Dissertations / Theses on the topic 'Homocysteine'
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Bellamy, Michael Francis. "Homocysteine and endothelial function." Thesis, University College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.271171.
Full textMartin, Steven Carl. "Homocysteine and vascular disease." Thesis, University of Glasgow, 2003. http://theses.gla.ac.uk/30939/.
Full textAlgaidi, Sami Awda H. "Homocysteine and learning in rats." Thesis, University of Aberdeen, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.446586.
Full textBrown, John Charles Woodside. "Homocysteine metabolism and copper status." Thesis, University of Ulster, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.333966.
Full textHill, D. M. "Plasma homocysteine, measurement and clinical application." Thesis, Cranfield University, 2006. http://hdl.handle.net/1826/1108.
Full textTsitsiou, Eleni. "Homocysteine transport across the human placenta." Thesis, University of Manchester, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.493441.
Full textMcEligot, Archana Jaiswal. "Relationships between smoking, homocysteine and folate /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2001. http://wwwlib.umi.com/cr/ucsd/fullcit?p3029638.
Full textBohjort, Emelie. "Method verification for homocysteine and a sustainability study on glucose, homocysteine and lactate in different sampling tubes." Thesis, Uppsala universitet, Institutionen för kvinnors och barns hälsa, 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-296043.
Full textSemmler, Alexander, Michael Linnebank, Dietmar Krex, Anika Götz, Susanna Moskau, Andreas Ziegler, and Matthias Simon. "Polymorphisms of Homocysteine Metabolism Are Associated with Intracranial Aneurysms." Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2014. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-135282.
Full textDieser Beitrag ist mit Zustimmung des Rechteinhabers aufgrund einer (DFG-geförderten) Allianz- bzw. Nationallizenz frei zugänglich
Wald, David Samuel. "Serum homocysteine, folic acid and cardiovascular disease." Thesis, Queen Mary, University of London, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.406062.
Full text陳雲浩 and Wan-ho Chan. "Homocysteine stimulates nitric oxide production in macrophages." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2001. http://hub.hku.hk/bib/B31970291.
Full textOld, Iain Graeme. "The two homocysteine transmethylases of Escherichia coli." Thesis, University of Nottingham, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.327743.
Full textChan, Wan-ho. "Homocysteine stimulates nitric oxide production in macrophages." Hong Kong : University of Hong Kong, 2001. http://sunzi.lib.hku.hk/hkuto/record.jsp?B23295028.
Full textMuda, Piibe. "Homocysteine and hypertension: associations between homocysteine and essential hypertension in treated and untreated hypertensive patients withand without coronary artery disease /." Online version, 2005. http://dspace.utlib.ee/dspace/bitstream/10062/692/5/muda.pdf.
Full textTrinidad, Marcy Camilla P. "Vitamin supplementation effects on homocysteine and psychological functioning." Connect to resource, 2005. http://hdl.handle.net/1811/5882.
Full textTitle from first page of PDF file. Document formatted into pages: contains 20 p.; also includes graphics. Includes bibliographical references (p. 13-15). Available online via Ohio State University's Knowledge Bank.
Silaste, M. L. (Marja-Leena). "Dietary effects on antioxidants, oxidised LDL and homocysteine." Doctoral thesis, University of Oulu, 2003. http://urn.fi/urn:isbn:9514270703.
Full textFisher, Andrea. "Niacin, aspirin and homocysteine interrelationships, a clinical study." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape9/PQDD_0017/MQ47027.pdf.
Full textJan, Michael. "Novel Mechanisms Underlying Homocysteine-Suppressed Endothelial Cell Growth." Diss., Temple University Libraries, 2014. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/264103.
Full textPh.D.
