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The Global ETD Search service is a free service for researchers
to find electronic theses and dissertations. This service is
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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.
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Showing 11 to 20 of 1875 (0.022 seconds)Spelling suggestions: "subject:"[een] NITRIC OXIDE"" "subject:"[enn] NITRIC OXIDE""
| 11 |
Mechanisms of β cell DNA damage and repair in type 1 diabetes mellitusRosales HernaÌndez, Alma L. January 2002 (has links)
No description available.
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| 12 |
Comparison of endothelial function in human and porcine isolated pulmonary arteriesLawrence, Rebecca Naomi January 1999 (has links)
No description available.
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| 13 |
Synthetic routes towards guanidino-functionalised argininesYu, Weiping January 1998 (has links)
No description available.
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| 14 |
Endothelial cells and platelet functionVickers, James January 1995 (has links)
No description available.
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| 15 |
L-arginine in hypercholesterolaemia and uraemiaMendes Ribeiro, Antonio Claudio January 1996 (has links)
No description available.
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| 16 |
Decomposition pathways of an S-nitroso sugar, S-nitroso dithiols and the reaction of S-nitrosothiols with iron complexesParkin, David January 2002 (has links)
No description available.
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| 17 |
Development of vascular dysfunction in experimental diabetes : role of oxidative stress, angiotensin II and lipidsInkster, Melanie E. January 2002 (has links)
The mesenteric vascular bed from the streptozotocin (STZ) diabetic model was used in this thesis to elucidate the mechanisms underlying diabetic vascular dysfunction. Treatment strategies targeting oxygen free radicals, angiotensin II, and lipids were investigated. In phenylephrine-preconstricted preparations, maximum vasodilation to acetylcholine, progressively deteriorated over 8 weeks of diabetes both before and after NO synthase inhibition which isolated the EDHF component. Chronic preventive treatment with silymarin, a free radical scavenger, or allopurinol, a xanthine oxidase inhibitor, partially protected against the development of 4-week diabetic deficits of the NO and EDHF systems. On the other hand, treatment with the semicarbizide-sensitive amine oxidase (SSAO) inhibitor, MDL74972A, only significantly improved the NO component. Preventive treatment with the transition metal chelator, trientine, produced significant protection of the NO and EDHF responses. Furthermore, intervention treatment not only protected against the development of an 8-week but also reversed some of the 4-week diabetic deficit. Both preventative and intervention treatments targeting angiotensin II production through either angiotensin-converting enzyme (ACE) inhibition with lisinopril or AT1 receptor blockade with candesartan provided some protection against the diabetic-induced decline in acetylcholine relaxations. Most notably, candesartan preventive treatment completely protected against a deficit in the EDHF response. Preventive treatment with rosuvastatin, a lipid-lowering drug, partially protected against the development of NO and EDHF deficits. The results show that experimental diabetes had deleterious effects on NO and EDHF-mediated vasodilation and suggest a role for free radicals, angiotensin II and lipids in this dysfunction.
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| 18 |
Inhibitory effect of tetramethylpyrazine (TMP) on nitric oxide production in macrophagesLam, Ho-keung. January 2001 (has links)
Thesis (M. Med. Sc.)--University of Hong Kong, 2001. / Includes bibliographical references (leaves 43-65).
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| 19 |
Homocysteine stimulates nitric oxide production in macrophagesChan, Wan-ho. January 2001 (has links)
Thesis (M. Med. Sc.)--University of Hong Kong, 2001. / Includes bibliographical references.
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| 20 |
Regulation of nitric oxide synthase expression in mammalian cells /Cheung, Filly. January 2001 (has links)
Thesis (Ph. D.)--University of Hong Kong, 2001. / Includes bibliographical references (leaves 128-151).
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