasileira
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Paim, Francine Chimelo. "Citocinas pró-inflamatórias em ratos experimentalmente infectados por Trypanosoma evansi." Universidade Federal de Santa Maria, 2011. http://repositorio.ufsm.br/handle/1/10087.
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Conselho Nacional de Desenvolvimento Científico e TecnológicoThe aim of this study was to measure the levels of interferon-gamma (IFN-γ), tumor necrosis factor-alpha (TNF-α), interleukin 1 (IL-1) and interleukin 6 (IL-6) in serum of rats experimentally infected with Trypanosoma evansi and to correlate with the hematological parameters. Seventy-six rats (Wistar) were divided into two groups. Group C (control) composed of twenty-eight non-inoculated rats distributed in four subgroups with seven animals each (C3, C5, C10 and C20), which received 0.2 mL saline by intraperitoneally. The group T (infected) formed of forty-eight rats was inoculated intraperitoneally with cryopreserved blood containing 1x106 trypomastigotes per animal. These, eight animals died between 5th -7th days post-infection. The remaining animals were divided into four subgroups with ten animals (T3, T5, T10 and T20) according to parasitemia degree. The blood samples were collected by cardiac puncture at the day 3 (C3, T3), 5 (C5, T5), 10 (C10, T10) and 20 (C20, T20) post infection (pi) to perform the complete blood count and determination of IFN-γ, TNF-α, IL-1 and IL-6 levels using an ELISA quantitative sandwich. Immediately after collection the animals were euthanized. The levels of all measured cytokines increased significantly (P < 0.01) in infected animals compared to the controls. T. evansi infection in rats caused an increase in serum IFN-γ, TNF-α, IL-1 and IL-6 and this increase was observed during the whole experimental infection. In addition, the increase in the cytokine levels was concomitant and directly correlated with parasitemia and anemia development at the parasitemia peak. These results suggest a synergism between these cytokines contributing to the development of anemia and the regulation of the immune response against the parasite.
O objetivo deste estudo foi avaliar os níveis séricos das citocinas pró-inflamatórias interferon-gama (INF-γ), fator de necrose tumoral-alfa (TNF-α), interleucina 1 (IL-1) e interleucina 6 (IL-6) em ratos experimentalmente infectados por Trypanosoma evansi e estabelecer uma correlação com os parâmetros hematológicos. Setenta e seis ratos (Wistar) machos foram divididos em dois grupos experimentais. O Grupo C (controle) foi composto por vinte e oito ratos não inoculados distribuídos em quatro subgrupos com sete animais cada (C3, C5, C10 e C20), que receberam 0,2 mL de solução fisiológica pela via intraperitoneal. O grupo T (infectados) formado por quarenta e oito ratos inoculados intraperitonealmente com sangue criopreservado, contendo 1x106 tripomastigotas de T. evansi por animal. Destes, oito morreram entre o 5º e 7º dia pós-infecção. Os animais restantes foram divididos em quatro subgrupos de dez animais cada (T3, T5, T10 e T20) de acordo com o grau de parasitemia. As amostras de sangue foram coletadas por punção cardíaca, nos dias 3 (C3, T3), 5 (C5, T5), 10 (C10, T10) e 20 (C20,T20) pós-infecção (pi) para a realização do hemograma e determinação dos níveis séricos de INF-γ, TNF-α, IL-1 e IL-6 pela técnica de ELISA tipo sanduíche. Imediatamente após as coletas os animais eram submetidos à eutanásia. Os níveis de citocinas pró-inflamatórias aumentaram significativamente (P<0,01) nos animais infectados em relação ao grupo controle. A infecção por T. evansi em ratos provocou um aumento nos níveis séricos de INF-γ, TNF-α, IL-1, IL-6 e esse aumento foi observado durante toda a infecção experimental. Além disso, o aumento nos níveis de citocinas foi diretamente correlacionado com a parasitemia e o desenvolvimento da anemia. Estes resultados sugerem um sinergismo entre essas citocinas contribuindo para o desenvolvimento da anemia e regulação da resposta imune contra o parasito.
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Hisada, Toru. "Indigenous Development and Self-Determination in West Papua: A Case Study of the Socio-Political and Economic Impacts of Mining upon the Amungme and Kamoro Communities of West Papua." The University of Waikato, 2007. http://hdl.handle.net/10289/2457.
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Since West Papua was colonized by Indonesia in 1963, West Papuans have endured one of the most disastrous experiences of cultural and environmental destruction, human rights abuses and mass killing of the twentieth century. In the Western Highlands of West Papua, where Freeport McMoRan, a mining company from Louisiana, United States (U.S.), operates, there have been long-standing disputes over environmental justice, human rights, the right to control development, and wealth distribution. Substantial research has been done on the negative impacts of the Freeport's operation on the Amungme and Kamoro communities who reside in the company's operating area. Yet, limited research has been done regarding Freeport's social policies and the possible solutions to the issues which are crucial for the further development of Amungme and Kamoro. Therefore, the thesis firstly examines Freeport's recent social policies which have attempted to address the two communities' concerns as well as the social problems the company has caused around its operating area. The examination suggests that genuine reconciliation between Amungme and Kamoro communities and Freeport is a crucial next step in achieving successful community development in the area. The thesis employs a case study of the South African reconciliation processes via Truth and Reconciliation Commission (TRC) to explore the prospects of achieving successful community development in Freeport's operating area of West Papua which might lead to prosperity for the Amungme and Kamoro peoples. In addition to this, the prospect of preventing the human rights violations by the Indonesian Military (Tentera Nasional Indonesia-TNI) is considered. The TNI, by carrying out the role of protecting the Freeport operation, has until today committed a large number of human rights violations against indigenous West Papuans around the mine thus preventing and inhibiting the future development of Amungme and Kamoro communities. Since major countries, including the U.S., the United Kingdom (UK), New Zealand and Australia, have until today, supported the Indonesia state and the TNI, the attitude of Pacific Island states towards the issue is examined. Finally, although the above processes are important, the study suggests the more important role of the Amungme and Kamoro themselves in taking responsibility for their plight and taking positive actions wherever possible to solve the issues surrounding them. Although the conflict continues to the present day, the research contained in the thesis outlines the situation in West Papua only up until November 2006.
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Castilho, Pereira Ione Aparecida Martins. "Em tudo semelhante, em nada parecido : uma an?lise comparativa dos planos urbanos das miss?es jesu?ticas de Mojos Chiquitos, Guarani e Maynas (1607-1767)." Pontif?cia Universidade Cat?lica do Rio Grande do Sul, 2014. http://tede2.pucrs.br/tede2/handle/tede/2485.