Cardiovascular disease (CVD) is the leading cause of death worldwide, and is projected to remain so for at least the next decade. Ever since its discovery in the urine and blood of children with inborn errors of metabolism, homocysteine (Hcy) at elevated plasma concentrations has been associated with CVD clinically and epidemiologically. Observational studies and meta-analyses have noted that changes in plasma Hcy by 5μM increase the odds ratio of developing coronary artery disease by 1.6-1.8 among other CVD. Clinical trials aimed at reducing plasma Hcy for benefit against development of subsequent cardiovascular events have had unconvincing results, but have moreover failed to address the mechanisms by which Hcy contributes to CVD. Recommendations from national agencies like the American Heart Association and the United States Preventive Services Task Force emphasize primordial prevention as a way to combat CVD. Reducing plasma Hcy as secondary and primary interventions does not fulfill this recommendation. In order to best understand the role of Hcy in CVD, an investigation into its mechanisms of action must be undertaken before measures of primordial prevention can be devised. Numerous experimental studies in the literature identify vascular endothelium as a target for the pathological effects of Hcy. Endothelial injury and impairment are contributory processes to atherosclerosis, and Hcy has been demonstrated to inhibit endothelial cell (EC) growth and proliferation through mechanisms involving cell cycle arrest, oxidative stress, and programmed cell death in vitro. Animal models have also confirmed that high levels of Hcy accelerate atherosclerotic plaque development and lead to impairment of vascular reendothelialization following injury. Hcy has been shown to have the opposite effect in vascular smooth muscle cells (SMC), causing their proliferation and again contributing to atherosclerosis. The cell-type specificity of Hcy remains to be understood, and among the aims of this research was to further characterize the effects of Hcy in EC. The overarching goal was discovery in order to direct future investigations of Hcy-mediated pathology. To begin, the first investigation considered the transcriptional and regulatory milieu in EC following exposure to Hcy. High-throughput screening using microarrays determined the effect of Hcy on 26,890 mRNA and 1,801 miRNA. Two different in vitro models of hyperhomocysteinemia (HHcy) were considered in this analysis. The first used a high dose of 500µ Hcy to mimic plasma concentrations of patients wherein the transsulfuration pathway of Hcy metabolism is impaired as in inborn cystathionine-ß-synthase deficiency. The other set of conditions used 50µ Hcy in the presence of adenosine to approximate impairment of the remethylation pathway of Hcy metabolism wherein s-adenosylhomocysteine accumulates, thus inhibiting s-adenosylmethionine formation and methylation reactions. These distinctions are important because most clinical trials do not distinguish between causes of HHcy, thereby ignoring the specific derangements underlying HHcy. mRNA and miRNA expression changes for both sets of treatment conditions identified CVD as a common network of Hcy-mediated pathology in EC. Moreover, methylation-specific conditions identified cell cycle modulation as a major contributory mechanism for this pathology, which agrees with recent findings in the literature. Analysis of significant mRNA changes and significant miRNA changes independently identified roles for Hcy in CVD and cell cycle regulation, thereby suggesting that miRNA may mediate the effects of Hcy in addition to gene expression changes alone. To investigate the role of Hcy in the cell cycle further, the next set of investigations considered the effect of Hcy under conditions approximating impaired remethylation in early cell cycle events. Previous studies have demonstrated that Hcy inhibits cyclin A transcription in EC via demethylation of its promoter. Conversely, Hcy induces cyclin A expression in SMC, again making the case for a cell type-specific mechanism in EC. Preceding cyclin A transcription and activation, canonical events in the early cell cycle include D-type cyclin activation, retinoblastoma protein (pRB) phosphorylation, and transcription factor E2F1 activation. In a series of in vitro experiments on EC, it was seen that Hcy inhibits expression of cyclin D2 and cyclin D3, but not cyclin D1. Next, pRB phosphorylation