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1

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.

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2

Martin, Steven Carl. "Homocysteine and vascular disease." Thesis, University of Glasgow, 2003. http://theses.gla.ac.uk/30939/.

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Cardiovascular disease is multifactorial. The main risk factors for developing cardiovascular disease (age, sex, smoking, diabetes, hyperlipidaemia and hypertension) do not explain its development in everyone. New risk factors are continually being sought in order to better understand and treat the disease process. In recent years homocysteine has been proposed as a risk factor for the development of premature cardiovascular disease as a consequence of the accelerated arterial and venous thrombotic disease seen in homocystinuria as a result of a single gene defect. This theory has been difficult to test because patients with premature cardiovascular disease are thankfully rare and because of the difficulties in measuring homocysteine itself. We propose that, if homocysteine is a causative risk factor for atherothrombosis, it will be involved in the development of cardiovascular disease regardless of age and have therefore studied affected patients from routine hospital clinics. Homocysteine analysis has become easier over the past decade with the development of HPLC methods utilising fluorescent detection, but these methods involve toxic chemicals and suffer from high background fluoresence. I have developed an HPLC method more suited to a routine hospital laboratory utilising coulometric detection for measuring plasma total homocysteine and used it to investigate the relationship between homocysteine levels and both micro- and macro-vascular atherothrombotic disease.
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3

Algaidi, Sami Awda H. "Homocysteine and learning in rats." Thesis, University of Aberdeen, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.446586.

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Rats were injected daily with two doses of HCY (20-mg/kg and 200-mg/kg) for variable duration and spatial memory was assessed in the water maze.  Animals were tested 30min after injection using two paradigms: 1) the reference memory (RM) paradigm in which the position of the platform in the water maze was kept constant over days in order to test long-term memory, 2) the delayed matching to position (DMTP) paradigm in which the platform position changed every day in order to test working/short-term memory.  We found that HCY induced a differential effect on memory depending on animal’s age and the task employed. In the first group of animals, HCY administration for 13 weeks, in contrast to all expectations, enhanced reversal learning in reference memory paradigm in 8-10 weeks old animals, with no effect on the acquisition or memory retention in the probe trials. In the second group of animals, in contrast to young animals, HCY administration enhanced memory of young-adult rats (5-month old) when a DMTP task was employed.  At the level of receptors, HCY enhancement is unlikely to be mediated via NMDA receptors alone, because HCY failed to revert MK801-induced (NMDA receptors antagonist) memory impairment observed with a DMTP task.  Surprisingly, we found that HCY partially reversed scopolamine-induced memory impairment, which may indicate that HCY has some activity on cholinergic system. In the third group of animals (1-year-old), HCY administration for 2 weeks, in contrast to the 5-month old rats, impaired memory in the DMTP task.  Also, we found that HCY plasma level in the 200-mg/kg group was about 600% more than controls.  This may reflect a reduced ability to clear HCY which may explain the absence of any impairment in young animals where HCY level increased by 50% only after 13 weeks of treatment. In conclusion, given that memory impairment was observed in old animals may indicate that hyperhomocysteinemia probably plays a role in AD.  However, HCY effects are overt only in already predisposed old patients.
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4

Brown, John Charles Woodside. "Homocysteine metabolism and copper status." Thesis, University of Ulster, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.333966.

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5

Hill, D. M. "Plasma homocysteine, measurement and clinical application." Thesis, Cranfield University, 2006. http://hdl.handle.net/1826/1108.