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Previous issue date: 2014-02-25This thesis intends to present a comparative analysis of the spatial organization of the urban plans of the jesuitic missions Guarani, Chiquitos, Mojos and Maynas. This study aims to know to what extent the evangelizer project undertook by Society of Jesus was similar and different concerning the spatial organization of these four missionary spatialities. To answer this inquiry, we established the years of 1607 to 1767 as a temporal delimitation. Such dates refer to the beginning of the jesuitic action in the Guarani missions, passing through Maynas missions foundation (1636), Mojos (1682), Chiquitos (1690), and finally the expulsion of the jesuits from Spanish America (1767). About the sources which are the focus of our analysis and comparison, they are both documental and bibliographic. Thus, what we seek is advance beyond the brief comparisons and the juxtapositions of informations in blocks of synthesis. Therefore, we intend to demonstrate, through a comparative analysis, that the diverse forms of existing, produced by indigenes and jesuits in these missionary spatialities, created not only differences, but also similarities from this relation with the inhabited space.
A presente tese tem por finalidade apresentar uma an?lise comparativa dos planos urbanos das miss?es jesu?ticas Guarani, Chiquitos, Mojos e Maynas. O objetivo deste estudo ? saber em que medida o projeto evangelizador empreendido pela Companhia de Jesus foi semelhante e diferente na organiza??o espacial destas quatro espacialidades missioneiras. Para responder a este questionamento, estabelecemos como delimita??o temporal os anos de 1607 a 1767. Tais datas referem-se ao in?cio da a??o jesu?tica nas miss?es Guarani, passando pelas funda??es das miss?es de Maynas (1636), Mojos (1682) e Chiquitos (1690), e, por fim, a data de expuls?o dos jesu?tas da Am?rica Espanhola (1767). J? as fontes que constituem o foco de nossa an?lise e compara??o s?o tanto documentais quanto bibliogr?ficas. Sendo assim, queremos ? avan?ar para al?m das breves compara??es e das justaposi??es de informa??es em blocos de s?nteses. Pretendemos demonstrar ent?o, atrav?s de uma an?lise comparativa, que as diversas formas do existir, produzidas por ind?genas e jesu?tas nestas espacialidades missioneiras, criaram como resultado desta rela??o com o espa?o habitado tanto diferen?as quanto semelhan?as.
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CONDE, Simone Regina Souza da Silva. "Correlação dos níveis séricos e dos polimorfismos nos genes de citocinas (TNF-α, INF-γ, TGF-β1 e IL-10) com a apresentação clínica da hepatite B crônica." Universidade Federal do Pará, 2010. http://repositorio.ufpa.br/jspui/handle/2011/4756.
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A hepatite B crônica apresenta amplo espectro de manifestações clínicas, resultante de diversos fatores, tais como o padrão de secreção e polimorfismo nos genes de citocinas. Este trabalho objetiva correlacionar os polimorfismos TNF-α -308G/A, INF-γ +874A/T, TGF-β1 -509C/T e IL-10 -1081A/G e os níveis séricos destas citocinas com a apresentação clínica da hepatite B. Foram selecionados 53 casos consecutivos de hepatite B, sendo divididos em grupo A (portador inativo= 30) e B (hepatite crônica/cirrose= 23). Como grupo controle, selecionaram-se 100 indivíduos com anti-HBc e anti-HBs positivos. Os níveis séricos das citocinas foram determinados por ensaios imunoenzimáticos, tipo ELISA (eBiosceince, Inc. Califórnia, San Diego, USA). A amplificação gênica das citocinas se realizou pela PCR e a análise histopatológica obedeceu à classificação METAVIR. Identificou-se maior prevalência do genótipo TNF-α -308AG (43,3% vs. 14,4%) no grupo B do que nos controles e a presença do alelo A se correlacionou com risco de infecção crônica pelo VHB (OR= 2,6). Os níveis séricos de INF-γ e de IL-10 foram maiores (p< 0,001) nos controles do que os demais grupos e, inversamente, as concentrações plasmáticas de TGF-β1 foram menores no grupo controle (p< 0,01). Observou-se, na histopatologia hepática, que atividade inflamatória > 2 se correlacionou com maiores níveis de TNF-α e de INF-γ (p< 0,05), assim como a fibrose > 2 com maiores níveis de INF-γ (p< 0,01). Na população pesquisada, menores níveis séricos de INF-γ e de IL-10 e maiores de TGF-β1 estiveram associados com a hepatite B crônica, bem como a presença do alelo A no gene TNF-α - 308 aumentou em 2,6 o risco de cronificação.
Chronic hepatitis B has a wide spectrum of clinical manifestations resulting from various factors, such as the pattern of secretion and polymorphism in cytokine genes. This work aims to correlate the TNF-α -308G/A, INF-γ +874A/T, TGF-β1 -509C/T e IL-10 -1081A/G polymorphisms and serum levels of these cytokines with the clinical presentation of hepatitis B. It was selected 53 consecutive cases of hepatitis B divided into group A (inactive carrier= 30) and B (chronic hepatitis / cirrhosis= 23). As a control, we selected 100 individuals anti-HBc and anti-HBs positives. Serum levels of cytokines were determined by enzyme immunoassays (eBiosceince, Inc. California, San Diego, USA). The gene amplification of cytokines was carried out by PCR and histopathological analysis followed by METAVIR classification. It was identified that genotype TNF-α -308GA was more prevalent among B group than controls and that presence of A allele increased the risk for chronic disease (OR= 2,6). The serum levels of INF-γ and IL-10 were higher (p <0,001) in controls than others groups A and B and the TGF-β1 levels were lower (p < 0,01) in controls. It was noted that inflammatory activity > 2 correlated with higher levels of TNF-α and IFN-γ (p<0.01) and fibrosis > 2 with higher levels of INF-γ (p <0.01). In the studied population, lower INF-γ and IL-10 levels and higher TGF-β1 level were associated with chronic hepatitis B, and that the presence TNF-α -308 A allele increased in 2,6 the risk for chronic disease .
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Dettogni, Raquel Spinassé. "Influência de polimorfismos nos genes FcγRIIa, CD209, VDR, TNF-α, IL-4, IL-6 e INF-γ na persistência de sintomas clínicos da dengue na fase de covalescença." reponame:Repositório Institucional da UFES, 2015. http://repositorio.ufes.br/handle/10/1311.