was seen to be decreased following treatment with Hcy. This also led to decreased E2F1 expression. However, this series of events could be reversed with E2F1 supplementation, allowing the cell cycle to proceed. As Hcy exerts a number of its effects via regulation of gene transcription, a final series of investigations aimed to predict potential targets of Hcy by examining patterns of transcription factor binding among known targets of Hcy regulation. Gene promoters of Hcy-modulated genes were analyzed in order to determine common transcription factors that potentially control their regulation. The locations of CpG-rich regions in promoters were identified to determine which regions would be most susceptible to regulation by DNA methylation. Next, high-throughput next-generation sequencing (NGS) and bisulfite NGS was performed for DNA from EC treated with Hcy in order to determine methylation changes after Hcy treatment. A number of potential transcription factors and their binding sites were identified as potential mediators of Hcy-mediated gene regulation. Taken together, these investigations represent an exploration of Hcy-mediated pathology in CVD, by focusing upon novel regulatory mechanisms in EC. Objective high-throughput arrays identified roles for Hcy in CVD and cell cycle pathways regulated by miRNA and gene expression, which were confirmed experimentally in vitro. These observations led to an investigation and identification of common transcription factors that potentially regulate Hcy-altered gene expression. This framework may be used to guide future investigations into the complex pathological network mediating the effects of Hcy in CVD. First, identification of a role for miRNA in mediating the effects of Hcy represents a novel regulatory mechanism, heretofore largely unexplored. Next, expanding the role of Hcy in EC cell cycle regulation to identify upstream mediators greatly adds to the published literature. Finally, noting that these changes center upon transcriptional and post-transcriptional regulation gives import to developing methods to characterize promoter and transcription factor regulation. The investigations presented herein and their results provide evidence that the future of Hcy research is vibrant, relevant, and not nearly surfeit.
Temple University--Theses
Rautiola, Davin. "Detection of Homocysteine with Bridged Viologen Chemical Probes." PDXScholar, 2014. https://pdxscholar.library.pdx.edu/open_access_etds/1541.
Full textSemmler, Alexander, Michael Linnebank, Dietmar Krex, Anika Götz, Susanna Moskau, Andreas Ziegler, and Matthias Simon. "Polymorphisms of Homocysteine Metabolism Are Associated with Intracranial Aneurysms." Karger, 2008. https://tud.qucosa.de/id/qucosa%3A27635.
Full textDieser Beitrag ist mit Zustimmung des Rechteinhabers aufgrund einer (DFG-geförderten) Allianz- bzw. Nationallizenz frei zugänglich.
宋蘭。 and Lan Fion Sung. "Role of homocysteine in the expression of monocyte Chemoattractant protein-1 (MCP-1)." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1999. http://hub.hku.hk/bib/B31221658.
Full textSung, Lan Fion. "Role of homocysteine in the expression of monocyte Chemoattractant protein-1 (MCP-1) /." Hong Kong : University of Hong Kong, 1999. http://sunzi.lib.hku.hk/hkuto/record.jsp?B21038338.
Full textChan, Sai Yen Victor, and 陳世欽. "Effect of homocysteine on nitric oxide production in cardiomyocytes." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2001. http://hub.hku.hk/bib/B31970321.
Full textYeung, King-yin Dennis, and 楊敬賢. "Effects of homocysteine and puerarin on coronary vasomotor responses." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2003. http://hub.hku.hk/bib/B29293923.
Full textChow, Ying-kit, and 周英傑. "Effect of lipoproteins and homocysteine on vascular endothelial function." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2000. http://hub.hku.hk/bib/B3122247X.
Full textDoshi, Sagar Navinchandra. "Homocysteine, folate and endothelial function in coronary heart disease." Thesis, Cardiff University, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.444121.
Full textChristie, Louisa A. "Homocysteine alters hippocampal signalling in vitro and ex vitro." Thesis, University of Aberdeen, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.440060.
Full textWeaving, Gary Ronald. "Measurement and clinic applications of homocysteine and methylated arginines." Thesis, University of Sussex, 2010. http://sro.sussex.ac.uk/id/eprint/2495/.
