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Toll-like Receptor 2-dependent Inhibition of Interferon gamma Signaling by <em>Mycobacterium tuberculosis</em>Pennini, Meghan E. 13 July 2006 (has links)
No description available.
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Regulation of Interferon Alpha Beta Induction and Dendritic Cell Function by CpG OligodeoxynucleotidesGray, Reginald Courtney January 2008 (has links)
No description available.
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Regulation of STAT6, STAT3 and STAT1 by the Cytoplasmic Tail of Polycystin-1, the Protein Affected in Polycystic Kidney DiseaseShivakumar, Vasanth 01 May 2007 (has links)
No description available.
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Suppressor of Cytokine Signaling (SOCS) 1 & 3 Expression in HSV-1- Infected and Interferon-γ-treated Neuro-2A CellsJones, Melinda 18 September 2012 (has links)
No description available.
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Inflammatory and oxidative mechanisms in endothelial cell activation and dysfunctionHuang, Hong 29 September 2004 (has links)
No description available.
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Detailed analysis of Japanese patients with adenosine deaminase 2 deficiency reveals characteristic elevation of type II interferon signature and STAT1 hyperactivation / 日本人ADA2欠損症患者における詳細な発現解析によりII型インターフェロンシグネチャーの特異的上昇とSTAT1過剰活性化が明らかとなったNihira, Hiroshi 23 March 2022 (has links)
京都大学 / 新制・課程博士 / 博士(医学) / 甲第23796号 / 医博第4842号 / 新制||医||1058(附属図書館) / 京都大学大学院医学研究科医学専攻 / (主査)教授 森信 暁雄, 教授 椛島 健治, 教授 杉田 昌彦 / 学位規則第4条第1項該当 / Doctor of Medical Science / Kyoto University / DFAM
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Distinct Inflammatory Biomarker Patterns in COVID-19 associated MIS-C suggest Overlap between Kawasaki Disease and Macrophage Activation SyndromeRodriguez-Smith, Jackeline J. 29 September 2021 (has links)
No description available.
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Role of Integrated Stress Response pathway in fish cells during VHSV Ia infectionShetty, Adarsh G. 15 September 2022 (has links)
No description available.
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Immunoteratological Studies of Diabetic Embryopathy Using Gene Expression AnalysisPunareewattana, Korawuth 23 April 2003 (has links)
Diabetic embryopathy is a major complication of pregnant women with type I diabetes. Immune defects in the pathogenesis of diabetic embryopathy have been suggested. We hypothesized that activated immune system can counteract diabetic effect and result in prevention of diabetic embryopathy. Diabetes was induced in pregnant ICR mice by streptozocin injection. Three different techniques of maternal immune stimulation, complete Freund's adjuvant (CFA), granulocyte-macrophage colony-stimulating factor (GM-CSF), or interferon-gamma (IFN-g), were used to stimulate the maternal immune system. Approximately 50% of fetuses from hyperglycemic (>27 mM/L) dams were malformed, with neural tube defects predominating. Maternal immune stimulation during the time of normoglycemia, i.e. prior to onset of hyperglycemia, was necessary for reducing teratogenic effects associated with hyperglycemia. The immune-stimulated diabetic mice then produced significantly lower numbers of malformed fetuses: CFA 20.9%, GM-CSF 23.3%, IFN-g 13.9%. A gene microarray was then used to examine a selected panel of placental and splenic genes. We hypothesized that a shared profile of placental or splenic gene expression changes may correlate to the reduced birth defect outcome induced by the different immune stimulation procedures. Diabetes did not cause significant changes in placenta or spleen gene expression profile. In placenta, CFA and GM-CSF changed placental gene expression relative to control or diabetes, but differentially affected such genes relative to each other; further, IFN-g did not affect gene expression relative to control or diabetes. Thus no common pattern of improved placental cytokine, cell-cycle, apoptotic, transcription factor, or other gene expression was identified in the immune-stimulated mice. In spleen, all 3 immune activators produced a common altered gene expression profile. The overall gene expression profile after all immune stimulation procedures suggested increased splenocyte activity and cytokine production. The cytokine GM-CSF, in particular, was up-regulated in splenic leukocytes. This cytokine has previously been associated with reduced cleft palate in urethane-exposed mice after immune stimulation, and with reduced limb malformations in cyclophosphamide-treated mice after intra-uterine administration. In contrast, the TGF-beta3 gene was down-regulated in immune-stimulated diabetic mice. This gene was up-regulated in urethane-exposed mice, an effect that may be associated with reduced cleft palate. Thus unlike urethane, TGF-beta3 gene expression did not show a relationship with reduced diabetes-induced birth defects. Taken together, these data prove our hypotheses and suggest that mechanistically diverse forms of immune activation result in protection against diabetes-related teratogenesis, but only if given prior to onset of hyperglycemia. Such immune stimulation in mice may act through systemic immune organs, i.e. spleen, over-riding adverse effects of diabetes on development. / Ph. D.
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Bovine Coccidiosis: Dynamics of infection in grazing cattle and the potential role of stress and immunityLucas, Aaron Scott 08 September 2011 (has links)
Eimerian parasites infect cattle worldwide. Information on the infection dynamics of these parasites is lacking in the central Appalachian region of the United States. Studies aimed at characterizing the seasonal dynamics of eimerian parasites in this region were carried out in order to assess the impact of these organisms in grazing systems. In these studies the prevalence of Eimeria spp. infection was highest in calves less than one year of age and subsequently decreased to stable levels in older animals. Although E. bovis was the most common species identified in calves, heifers and cows, mixed species infections dominated. Additional studies were carried out to investigate the effect of stress on Eimeria spp. infection in beef calves. Lower stress, two-stage, weaning methods had no effect on Eimeria spp. infection dynamics in beef calves. These findings must be interpreted in light of the fact that calves used in this study were not managed in a way typical of many calves in the U.S.A. The fact that they were only transported short distances, never commingled, or exposed to a livestock market may explain why a rise in post weaning FOC was not observed. A model of stress- induced coccidiosis was developed using dexamethasone and E. bovis challenge. In this model, an oral challenge of at least 500,000 sporulated E. bovis oocysts in addition to dexamethasone injection at 7 days post challenge increased subsequent FOC. Further investigation of the immune response to E. bovis challenge during times of stress indicates that stress-induced suppression of cell mediated immunity and E. bovis challenge are required to increase subsequent oocyst shedding. These findings may represent the mechanism associated with stress-induced outbreaks of coccidiosis reported to occur in beef cattle in the United States. / Ph. D.
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