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CAPES, FAPES
Diferenças na susceptibilidade do hospedeiro à infecção, na gravidade e na permanência do quadro clínico da doença podem ser atribuídas, em parte, às variações da resposta imune. Estas variações são associadas a polimorfismos de nucleotídeo único (do inglês: single nucleotide polymorphisms - SNPs). Como estudo prévio, foi realizada a caracterização da população geral do Espírito Santo (ES) - Brasil e de uma subpopulação do estado, de origem Pomerana, quanto aos SNPs -131 H/R, -336 A/G, TaqI, -308 A/G, -590 C/T, -174 G/C e +874 A/T nos genes FcγRIIa, CD209, VDR, TNFα, IL-4, IL-6 e INF-γ, respectivamente. Cem indivíduos da Grande Vitória representaram a população geral do ES e 59 indivíduos de Santa Maria de Jetibá representaram a população de origem Pomerana. Como a fase aguda da dengue é bem caracterizada, este estudo objetivou ampliar o conhecimento da fase de convalescença. Noventa e seis indivíduos diagnosticados com dengue sintomática no final de 2012 e início de 2013, no ES, foram acompanhados por 60 dias a partir do início dos sintomas por meio do preenchimento de um questionário clínico e epidemiológico em quatro entrevistas. A persistência de 37 sintomas clínicos da dengue foi avaliada. Para analisar a influência da genética do sistema imunológico do hospedeiro na persistência de sintomas clínicos da dengue na fase de convalescença, foi determinada a associação entre os sete SNPs, para os quais a população do ES foi caracterizada, e a persistência de sintomas. O DNA genômico dos participantes do estudo foi extraído do sangue periférico e a genotipagem dos SNPs foi realizada por reação em cadeia da polimerase - polimorfismo de comprimento de fragmento de restrição (do inglês: polymerase chain reaction - restriction fragment length polymorphism - PCR-RFLP) As frequências genotípicas de todos os SNPs encontraram-se em equilíbrio de Hardy-Weinberg (do inglês: Hardy-Weinberg equilibrium - HWE), com exceção do SNP no gene IL-6. Não houve diferença estatisticamente significante nas frequências genotípicas dos SNPs nos genes FcγRIIa, CD209, VDR, TNF-α e IL-4 entre as duas populações. Diferença estatisticamente significante foi encontrada entre as duas populações nas distribuições genotípicas dos SNPs nos genes IL-6 (p = 0,03) e INF-γ (p = 0,007). Trinta e sessenta dias após o início dos sintomas, 38,5% e 11,5% dos indivíduos com dengue sintomática reportaram ter pelo menos um sintoma clínico da dengue, respectivamente. Dos sintomas analisados, os mais persistentes foram os relacionados à síndrome da fadiga como mialgia, artralgia, astenia e mal-estar, sendo a mialgia o mais frequente. A persistência de sintomas em 30 dias foi associada ao gênero feminino (p = 0,044) e a persistência de sintomas constitucionais foi associada à dengue secundária (p = 0,041). O SNP no gene FcγRIIa, foi associado à persistência de sintomas em 30 dias, no subgrupo de indivíduos com dengue secundária (p = 0,046), sendo a presença do alelo H associada à não persistência de sintomas (p = 0,014). A presença do alelo A do SNP no gene TNF-α foi associada à não persistência de sintomas no subgrupo de indivíduos com dengue secundária (p = 0,025), sendo o genótipo GG associado à persistência de sintomas neurológicos, psicológicos e comportamentais em 30 dias (p = 0,038). A presença do alelo C do SNP no gene IL-6 foi associado à persistência de sintomas dermatológicos em 30 dias (p = 0,005). O perfil genético desses SNPs pode favorecer o estabelecimento de marcadores imunogenéticos associados à fase convalescente da infecção pelo vírus da dengue (do inglês: dengue virus - DENV).
Differences in host susceptibility to infection, in the severity and permanence of the clinical picture of disease can be attributed, in part, to variations in the immune response. These variations are associated with single nucleotide polymorphisms (SNPs). As a previous study, the characterization of the general population of the Espírito Santo (ES)-Brazil and of a subpopulation of the state, of pomeranian origin, was performed as the SNPs -131 H/R, -336 A/G, TaqI, -308 A/G, -590 T/C, -174 G/C and +874 A/T in FcγRIIa, CD209, VDR, TNF-α, IL-4, IL-6 and IFN-γ genes, respectively. One hundred individuals of the Grande Vitória represented the general population of ES and 59 individuals of Santa Maria de Jetibá represented the population of Pomeranian origin. As the acute phase of dengue is well characterized, this study aimed to expand the knowledge of the phase of convalescence. Ninety-six individuals diagnosed with symptomatic dengue in late 2012 and early 2013, in ES, were followed for 60 days from the onset of symptoms by completing a clinical and epidemiological questionnaire in four interviews. The persistence of 37 clinical symptoms of dengue was assessed. To analyze the influence of the genetics of the host immune system in the persistence of clinical symptoms of dengue in the convalescent phase, the association between seven SNPs, for which the population of ES was characterized, and the persistence of symptoms was determined. Genomic DNA of study participants was extracted from peripheral blood and genotyping of SNPs was performed by polymerase chain reaction - restriction fragment length polymorphism (PCR-RFLP). The genotype frequencies of all SNPs were found in Hardy-Weinberg equilibrium (HWE), except for the SNP in the IL-6 gene. There was no statistically significant difference in genotype frequencies of SNPs in FcγRIIa, CD209, VDR, TNF-α and IL-4 genes between the two populations. A statistically significant difference was found between the two populations in the genotypic distributions of SNPs in IL-6 (p = 0.03) and INF-γ (p = 0.007) genes. Thirty and sixty days after the onset of symptoms, 38.5% and 11.5% of symptomatic patients with dengue reported having at least one clinical symptom of dengue, respectively. Symptoms among, the most persistent were related to fatigue syndrome as myalgia, arthralgia, asthenia and malaise, myalgia being the most frequent. The persistence of symptoms at 30 days was associated with female gender (p = 0.044) and persistent constitutional symptoms was associated with secondary dengue (p = 0.041). FcγRIIa gene SNP, was associated with persistent symptoms at 30 days in the subgroup of patients with secondary dengue (p = 0.046), and presence of the H allele was associated with non-persistence of symptoms (p = 0.014). The presence of the A allele in the TNF-α gene SNP was associated with non-persistence of symptoms in the subgroup of patients with secondary dengue (p = 0.025), with the GG genotype associated with persistent neurological, psychological and behavioral symptoms in 30 days (p = 0.038). The presence of the C allele in the IL-6 gene SNP was associated with persistent dermatological symptoms at 30 days (p = 0.005). Genetic profiling of these SNPs may favor the establishment of immunogenetic markers associated with the convalescent infection phase by the dengue virus (DENV).
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DETTOGNI, R. S. "Influência de Polimorfismos nos Genes Fcyrlla, Cd209, Vdr, Tnf-a, Il-4, Il-6 e Inf-y na Persistência de Sintomas Clínicos da Dengue na Fase de Convalescença." Universidade Federal do Espírito Santo, 2015. http://repositorio.ufes.br/handle/10/4523.