Full textSkipsey, Mark. "Cloning and characterisation of S-adenosyl-L-homocysteine hydrolase." Thesis, University of Leicester, 1996. http://hdl.handle.net/2381/35350.
Full textOyesanya, Olufemi. "Mechanistic Studies on the Electrochemistry of Glutathione and Homocysteine." VCU Scholars Compass, 2008. http://scholarscompass.vcu.edu/etd/1583.
Full textChan, Sai-yen Victor. "Effect of homocysteine on nitric oxide production in cardiomyocytes." Hong Kong : University of Hong Kong, 2001. http://sunzi.lib.hku.hk/hkuto/record.jsp?B23476552.
Full textChaudhry, Shazia Hira. "The Association of Homocysteine with Placenta-Mediated Pregnancy Complications." Thesis, Université d'Ottawa / University of Ottawa, 2019. http://hdl.handle.net/10393/39425.
Full textMalaguarnera, Giulia Anna. "Diabetic retinopathy and Type 3 Diabetes Role of Homocysteine." Doctoral thesis, Università di Catania, 2015. http://hdl.handle.net/10761/3950.
Full textCrew, Elizabeth. "Nanoparticle-based analytical/bioanalytical probes investigation of interactions and reactivities between gold nanoparticles and homocysteine /." Diss., Online access via UMI:, 2005. http://wwwlib.umi.com/dissertations/fullcit/1425749.
Full text朱瑞中 and Sui-chung Chu. "Regulation of lipoprotein uptake in mammalian cells." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2000. http://hub.hku.hk/bib/B31969707.
Full textDemuth, Marion. "Hyperhomocysteinemie et atherosclerose : aspects clinico-biologiques et moleculaires (doctorat : structure et fonctionnement des systemes biologiques integres)." Paris 11, 1998. http://www.theses.fr/1998PA114845.
Full textChu, Sui-chung. "Regulation of lipoprotein uptake in mammalian cells." Hong Kong : University of Hong Kong, 2000. http://sunzi.lib.hku.hk/hkuto/record.jsp?B22088982.
Full textŠkovierova, H., S. Mahmood, E. Blahovcova, J. Strnadel, J. Sopkova, and E. Halašova. "Homocystene and human astrocytes." Thesis, Сумський державний університет, 2016. http://essuir.sumdu.edu.ua/handle/123456789/44950.
Full textGao, Chao. "HOMOCYSTEINE-METHIONINE CYCLE IS A KEY METABOLIC SENSOR SYSTEM CONTROLLING METHYLATION-REGULATED PATHOLOGICAL SIGNALING - CD40 IS A PROTOTYPIC HOMOCYSTEINE-METHIONINE CYCLE REGULATED MASTER GENE." Master's thesis, Temple University Libraries, 2019. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/603000.
Full textM.S.
