151 |
Effects of enhanced glutathione biosynthesis on oxidative stress-mediated hepatocellular injury and gene expression in mice /Shi, Shengli, January 2004 (has links)
Thesis (Ph. D.)--University of Washington, 2004. / Vita. Includes bibliographical references (leaves 116-130).
|
152 |
Rheumatoid arthritis and major depression : effects of antidepressant therapy on markers of inflammation /Johnston, Sandra K. January 2004 (has links)
Thesis (Ph. D.)--University of Washington, 2004. / Vita. Includes bibliographical references (leaves 121-138).
|
153 |
Effect of microbial lipopolysaccharide and inflammatory cytokines on IL-6 induction by human gingival fibroblasts from healthy and periodontally diseased tissueKent, Leigh Whitfield. January 1997 (has links)
Thesis (Ph. D.)--University of Alabama at Birmingham, School of Joint Health Sciences, 1997. / eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references.
|
154 |
Mechanisms underlying the hyper-induction of tumour necrosis factor alpha (TNF-? by avian influenza virus in human macrophages /Tam, Ho-man, Alex. January 2008 (has links)
Thesis (M. Phil.)--University of Hong Kong, 2009. / Includes bibliographical references (leaves 78-89) Also available online.
|
155 |
Apoptosis-related genetic polymorphisms in sarcoidosis /Wasfi, Yasmine S. January 2005 (has links)
Thesis (Ph.D. in Clinical Sciences) -- University of Colorado at Denver and Health Sciences Center, 2005. / Typescript. Includes bibliographical references (leaves 88-108).
|
156 |
Effector function of pathogenic CD4 TH1 T cells in autoimmune diabetes /Cantor, Joseph M. January 2005 (has links)
Thesis (Ph.D. in Immunology) -- University of Colorado, 2005. / Typescript. Includes bibliographical references (leaves 180-202). Free to UCDHSC affiliates. Online version available via ProQuest Digital Dissertations;
|
157 |
Genetic susceptibility in Alzheimer's Disease and the role of lipid metabolismMiller, Katherine. January 2007 (has links)
Thesis (Ph. D.)--Case Western Reserve University, 2006. / [School of Medicine] Department of Epidemiology and Biostatistics. Includes bibliographical references. Available online via OhioLINK's ETD Center.
|
158 |
Effect of microbial lipopolysaccharide and inflammatory cytokines on IL-6 induction by human gingival fibroblasts from healthy and periodontally diseased tissueKent, Leigh Whitfield. January 1997 (has links)
Thesis (Ph. D.)--University of Alabama at Birmingham, School of Joint Health Sciences, 1997. / Includes bibliographical references.
|
159 |
Avaliação da citotoxicidade de materiais obturadores de canais radiculares : influência na liberação de fator de necrose tumoral alfa, interferon-y e óxido nítrico em cultura de células murinas /Rivas Gutiérrez, José Carlos. January 2006 (has links)
Orientador: Iracilda Zeppone Carlos / Banca: Idomeo Bonetti Filho / Banca: Fábio Luiz Camargo Villela Berbert / Banca: Ivaldo Gomes de Moraes / Banca: Abílio Albuquerque Maranhão de Moura / Resumo: Os macrófagos constituem uma população celular do sistema imune. Estas células podem ser ativadas por uma variedade de estímulos e suas principais funções incluem a fagocitose de partículas estranhas, apresentação de antígenos, produção de citocinas e compostos intermediários do nitrogênio (NO) e do oxigênio (H202). Os cimentos endodônticos são capazes de promover uma estimulação do sistema imune. Neste estudo, foram analisados os níveis de quantificação das citocinas, além do mediador óxido nítrico, como uma medida de estimulação de macrófagos peritoneais de camundongos. Através de análise estatística dos dados, foram observados os níveis de citotoxicidade dos macrófagos de camundongos estimulados pelos diferentes cimentos endodônticos, meio RPMI-1640 (grupo controle -) e LPS (grupo controle +). Os diferentes cimentos testados apresentaram concentrações com diferentes citotoxicidades: Sealapex 35ug/ml, Polímero