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Previous issue date: 2015-02-13Influência de polimorfismos nos genes FcγRlla, CD209, VDR, TNF-α, IL-4, IL-6 e INF-γ na persistência de sintomas clínicos da dengue na fase de convalescença
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Stumpf, Ana Rita Lancini. "Perfil de citocinas pró- e anti-inflamatória e da proteína c-reativa no tratamento do tumor venéreo transmissível canino." Universidade Federal de Santa Maria, 2014. http://repositorio.ufsm.br/handle/1/10174.
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The canine transmissible venereal tumor (CTVT) is unique in various
aspects, and the
principal is that the tumoral cells are not originated from the hos
t. Recent findings showed that
the CTVT is a transplantable tumor that first appeared in a
dog ancestor approximately 10000
years ago. The tumoral cells propagate mainly through coitus, develop a
s a graft, and have the
capability of installing themselves by mechanisms of escape
from the host's immunologic
response. This specific response involves cellular and humoral immunity
and varies according to
some factors not yet very elucidated. Beyond the well-known role of fi
ghting the tumor cells, the
inflammatory response also plays an involuntary and paradoxical role, w
hich results in the
promotion of tumor growth by releasing vasculogenic, antiapoptotic, and
cellular growth-
promoting substances. The fact that tumors can benefit from the inf
lammatory response makes
the investigation of the mechanisms involved important for the development
of new therapies
focused on the modulation of the inflammatory response to control the tumor
development. The
aim of this work is to better understand the mechanisms behind tumora
l growth by the
measurement of the levels of pro-inflammatory (IL-1, IL-6, TNF-
α
and INF-
γ
) and anti-
inflammatory (IL-10) cytokines and the C-reactive protein (CRP) ove
r the treatment of dogs
naturally infected with CTVT. The quantification of the cytokines and
CRP was performed in the
animals' serum from samples obtained at the moments of the diagnosis
and pre-therapy, immediately before chemotherapy, and after the confirmation of
the cure of each animal.
According to therapy response, two groups were identified, R, were t
he tumor was resistant to
therapy and NR, which was susceptible. A cure probability was define
d in relation to time of
treatment and tumor response to vincristin. In group R all parameter
s varied significantly: The
expression of pro-inflammatory cytokines and CRP were higher, and of I
L-10, lower, comparing
to group NR. For pro-inflammatory cytokines, this difference was ma
intained until cure.
Statistical analysis was able to detect correlations betwee
n all variables, demonstrating the
participation of cytokines during tumor evolution. The role of inflammati
on has been postulated
and, although the mechanisms remain unclear, a correlation of chronic i
nflammation and cancer
susceptibility has been demonstrated. Because CTVT is a tumor of
foreign cells, it is a suitable
model to investigate the mechanisms involved in tumor maintenance and deve
loping, as well as
the associated immune response.O tumor venéreo transmissível canino (TVTc) é um tumor único em vários aspectos, sendo o principal, o fato de as células tumorais não serem originárias do animal acometido. Resultados de pesquisas recentes demonstraram que o TVTc é um tumor transplantável que surgiu em ancestrais do cão doméstico há aproximadamente 10000 anos. As células, que se propagam principalmente pelo coito, se desenvolvem como um enxerto e apresentam a capacidade de se implantar através de mecanismos de escape à resposta imunológica do hospedeiro. Essa resposta envolve a imunidade celular e humoral e varia de acordo com fatores não totalmente elucidados. Além do conhecido papel na resposta imune com o objetivo de combater tumores, a resposta inflamatória desempenha um papel involuntário e paradoxal que resulta na promoção do crescimento tumoral pela liberação de substâncias vasculogênicas, antiapoptóticas e promotoras de crescimento celular. O fato de que os tumores possam se beneficiar da resposta inflamatória torna necessárias pesquisas visando o desenvolvimento de terapias direcionadas à modulação da resposta inflamatória para o controle do desenvolvimento tumoral. Dessa forma, o objetivo deste estudo foi compreender melhor os mecanismos envolvidos no desenvolvimento do tumor através da mensuração dos níveis das citocinas pró-inflamatórias (IL- 1, IL-6, TNF-α e INF-γ) e da anti-inflamatória (IL-10) e de uma proteína de fase aguda da inflamação, a Proteína C-reativa (PCR) durante o tratamento de cães naturalmente infectados pelo TVTc. A quantificação das citocinas e da PCR foi realizada no soro dos animais a partir de amostras obtidas no diagnóstico e pré-terapia, imediatamente antes de cada nova aplicação 9 quimioterápica e no momento em que o animal era considerado curado. A partir da resposta à quimioterapia foram caracterizados grupos de animais de acordo com os tumores resistentes (R) e não-resistentes (NR). Foi estabelecida a probabilidade de cura em relação ao tempo de terapia, de acordo com o tipo de tumor. No grupo R, foi observada variação significativa em todos os parâmetros, sendo a expressão das citocinas pró-inflamatórias e da PCR, mais elevadas e a expressão da IL-10 inferior em relação à expressão observada em amostras dos animais do grupo NR. No caso das citocinas pró-inflamatórias e da PCR, essa diferença se manteve até a cura dos animais, diferindo da IL-10, cujas concentrações foram similares nos dois grupos ao final do tratamento. A análise estatística realizada detectou a presença de correlações entre as variáveis, demonstrando a participação das citocinas durante o processo de evolução tumoral. O papel da inflamação no desenvolvimento do câncer foi postulado, apesar de os mecanismos moleculares não terem sido elucidados, sabe-se que a inflamação crônica eleva a probabilidade do desenvolvimento de tumores. Pelo fato de o TVTc ser um tumor de células estranhas ao organismo, seu estudo é importante para verificar os mecanismos relacionados com a manutenção e desenvolvimento dos tumores, bem como da resposta imune associada.
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Pawley, Adam David. "Novel TMS and EEG markers of diagnosis and treatment response in epilepsy." Thesis, King's College London (University of London), 2015. https://kclpure.kcl.ac.uk/portal/en/theses/novel-tms-and-eeg-markers-of-diagnosis-and-treatment-response-in-epilepsy(02e6922a-e038-41af-bac9-169770fb7d05).html.