Homocysteine-Methionine (HM) cycle produces a universal methyl group donor S-adenosylmethionine (SAM), a competitive methylation inhibitor S-adenosylhomocysteine (SAH), and an intermediate amino acid product homocysteine (Hcy). Elevated plasma levels of Hcy is termed as hyperhomocycteinemia (HHcy) which is an established risk factor for cardiovascular disease (CVD) and neural degenerative disease. We were the first to describe methylation inhibition as a mediating biochemical mechanism for endothelial injury and inflammatory monocyte differentiation in HHcy-related CVD and diabetes. We proposed metabolism-associated danger signal (MADS) recognition as a novel mechanism for metabolic risk factor-induced inflammatory responses, independent from pattern recognition receptor (PRR)-mediated pathogen-associated molecular pattern (PAMP)/danger-associated molecular pattern (DAMP) recognition. In this study, we examined the relationship of HM cycle gene expression with methylation regulation in human disease. We selected 115 genes in the extended HM cycle, including 31 metabolic enzymes and 84 methyltransferases (MT), examined their mRNA levels in 35 human disease conditions using a set of public databases. We discovered that: 1) HM cycle senses metabolic risk factor and controls SAM/SAH-dependent methylation. 2) Most of metabolic enzymes in HM cycle (8/11) are located in cytosol, while most of the SAM-dependent MTs (61/84) are located in the nucleus, and Hcy metabolism is absent in the nucleus. 3) 11 up-regulated, 3 down-regulated and 24 differentially regulated SAM/SAH-responsive signal pathways are involved in 7 human disease categories. 4) 8 SAM/SAH-responsive H3/H4 hypomethylation sites are identified in 8 disease conditions. We conclude that HM cycle is a key metabolic sensor system which mediates receptor-independent MADS recognition and modulates SAM/SAH-dependent methylation in human disease. We propose that HM metabolism takes place in cytosol and that nuclear methylation equilibration requires nuclear-cytosol transfer of SAM, SAH and Hcy. CD40 is a cell surface molecule which is expressed on antigen presenting cells such as monocyte, macrophage, dendritic cells and neutrophils. The costimulatory pair, CD40 and CD40L, enhances T cell activation and induce chronic inflammatory disease. Also, DNA hypomethylation on CD40 promotor induces inflammatory monocyte differentiation in chronic kidney disease. In order to figure out if CD40 is a prototypic HM cycle regulated master gene, RNA-seq analysis were performed for CD40+ and CD40- monocytes from mouse peripheral blood and 1,093 differentially expressed genes (DEGs) were selected from those two groups. All the DEGs modulate as much as 15 functional gene groups such as cytokines, enzymes and transcriptional factors. Furthermore, CD40+ monocytes activated trained immunity pathways especially in Acetyl-CoA generation and mevalonate pathway. In HM cycle, CD40 is a prototypic HM cycle regulated master gene to induce the most of the Hcy metabolic enzymes as well as MT, which can further modulate the methylation-regulated pathological signaling.
Temple University--Theses
Hultdin, Johan. "Homocysteine in cardiovascular disease with special reference to longitudinal changes." Doctoral thesis, Umeå : Medical Biosciences, 2005. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-529.
Full textNakano, Emi. "Studies of homocysteine metabolism and its relevance to cardiovascular disease." Thesis, University of Sheffield, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.420807.
Full textVARKADOS, MARGARET. "Synthese d'inhibiteurs specifiques des s-adenosyl-homocysteine hydrolase et nucleosidase." Paris 6, 1989. http://www.theses.fr/1989PA066499.
Full textOwen, Laura Jean. "Modulation of the Cardiac Calcium Release Channel by Homocysteine Thiolactone." PDXScholar, 2014. https://pdxscholar.library.pdx.edu/open_access_etds/2071.
Full textKitami, Toshimori. "GENETIC, EVOLUTIONARY, AND GENOMIC ANALYSIS OF HOMOCYSTEINE AND FOLATE PATHWAY REGULATION." Connect to text online, 2006. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=case1127865525.
Full textHyndman, Matthew Eric. "Biochemical and functional interactions of methyltetrahydrofolate and homocysteine in vascular disease." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/NQ64814.pdf.
Full textThomas, J. "The effects of homocysteine on potassium channel function in human platelets." Thesis, University of Oxford, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.270751.
Full textKaramanoli, Zoe. "Interactions between homocysteine and selenium metabolism in renal proximal tubular cells." Thesis, University of Liverpool, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.534001.
Full textMeiklejohn, David J. "Genetic polymorphisms, platelet activation and plasma homocysteine concentrations in atherothrombotic stroke." Thesis, University of Glasgow, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.390772.
Full textMoat, Stuart James. "Investigations of mechanisms of homocysteine mediated-vascular dysfunction and its amelioration." Thesis, University of Sheffield, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.324428.
Full textWard, Mary. "Dietary influences on plasma homocysteine, a risk factor for cardiovascular disease." Thesis, University of Ulster, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.267782.
Full text