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Raised plasma homocysteine (Hcy) levels have been cited as a major risk factor for several vascular disorders. Yet hyperhomocysteinaemia is easily treated through dietary intervention and vitamin supplementation. Commercial assays have facilitated routine plasma Hcy analysis. However, the problem faced by clinicians is stabilisation of Hcy in whole blood samples prior to delivery to the laboratory. Following blood collection, erythrocytes continue to produce and excrete Hcy increasing plasma concentrations by up to 10% per hour. This thesis describes the investigation of stabilising plasma Hcy in whole blood, allowing wide scale screening for hyperhomocysteinaemia. The most effective method appears to be inhibition of the enzyme responsible for Hcy production, Sadenosylhomocysteine hydrolase (SAHH), using a competitive inhibitor 3- deazaadenosine (3DA). Clinical trials were conducted on a pilot batch of evacuated blood tubes. Samples were stored in EDTA whole blood in the presence and absence of 3DA, at ambient temperatures (20 to 25ºC), and under refrigerated conditions (2 to 8ºC). Only samples that were collected into EDTA plus 3DA tubes and stored refrigerated showed stability over 72 hours (p = 0.2761). For wide scale screening, samples must be stable under ambient conditions. As the structure of SAHH is known a molecular modelling approach was adopted in an attempt to identify other potential inhibitors from screened databases. Interference of SAHH, in an immunochemical method for Hcy, was to be utilised for in vitro screening before any further clinical trials were conducted. The thesis also focuses on Hcy as a marker of vitamin deficiency and explores links between thiol metabolism and the development of cognitive decline eventually leading to dementia. Disruption of single carbon metabolism can lead to an increase in Hcy and a decrease in available methyl groups important in regulation of several metabolic pathways. Increased oxidative stress may also be a causative factor.
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6

Tsitsiou, Eleni. "Homocysteine transport across the human placenta." Thesis, University of Manchester, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.493441.

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Elevated maternal levels of the neutral amino acid homocysteine (Hcy) during pregnancy are associated with various complications of pregnancy and adverse neonatal outcomes, suggesting placental transport of Hcy may influence fetal development. The primary aim of this study was to characterise Hcy transport across the microvillous plasma membrane (MVM) of the syncytiotrophoblast, the transporting epithelium of human placenta.
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7

McEligot, 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.

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8

Bohjort, 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.

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The pre-analytical phase is known for being the most important step in the laboratory process to reach reliable test results. If handling, transport or preparation of the sample is performed incorrectly the results can deviate from the true value. Today, sampling tubes contains various additives to stabilize concentration levels. The aim of this study was to test a new sampling tube containing fluoride/citrate for glucose, lactate and homocysteine. It was also of interest to evaluate the stability of those three analytes in lithium-heparin, sodium-fluoride/potassium oxalate and fluoride/citrate tubes. To perform the sustainability study, a method verification was done for homocysteine in plasma. The study was performed in a hospital laboratory on the routine instrument Roche Cobas 6000 analyzer. Blood was drawn from 20 patients and was analyzed at the hospital laboratory in Gävle. The blood samples were transported frozen to the laboratory in Hudiksvall and were used in the method verification. For the sustainability study, blood was drawn from 10 healthy volunteers in lithium-heparin, sodium-fluoride/potassium oxalate and fluoride/citrate tubes. The method verification was approved. The results showed that glucose was stable for up to 72 hours in Vacuette Glycaemia tube with fluoride/citrate and this tube also gave more accurate results. Lactate and homocysteine were also stable in fluoride/citrate, but needs further studies. All three analytes were more stable if the sample tubes were centrifuged as soon as possible after blood collection. Fluoride/citrate tubes were stable without centrifugation directly.
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9

Semmler, 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.