de Mamona 8,75 ug/ml, do Epiphany 17,5 ug/ml, do Epiphany + Primer 17,5 ug/ml, do Primer 35 ug/ml, do EndoRez 17,5 ug/ml e do AH Plus 70 ug/ml. Após a adequação das concentrações viáveis dos cimentos testados conclui-se que o material que mais estimulou a liberação de NO foi Primer, seguido do Endorez, AH Plus, Ephiphany, Sealapex, Epiphany + Primer. O Polímero de Mamona foi o que estimulou a uma menor produção de NO. Em relação à produção de TNF-alfa o material que estimulou maior produção foi o Primer, seguido de Epiphany, AH Plus, Epiphany + Primer, Sealapex e Polímero de Mamona. O EndoRez não foi capaz de estimular a produção de TNF-alfa. Nenhum dos cimentos testados induziu à liberação de IFN-y, sugerindo que outro mediadores tais como IL-1 e IL-12 possam estar envolvidos na liberação de NO observada no presente estudo. / Abstract: It was evaluated the citotoxicity of the sealers, Sealapex, Polímero de Mamona, Epiphany, EndoRez and AH Plus in relation to the release of Nitric Oxide, Tumor Necrotic Factor-Alpha and Interferon Gamma in murine cells culture. After the ideal concentration was found, according to MTT test, it was conduded that the sealers with higher release were Polímero de Mamona, EndoRez, Epiphany + Primer, Epiphany, Primer do Epiphany = Sealapex and AH Plus. All sealers reached lower levels of citotoxicity than control. / Doutor
|
160 |
Ginsenosides enhance the cytotoxicity of tumor necrosis factor-α in human MDA-MB 231 and MCF-7 breast cancer cells in a caspase-dependent mannerHantak, Alison Marie 01 December 2009 (has links)
Ginsenosides (GF) are a major bioactive constituent of ginseng and have been shown to elicit a multitude of actions ranging from the improvement of synaptic plasticity to the improved uptake of glucose into a cell. Furthermore, ginsenosides and their metabolites have been shown to be potent anti-cancer agents in multiple experimental cancer models. The aim of this study was to investigate the potential influence of GF derived from American ginseng root (Panax quinquefolius), and a ginsenoside metabolite Rh2, on tumor necrosis factor-α (TNF-α) cytotoxicity in MDA-MB 231 and MCF-7 human breast cancer cells. In combination, these agents significantly increased cell death in both cell lines. Together, ginsenosides and TNF-α induced a robust increase of the pre-G0/G1 and accompanying decrease in S phase cell populations in breast cancer cells. This cell death was the result of the induction of apoptosis, as determined by annexin-V/7-AAD and Hoechst staining. Furthermore, the mechanism of ginsenoside and TNF-α induced apoptosis is caspase-dependent, as determined by the pan-caspase inhibitor Z-VAD-FMK, with caspase-8, but not caspase-9, serving as initiator caspase in both cell lines. Additionally, ginsenoside treatment significantly XIAP expression in both MDA-MB 231 and MCF-7 cells, in the absence of TNF-α. In addition to enhancing apoptosis, it was also hypothesized that ginsenosides would abrogate pro-survival pathways induced by TNF-α. However, ginsenosides failed to block TNF-α effects on NFκB expression in either cell line. JNK which, when activated by TNF-α in MDA-MB 231 cells has a pro-survival function, was reduced by ginsenosides. However, JNK inhibition had no effect on cell death, suggesting that it does not play an integral role in the mechanism of action. In MCF-7 cells, JNK has been shown to have a pro-apoptotic function. Treatment with ginsenosides had no effect on TNF-α activation of JNK, but inhibition of JNK significantly reduced cell death in combined ginsenoside and TNF-α treated cells. To conclude, combined treatment with ginsenosides and TNF-α can enhance cell death in the sensitive MCF-7 cell line, and induce cell death in the insensitive MDA-MB 231 cell line in a caspase-dependent manner that is aided by the reduction of XIAP by ginsenosides.
|
Page generated in 0.0742 seconds