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Approximately 30% of epilepsy patients do not respond to treatment, whereas others attain seizure freedom with the same medication, the reasons remain unclear. Previous work utilised transcranial magnetic stimulation (TMS) to reveal predictive markers of treatment response in new-onset drug-naïve patients, distinguishing good responders from those who become intractable. I hypothesised that these markers should also be present in long-term treatment resistant epilepsy, allowing outcome prediction in patients commencing new medications. A central hypothesis in this thesis is that, interictal brain dynamics in epilepsy differ from the stable state of the healthy brain and are related to seizure frequency. I addressed this using TMS measures of excitation and inhibition, and electroencephalography (EEG) as a measure of the larger-scale electrophysiological dynamic system. Using existing TMS data I examined motor evoked potentials (MEPs) in Idiopathic generalised epilepsy (IGE). MEPs were more polyphasic in patients and their relatives than controls, which may represent an inherited endophenotype. TMS measures were also compared between patients with well and poorly controlled epilepsy. Findings broadly indicated that poorly controlled patients have reduced excitability vs well controlled, the reasons are unknown, although a protective homeostatic mechanism may be responsible. Furthermore, TMS parameters in well-controlled epilepsy were closer to healthy controls than poorly controlled patients. A longitudinal TMS study in chronic epilepsy with patients studied before and after treatment change, revealed a weak effect suggesting reduced excitability in poor responders, although a range of factors suggested that TMS would not have utility as a predictive marker clinically. A pilot study also investigated whether external trigeminal nerve stimulation (eTNS) has a measureable effect on brain excitability. There was a small effect which may associate with treatment outcome. Finally, EEG measures were compared in well and poorly-controlled epilepsy, with the profile of a well-controlled patient closer to that of the healthy brain. Future work focusing on EEG as a marker of response in newly diagnosed epilepsy, utilising TMS-EEG for revealing mechanisms underlying treatment response would be appropriate.
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Arruda, Ariane Aparecida Carvalho de. "Condicionantes ?tnicos na cria??o das Miss?es de Chiquitos : alian?as e conflitos na Chiquitania e no Pantanal (1609-1691)." Pontif?cia Universidade Cat?lica do Rio Grande do Sul, 2011. http://tede2.pucrs.br/tede2/handle/tede/2378.
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Previous issue date: 2011-03-11Este estudo tem como objetivo estabelecer os condicionantes ?tnicos que dificultaram e/ou facilitaram a instala??o das Miss?es de Chiquitos na Bol?via. A partir do contato inter?tnico, surgiram alian?as e conflitos entre ind?genas/ind?genas e entre ind?genas/europeus, que possibilitaram o estabelecimento da sociedade europeia em seus territ?rios, a implanta??o do sistema de encomiendas em Assun??o e Santa Cruz de la Sierra e, finalmente, a funda??o das miss?es jesu?ticas entre os ind?genas da Chiquitania. O recorte temporal inicia em meados do s?culo XVI, quando os conquistadores europeus entram na regi?o do Pantanal e da Chiquitania na tentativa de alcan?ar as riquezas minerais do Peru e de Potosi na Bol?via. Nesse contexto, ocorrem v?rios epis?dios de intensos conflitos entre ind?genas e espanh?is encomenderos at? que, a partir de 1609, os mission?rios jesu?tas aparecem como uma possibilidade de salva??o dos ind?genas e de inser??o em um novo contexto colonial por meio das redu??es religiosas, primeiro, junto aos Guarani, nas margens do rio Paranapanema (no atual estado do Paran?) e, posteriormente, em 1691, na Chiquitania, junto aos ind?genas conhecidos como Chiquito. Assim, surgem conflitos e alian?as entre os europeus que almejavam conquistar riquezas e territ?rios para a Coroa espanhola, ocorre o genoc?dio e a explora??o de muitos ind?genas, a migra??o de ind?genas para regi?es mais seguras, como a das pr?prias Miss?es de Chiquitos e a miscigena??o de grupos ind?genas com culturas e l?nguas distintas. Para a interpreta??o dos epis?dios gerados pelo contato inter?tnico entre ind?genas e europeus, a an?lise de discurso foi utilizada na compreens?o de como a sociedade europeia construiu a imagem do ind?gena como um ser sem f?, sem lei e sem Rei.
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Mercer, Louise. "Safety of long-term anti-TNF use, with respect to malignancy, in a national cohort of people with rheumatoid arthritis." Thesis, University of Manchester, 2013. https://www.research.manchester.ac.uk/portal/en/theses/safety-of-longterm-antitnf-use-with-respect-to-malignancy-in-a-national-cohort-of-people-with-rheumatoid-arthritis(be2ba2c3-a9a2-4a23-a3fb-c5688e990f93).html.
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AimThe broad aim of this thesis was to explore the risk of malignancy in people with rheumatoid arthritis (RA), treated with anti-tumour necrosis factor (TNF) drugs.MethodsThis thesis used data from patients with RA registered with the British Society of Rheumatology Biologics Register-RA. The risk of cancer in biologic-naive patients treated with traditional disease modifying drugs (nbDMARD) was compared to that in the general population by calculating standardised incidence ratios (SIR). The influence of anti-TNF on cancer risk was then explored by comparing the risk in the anti-TNF cohort to that in the nbDMARD cohort using Cox proportional hazard models.ResultsThe risk of cancer was increased in the nbDMARD cohort by 28% compared to the general population (SIR 1.28, 95% confidence interval (CI) 1.10, 1.48). Risks of lung cancer (SIR 2.39, 95% CI 1.75, 3.19), Hodgkin lymphoma (SIR 12.82, 95% CI 4.16, 29.92) and Non-Hodgkin Lymphoma (SIR 3.12, 95% CI 1.79, 5.07) were increased compared to the general population and both prostate cancer and cancers of the female genital organs reduced; SIRs 0.35 (95% CI 0.11, 0.82) and 0.35 (95% CI 0.10, 0.90) respectively. There was no difference in the risk of cancer in patients treated with anti-TNF compared to nbDMARD, after adjusting for differences in baseline characteristics; Hazard ratio for lymphoma: 1.00 (95% CI 0.49, 2.05); cancers of the solid organs: 0.83 (95% CI 0.64, 1.07); and keratinocyte skin cancer: basal cell carcinoma 1.06 (95% CI 0.64, 1.75), squamous cell carcinoma 1.62 (95% CI 0.44, 5.90). ConclusionsSubjects with RA, treated with nbDMARD were at increased risk of cancer compared to the general population. In particular, lung cancer, lymphoma and KSC were increased. Treatment with the TNF inhibitors ETA, INF or ADA was not associated with a difference in relative risk of lymphoma, solid cancer or skin cancers when compared to nbDMARD.
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Hicks, Alexander Peter. "The role of the Coxsackie and Adenoviral Receptor in TNF alpha driven inflammation." Thesis, King's College London (University of London), 2016. http://kclpure.kcl.ac.uk/portal/en/theses/the-role-of-the-coxsackie-and-adenoviral-receptor-in-tnf-alpha-driven-inflammation(4271fb76-92b2-4edf-86ea-d002aab902c9).html.
