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The Global ETD Search service is a free service for researchers
to find electronic theses and dissertations. This service is
provided by the
Networked Digital Library of Theses and Dissertations.
Our metadata is collected from universities around the world. If you manage a university/consortium/country archive and want to be added, details can be found on the NDLTD website.
Search results
Showing 1 to 10 of 10 (0.064 seconds)| 1 |
The role of cannabinoids and cannabinoid receptors in enteric neuronal survivalLi, Yan, January 1900 (has links)
Thesis (Ph.D.)--Virginia Commonwealth University, 2009. / Prepared for: Dept. of Physiology. Title from title-page of electronic thesis. Bibliography: leaves 145-[160].
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Fatty acid amide hydrolase - a target for anti-inflammatory therapies? /Holt, Sandra, Unknown Date (has links)
Diss. (sammanfattning) Umeå : Umeå universitet, 2005. / Härtill 4 uppsatser.
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Regulation of phospholipase A₂ in astrocytes : role in oxidative and inflammatory responses /Xu, Jianfeng, January 2002 (has links)
Thesis (Ph. D.)--University of Missouri--Columbia, 2002. / "May 2002." Typescript. Includes bibliographical references. Also available on the Internet.
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Regulation of 5-oxo-ETE synthesis by pyridine nucleotides in aging neutrophilsGraham, François. January 2008 (has links)
Neutrophils (polymorphonuclear leukocytes) are short lived granulocytes that playa primordial role in host innate defense against invading pathogens. Freshly isolated neutrophils spontaneously undergo apoptosis when cultured, which is associated with oxidative stress. We found that there is a dramatic shift in the metabolism of the 5-lipoxygenase product 5-hydroxy-6,8,11,14-eicosatetraenoic acid (5-HETE) from its biologically inactive o-oxidation product in freshly isolated neutrophils to the potent granulocyte chemoattractant 5-oxo-6,8,11,14-eicosatetraenoic acid (5-oxo-ETE) in neutrophils cultured for 24 h. o-oxidation of the chemoattractant leukotriene B4 (LTB4) was also reduced in aging neutrophils incubated with arachidonic acid, resulting in higher levels of LTB4. The reduced o-oxidation activity appeared to be due to a decrease in active LTB4 20-hydroxylase. In contrast, the increased 5-oxo-ETE formation was not associated with an increase in the amount of active 5-hydroxyeicosanoid dehydrogenase, which is required for its formation, but rather with a dramatic increase in its cofactor NADP +. NAD+ levels also increased, but NADPH levels remained unchanged after 24 h. There was also evidence for increased oxidative stress (high GSSG/GSH) in aging neutrophils. The changes in 5-HETE metabolism and pyridine nucleotides in cultured neutrophils could be inhibited by neutrophil survival factors and antioxidants. These results suggest that in severe inflammation, aging neutrophils that have evaded rapid uptake by macrophages may produce increased amounts of the chemoattractants 5-oxo-ETE and LTB4, resulting in delayed resolution of inflammation. Similarly, we found that the NADPH oxidase activator PMA caused a very rapid and dramatic increase in NADP + levels in both freshly isolated and cultured neutrophils, accompanied by a rapid increase in 5-oxo-ETE synthesis and reduced o-oxidation activity. Surprisingly, this was not accompanied by a corresponding decline in NADPH levels, which instead initially increased, but rather by a precipitous reduction in NAD+, which mirrored the increase in NADP+. These results suggest that the phosphorylation of NAD+ by NAD kinase may be very important for providing both NADP+ for 5-oxo-ETE synthesis and NADPH for the respiratory burst.
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Signaling pathways involved in regulation of glucose-6-phosphate dehydrogenase (G6PD) by arachidonic acidTalukdar, Indrani. January 2006 (has links)
Thesis (Ph. D.)--West Virginia University, 2006. / Title from document title page. Document formatted into pages; contains viii, 123 p. : ill. (some col.). Includes abstract. Includes bibliographical references.
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Regulation of 5-oxo-ETE synthesis by pyridine nucleotides in aging neutrophilsGraham, François. January 2008 (has links)
No description available.
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Regulation of phospholipase A₂ in astrocytes role in oxidative and inflammatory responses /Xu, Jianfeng, January 2002 (has links)
Thesis (Ph. D.)--University of Missouri--Columbia, 2002. / Typescript. Includes bibliographical references. Also available on the Internet.
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Uncovering the mechanisms of trans-arachidonic acids : function and implications for cerebral ischemia and beyondKooli, Amna. January 2008 (has links)
Cerebral ischemia is the principal cause of morbidity and mortality worldwide. In addition to neuronal loss associated with hypoxic-ischemic damage, cerebral ischemia is characterized by a neuromicrovascular injury. Nitrative stress and lipid peroxidation increase in hypoxic-ischemic damages and play an essential role in neuromicrovascular injury leading to cerebral ischemia. We hypothesized that newly described lipid peroxidation products, termed trans-arachidonic acids (TAA), could be implicated in the pathogenesis of hypoxia-ischemia by affecting the cerebral vasomotricity and microvascular integrity. / The effects of TAA on neuromicrovascular tone were tested ex vivo by monitoring the changes in vascular diameter of rat cerebral pial microvessels. Four isomers of TAA, namely 5 E-AA, 8E-AA, IIE-AA and 14 E-AA induced an endothelium-dependent vasorelaxation. Possible mechanisms involved in TAA-induced vasorelaxation were thoroughly investigated. Collectively, data enclosed revealed that TAA induce cerebral vasorelaxation through the interactive activation of BKCa channels with heme oxygenase-2. This interaction leads to generation of carbon monoxide which in turn activates soluble guanylate cyclase and triggers vasorelaxation. / Chronic effects of TAA on microvascular integrity were examined by generating a unilateral hypoxic-ischemic (HI) model of cerebral ischemia on newborn rat pups. Our HI model showed microvascular degeneration as early as 24h post-HI, preceded by an increase in cerebral TAA levels. HI-induced microvascular lesions were dependent on nitric oxide synthase activation and ensued TAA formation. Although the molecular mechanisms leading to TAA-induced microvascular degeneration were, in part uncovered for the retina, the primary site of action of TAA remains unknown. We demonstrated that TAA binds and activates GPR40 receptor, a newly described free fatty acid receptor. Importantly, GPR40 receptor knock-out prevents TAA-induced reduction in cerebral microvascular density and limits HI-induced brain infarct.
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Uncovering the mechanisms of trans-arachidonic acids : function and implications for cerebral ischemia and beyondKooli, Amna. January 2008 (has links)
No description available.
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Chemoprevention for Colorectal CancerKrishnan, K, Ruffin, M T., Brenner, D E. 01 March 2000 (has links)
No description available.
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