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Transepithelial migration (TEpM) of leucocytes during the inflammatory process requires engagement with receptors expressed on the basolateral surface of the epithelium. One such receptor is Coxsackie and Adenovirus Receptor (CAR) which binds to Junction Adhesion Molecule - L (JAM-L) on leucocytes during TEpM. This study reports the first evidence that TEpM of leucocyte cells requires, and is controlled by, phosphorylation of the cytoplasmic tail of CAR. The in vitro data shows that these leucocyte cells can adhere to an epithelial layer but where the cytoplasmic tail of CAR is prevented from undergoing phosphorylation the leucocytes are unable to transmigrate. Furthermore it shows that this CAR phosphorylation step is driven by TNF α signalling via a TNFR1-PI3K-PKCδ dependent signalling pathway. The work demonstrates that THP-1 cells can secrete TNF α thereby activating the CAR phosphorylation pathway leading to TEpM without addition of exogenous TNF α but importantly where TNF α is added this process is augmented suggesting a role for CAR in inflammatory conditions. Mouse models also confirm that CAR phosphorylation in response to inflammatory stimuli occur in vivo. Both acute (a 24 hour inhaled TNF α challenge) and chronic (a 34 day ovalbumin challenge) inflammatory conditions are studied. Confocal microscopy techniques are used to show that the cytoplasmic tail of CAR is phosphorylated. Specifically this is seen at the cell membrane of epithelial cells of bronchioles with associated inflammatory cells in the interstitium. Taken together these data describe a novel method for the control of TEpM by transmigrating leucocytes that can also be heightened by the presence of proinflammatory cytokines during inflammation. This provides a novel target for controlling inflammation at the epithelium, a key component of the pathogenesis of many diseases including asthma.
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Mastroeni, Pietro. "Immunity to Salmonella, role of : antibodies, T-cells, TNF#alpha# and INF#gamma# in resistance to infection and in delayed type hypersensitivity in mice immunised with aroA S. typhimurium SL3261 live attenuated vaccine strain." Thesis, University of Cambridge, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.320407.
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Montgomery, Travis Dale. "Re(orient)ing America : the imagined Middle East in the early works of Edgar Allan Poe /." Full text available from ProQuest UM Digital Dissertations, 2009. http://0-proquest.umi.com.umiss.lib.olemiss.edu/pqdweb?index=0&did=1800249041&SrchMode=1&sid=2&Fmt=2&VInst=PROD&VType=PQD&RQT=309&VName=PQD&TS=1269372830&clientId=22256.
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Thesis (Ph.D.)--University of Mississippi, 2009.Typescript. Vita. "April 2009." Dissertation director: Dr. Benjamin F. Fisher Includes bibliographical references (leaves 188-207). Also available online via ProQuest to authorized users.
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Shelton, Heath W. "The Effects of Two Novel Anti-Inflammatory Compounds On Prepulse Inhibition and Neural Microglia Cell Activation in a Rodent Model of Schizophrenia." Digital Commons @ East Tennessee State University, 2019. https://dc.etsu.edu/etd/3537.
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Recent studies have shown elevated neuroinflammation in a large subset of individuals diagnosed with schizophrenia. A pro-inflammatory cytokine, tumor necrosis factor-alpha (TNFα), has been directly linked to this neuroinflammation. This study examined the effects of two TNFα modulators (PD2024 and PD340) produced by our collaborators at P2D Bioscience, Inc., to alleviate auditory sensorimotor gating deficits and reduce microglial cell activation present in the polyinosinic:polycytidylic (Poly I:C) rodent model of schizophrenia. Auditory sensorimotor gating was assessed using prepulse inhibition and microglial activation was examined and quantified using immunohistochemistry and confocal microscopy, respectively. Both PD2024 and PD340 alleviated auditory sensorimotor gating deficits and reduced microglia activation and thereby demonstrated the ability to treat both the behavioral and neuroinflammatory aspects of the disorder. These results are significant and suggest that neural TNFα is a potential pharmacological target for the treatment of schizophrenia.
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Gauby, Sidney F. "The effect of fasting upon the development of servant leaders at Saint Joseph United Methodist Church, Fort Wayne, Indiana." 24-page ProQuest preview, 2007. http://proquest.umi.com/pqdweb?index=0&did=1328051311&SrchMode=1&sid=7&Fmt=14&VInst=PROD&VType=PQD&RQT=309&VName=PQD&TS=1220031263&clientId=10355.
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Stepp, Todd Alan. "Scriptural and rational piety." 24-page ProQuest preview, 2007. http://proquest.umi.com/pqdweb?index=0&did=1375508181&SrchMode=1&sid=2&Fmt=14&VInst=PROD&VType=PQD&RQT=309&VName=PQD&TS=1220040920&clientId=10355.
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Cavalcante, Roselli Aparecida. "Funda??o de Vila Maria com a presen?a Chiquitana : os povoadores da fronteira oeste da Capitania de Mato Grosso (1778-1827)." Pontif?cia Universidade Cat?lica do Rio Grande do Sul, 2015. http://tede2.pucrs.br/tede2/handle/tede/5921.
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This study aims to analyze the foundation of Vila Maria of Paraguay, current C?ceres - MT, with the presence of Chiquitano Indians from Chiquitano Jesuit missions on the eastern side of the Spanish colony in America, now Bolivia, probably, Santa Ana, Santa Rosa, St. John and the Holy Heart of Jesus de Chiquitos. Seeks to highlight the Portuguese settlement strategies with these Indians in the period they were created and consolidated the Portuguese-Spanish border in western Mato Grosso Captaincy with the lands of the Spanish colony in South America especially in Vila Maria of Paraguay. The time frame covers the foundation of Vila Maria from 1778 to 1827, during the view of Hercules Florence to that village. Vila Maria becomes important strategic point between the villages of Cuiab? and Vila Bela of the Trinity in the Guapor? valley and the lack of "white people" to populate it, the Chiquitano and Indians from other ethnic groups, served the Lusitanian project of settlement, occupation and consolidation of their land in this part of the colony. The royal instructions and the urbanization project of the Portuguese crown and the Marquis of Pombal will be the hallmarks of this settlement.
Este estudo tem como objetivo analisar a funda??o de Vila Maria do Paraguai, atual C?ceres ? MT, com a presen?a de ?ndios Chiquitano provenientes de miss?es jesu?ticas Chiquitanas do lado oriental da col?nia espanhola na Am?rica, atual Bol?via, provavelmente de, Santa Ana, Santa Rosa, S?o Jo?o e do Santo Cora??o de Jesus de Chiquitos. Procura evidenciar as estrat?gias de povoamento dos portugueses com esses ?ndios no per?odo em que se criavam e consolidavam a fronteira luso-espanhola no oeste da Capitania de Mato Grosso com as terras da col?nia espanhola na Am?rica do sul, especialmente em Vila Maria do Paraguai. O recorte temporal abrange a funda??o de Vila Maria 1778 a 1827, ocasi?o da vista de Hercules de Florence a essa Vila. Vila Maria torna-se importante ponto estrat?gico entre as Vilas de Cuiab? e Vila Bela da Sant?ssima Trindade no vale do Guapor? e na falta de ?gente branca? para povo?-la, os Chiquitano, bem como ?ndios de outras etnias, serviram ao projeto lusitano de povoamento, ocupa??o e consolida??o de suas terras nesta parte da col?nia. As instru??es r?gias e o projeto de urbaniza??o da coroa portuguesa e do Marqu?s de Pombal ser?o os balizadores deste povoamento.
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Söderlund, Erik. "Transnational Corporations and Human Rights : Assessing the position of TNCs within international human rights law, and the appropriateness of an international treaty on business and human rights." Thesis, Uppsala universitet, Juridiska institutionen, 2018. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-363144.
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Transnational corporations are playing an important role in the global economy of today. Many of these corporations have great economic resources and have the possibility of contributing to the development of societies in developing states. At the same time, in their search for profit, the activities of TNCs have proven fatal to some of the individuals employed by them, or otherwise in contact with their activities. Within the international legal framework, corporations are not traditionally treated as subjects and if a TNC allocates its production to a state with lax human rights protection, no binding international standards exist to regulate the conduct of the corporation. In my thesis I will assess the position of TNCs under the present core human rights instruments and soft law initiatives. I will also analyze a draft treaty text produced by the Intergovernmental Working Group on Business and Human Rights, released in July 2018, to reach a conclusion on whether such an instrument would affect the international legal status of TNCs and provide a more robust protection of international human rights.
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Griffith, Luke. ""Green Cheese" and "the Moon": Jimmy Carter, Ronald Reagan, and the Euromissiles." Ohio University / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1542113024275818.
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Papen, Uta. "Tour guides, textbooks and TV's : uses and meanings of literacy in Namibia." Thesis, King's College London (University of London), 2002. https://kclpure.kcl.ac.uk/portal/en/theses/tour-guides-textbooks-and-tvs--uses-and-meanings-of-literacy-in-namibia(fade0753-f924-4bbe-848b-5902b7fae59c).html.
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Myles, Benita J. "A study of methamphetamine-induced hyperthermia in the rat: development of tolerance, effects of ambient temperature and dose escalation, and the critical role of core temperature in neurotoxicity /." Full text available from ProQuest UM Digital Dissertations, 2005. http://0-proquest.umi.com.umiss.lib.olemiss.edu/pqdweb?vinst=PROD&clientid=22256&dbid=21651&jsenabled=1&vname=PQD&date=ALL&querysyntax=PQ&sq=a+study+of+methamphetamine+induced++hyperthermia++in+the+rat&sortby=REVERSE_CHRON&searchinterface=1&la=any&ts=1184868959&vtype=PQD&moreoptstate=CLOSED&rqt=305&mtype=all&sck=0&TS=1184868984&clientId=22256.
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Casselman, James Edwin. "A study into the non-invasive manipulation of skin blood flow utilizing electrotherapy techniques integrating Eastern and Western research to create an engaging, open-ended classroom experiences." Thesis, 2013. http://hdl.handle.net/2152/23988.
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The research to date, of transcutaneous electric nerve stimulation on cutaneous blood flow, is equivocal. The purpose of this report is to review the TENS body of knowledge, in particular synthesizing the literature on acupuncture stimulation of cutaneous blood flow with the two fold goal of creating a protocol to increase skin blood flow through the exogenous application of electrical stimulation, as well as creating an engaging engineering challenge for high school anatomy and physiology students. The hypothesis developed was TENS stimulation with electrode placement on specific acupuncture points would influence cutaneous blood flow as measured using laser Doppler flowmetry.
The findings of this project did not support the hypothesis of TENS or Interferential electrical stimulation, in combination with acupuncture points or not, influencing skin blood flow. Perhaps this is due to the physiological differences between glabrous and non-glabrous skin and the different electrical resistances of each dermal layer, nerve stimulation, age and gender of subject or some combination thereof. These equivocal findings may also be the result of inconsistencies in testing protocols, such as subject preconditioning or not, subject’s position during administration of stimulation, electrode size and placement to name a few.
Ultimately, this report provides a summary of the research to date, as well as outlining how this research could be adapted to supply engaging bio engineering challenges in the classroom including challenges to develop a model for delivering current to muscle; develop a model for skin blood flow management to name a few.text
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Paschalinou, Eleni [Verfasser]. "Nachweis von Punktmutationen im TNF-α- [TNF-alpha-] und IFN-γ-Promotior [INF-gamma-Promotor] bei Patienten nach allogener Stammzelltransplantation oder Knochenmarktransplantation / vorgelegt von Eleni Paschalinou." 2009. http://d-nb.info/992033284/34.
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"Ação do fator de necrose tumoral alfa (TNF-'alfa') no hipotalamo : efeitos sobre expressão proteica, ingestão alimentar e consumo de 'O IND.2'/produção de 'CO IND.2'." Tese, Biblioteca Digital da Unicamp, 2006. http://libdigi.unicamp.br/document/?code=vtls000396609.
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Farshadmanesh, Farshad. "Three dimensional eye-head coordination after unilateral inactivation of the interstitial nucleus of Cajal (INC) in the primate /." 2006. http://proquest.umi.com/pqdweb?index=0&did=1240690631&SrchMode=1&sid=2&Fmt=2&VInst=PROD&VType=PQD&RQT=309&VName=PQD&TS=1195653182&clientId=5220.
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Thesis (M.Sc.)--York University, 2006. Graduate Programme in Biology.Typescript. Includes bibliographical references (leaves 101-125). Also available on the Internet. MODE OF ACCESS via web browser by entering the following URL: http://proquest.umi.com/pqdweb?index=0&did=1240690631&SrchMode=1&sid=2&Fmt=2&VInst=PROD&VType=PQD&RQT=309&VName=PQD&TS=1195653182&clientId=5220
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Dufour, Florent. "Étude de la fonction anti-apoptotique de la sous-unité R1 de la ribonucléotide réductase des virus de l’herpès simplex." Thèse, 2010. http://hdl.handle.net/1866/4653.
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L’élimination des cellules infectées par apoptose constitue un mécanisme de défense antivirale. Les virus de l’herpès simplex (HSV) de type 1 et 2 encodent des facteurs qui inhibent l’apoptose induite par la réponse antivirale. La sous-unité R1 de la ribonucléotide réductase d’HSV-2 (ICP10) possède une fonction anti-apoptotique qui protège les cellules épithéliales de l’apoptose induite par les récepteurs de mort en agissant en amont ou au niveau de l’activation de la procaspase-8. Puisqu’une infection avec un mutant HSV-1 déficient pour la R1 diminue la résistance des cellules infectées vis à vis du TNFα, il a été suggéré que la R1 d’HSV-1 (ICP6) pourrait posséder une fonction anti-apoptotique. Le but principal de cette thèse est d’étudier le mécanisme et le potentiel de la fonction anti-apoptotique de la R1 d’HSV-1 et de la R1 d'HSV-2.
Dans une première étude, nous avons investigué le mécanisme de la fonction anti-apoptotique de la R1 d’HSV en utilisant le TNFα et le FasL, deux inducteurs des récepteurs de mort impliqués dans la réponse immune anti-HSV. Cette étude a permis d’obtenir trois principaux résultats concernant la fonction anti-apoptotique de la R1 d’HSV. Premièrement, la R1 d’HSV-1 inhibe l’apoptose induite par le TNFα et par le FasL aussi efficacement que la R1 d’HSV-2. Deuxièmement, la R1 d’HSV-1 est essentielle à l’inhibition de l’apoptose induite par le FasL. Troisièmement, la R1 d’HSV interagit constitutivement avec la procaspase-8 d’une manière qui inhibe la dimérisation et donc l’activation de la caspase-8. Ces résultats suggèrent qu’en plus d’inhiber l’apoptose induite par les récepteurs de mort la R1 d’HSV peut prévenir l’activation de la caspase-8 induite par d’autres stimuli pro-apoptotiques. Les ARN double-brins (ARNdb) constituant un intermédiaire de la transcription du génome des HSV et activant l’apoptose par une voie dépendante de la caspase-8, nous avons testé dans une seconde étude l’impact de la R1 d’HSV sur l’apoptose induite par l’acide polyriboinosinique : polyribocytidylique (poly(I:C)), un analogue synthétique des ARNdb. Ces travaux ont montré qu’une infection avec les HSV protège les cellules épithéliales de l’apoptose induite par le poly(I:C). La R1 d’HSV-1 joue un rôle majeur dans l’inhibition de l’activation de la caspase-8 induite par le poly(I:C). La R1 d’HSV interagit non seulement avec la procaspase-8 mais aussi avec RIP1 (receptor interacting protein 1). En interagissant avec RIP1, la R1 d’HSV-2 inhibe l’interaction entre RIP1 et TRIF (Toll/interleukine-1 receptor-domain-containing adapter-inducing interferon β), l’adaptateur du Toll-like receptor 3 qui est un détecteur d’ARNdb , laquelle est essentielle pour signaler l’apoptose induite par le poly(I:C) extracellulaire et la surexpression de TRIF.
Ces travaux démontrent la capacité de la R1 d’HSV à inhiber l’apoptose induite par divers stimuli et ils ont permis de déterminer le mécanisme de l’activité anti-apoptotique de la R1 d’HSV. Très tôt durant l’infection, cFLIP, un inhibiteur cellulaire de la caspase-8, est dégradé alors que la R1 d’HSV s’accumule de manière concomitante. En interagissant avec la procapsase-8 et RIP1, la R1 d’HSV se comporte comme un inhibiteur viral de l’activation de la procaspase-8 inhibant l’apoptose induite par les récepteurs de mort et les détecteurs aux ARNdb.Elimination of infected cells by apoptosis constitutes an ancestral mechanism of host defense against viral infection. Herpes simplex viruses (HSVs) encode several viral factors to counteract the apoptotic antiviral response. Among them, the R1 subunit of HSV type-2 ribonucleotide reductase (HSV-2 R1, also named ICP10), protects cells by interrupting death receptor-mediated signaling at, or upstream of, caspase-8 activation. Since protection against tumor necrosis factor alpha (TNFα)-induced apoptosis is decreased un cells infected with an HSV type-1 R1 null mutant, it has been proposed that HSV-1 R1 (ICP6) could also possess an antiapoptotic activity. The fundamental goal of this thesis is to better understand the mechanism and the potential of the HSV R1s antiapoptotic activity. In a first study, we investigated the mechanism of the antiapoptotic activity of HSV R1s by using TNFα and Fas ligand (FasL), two death-receptor inducers involved in anti-HSVs immune response. From this work, we report three main findings on the antiapoptotic activity of HSV R1s. First, HSV-1 R1 like HSV-2 R1 has the ability to protect cells against TNFα- and FasL-induced apoptosis. Second, HSV-1 R1 contributes in protecting infected cells against FasL. Third, HSV R1s and procaspase-8 interact in a way that inhibits the dimerization/activation of caspase-8. These results suggest that in addition to counteracting death receptor-induced apoptosis, HSV R1s could inhibit apoptosis induced by other signals that trigger caspase-8 activation during HSV infection. Double-stranded RNA (dsRNA) are viral intermediates notably produced by HSVs and have been shown to induce apoptosis via caspase-8 activation. We tested in a second study whether HSV R1s have the ability to counteract apoptosis triggered by polyriboinosinic : polyribocytidylic acid (poly(I:C)), a synthetic analog of dsRNA that triggers caspase-8 activation. We showed that HSVs infection protect epithelial cells from apoptosis induced by poly(I:C). We established that HSV-1 R1 is essential for the protection of HSV-1-infected cells against poly(I:C)-induced caspase-8 activation. HSV R1s interact not only with procaspase-8 but also with the receptor interacting protein 1 (RIP1). The interaction between RIP1 and HSV-2 R1 inhibits the binding of RIP1 to the Toll/interleukine-1 receptor-domain-containing adapter-inducing interferon β (TRIF), the adaptor of Toll-like receptor 3 that is an extracellular dsRNA sensor, which is required to activate caspase-8 following extracellular poly(I:C) stimulation and TRIF overexpression. Thus, HSV R1s have the ability to inhibit poly(I:C)-induced apoptosis at several levels by preventing caspase-8 dimerization/activation and TRIF RIP1 interaction. This work sheds light on the ability of HSV R1s to manipulate apoptosis. Early during the lytic cycle, protein levels of the cellular inhibitors of caspase-8 as cFLIP drop but HSV R1s accumulate concomitantly and act as a viral inhibitor of apoptosis by binding to procaspase-8 and RIP1 in a way that impairs caspase-8 activation by death-receptors and dsRNA detectors stimulation.