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Background: Impaired homocysteine metabolism is associated with a number of vasculopathies including extracranial aneurysms. We analyzed the possible association of nine genetic variants of homocysteine metabolism with the occurrence of intracranial aneurysms. Methods: Caucasian patients (n = 255) treated at two German hospitals for intracranial aneurysms and local controls (n = 348) were genotyped for the following polymorphisms: methionine synthase (MTR) c.2756A→G, methylenetetrahydrofolate reductase (MTHFR) c.677C→T, MTHFR c.1298A→C, cystathionine β-synthase (CBS) c.844_855ins68, CBS c.833T→C, dihydrofolate reductase (DHFR) c.594 + 59del19bp, glutathione S-transferase Ω-1 (GSTO1) c.428C→A, reduced folate carrier 1 (RFC1) c.80G→A and transcobalamin 2 (Tc2) c.776C→G. Results: The G-allele of the missense polymorphism Tc2 c.777C→G was found to be underrepresented in patients, suggesting that this variant may protect from the formation of cerebral aneurysms [odds ratio per two risk alleles (OR) 0.48; 95% confidence interval (CI) 0.30–0.77; p = 0.002]. We obtained borderline results for the G-allele of RFC1 c.80G→A (OR 1.64; 95% CI 1.01–2.65; p = 0.051) and the insertion allele of DHFR c.594 + 59del19bp (OR 1.61; 95% CI 1.00–2.60; p = 0.059), which were found to be overrepresented in patients. Conclusion: Polymorphisms of homocysteine metabolism are possible risk factors for the formation of intracranial aneurysms
Dieser Beitrag ist mit Zustimmung des Rechteinhabers aufgrund einer (DFG-geförderten) Allianz- bzw. Nationallizenz frei zugänglich
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10

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.

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11

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.

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12

Old, 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.

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13

Chan, 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.

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14

Muda, 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.

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15

Trinidad, Marcy Camilla P. "Vitamin supplementation effects on homocysteine and psychological functioning." Connect to resource, 2005. http://hdl.handle.net/1811/5882.

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Thesis (Honors)--Ohio State University, 2005.
Title 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.
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16

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.

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Abstract Dietary vegetables and fruit may play a significant role in atherosclerosis. We investigated the effects of a high intake of vegetables, berries, and citrus fruit along with a diet low in total and saturated fat on plasma concentrations of lipids, lipoprotein(a), antioxidants, oxidised LDL (OxLDL), folate, homocysteine, and on serum paraoxonase-1 activity. We also determined whether gene polymorphisms affect diet response of plasma homocysteine and serum paraoxonase-1 activity. Thirty-seven healthy females consumed two diets (low and high vegetable diets) in a controlled crossover intervention. The plasma measurements were determined at the baseline and at the end of diet periods. The average plasma concentrations of total, LDL, and HDL cholesterol were 5.0 mmol/l, 2.8 mmol/l, and 1.7 mmol/l, respectively, on the low vegetable diet, and decreased by 8%, 8%,and 5%, respectively, in response to the high vegetable diet. The high vegetable diet increased the plasma concentrations of alpha-carotene, beta-carotene, lutein-zeaxanthin, beta-cryptoxanthin, and vitamin C by 133%, 134%, 107%, 65%, and 25%, respectively, compared with the low vegetable diet. There were no differences in the plasma concentrations of OxLDL between the low and high vegetable diets. The mean serum paraoxonase-1 activity was lower at the end of the high vegetable diet (226 U/l) than at the end of the low vegetable diet (240 U/l). Subjects having a genotype with high baseline paraoxonase-1 activity showed the most extensive reduction in their serum enzyme activities. The high vegetable diet enhanced the serum and erythrocyte folate concentrations by 78% and 14%, respectively, and reduced the plasma homocysteine by 13% compared with the low vegetable diet. The dietary treatment was effective even among subjects homozygous for C677T mutation in methylenetetrahydrofolate reductase gene, who are susceptible to high homocysteine levels. In conclusion, a high intake of vegetables, berries, and citrus fruit resulted in reduced plasma total and LDL cholesterol concentrations and enhanced plasma antioxidant levels. The high vegetable diet also effectively increased blood folate concentrations and reduced plasma homocysteine concentration.
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17

Fisher, 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.

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18

Jan, 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.

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Pharmacology
Ph.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
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19

Rautiola, Davin. "Detection of Homocysteine with Bridged Viologen Chemical Probes." PDXScholar, 2014. https://pdxscholar.library.pdx.edu/open_access_etds/1541.

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Increased blood plasma concentrations of the aminothiol homocysteine (Hcy) are associated with a variety of disease states including those which cause impaired renal function, many forms of cardiovascular disease, and neurodegenerative diseases such as Alzheimer's. Therefore, Hcy has the potential to be a significant diagnostic biomarker. Routine monitoring of Hcy plasma concentration is encumbered by the time and resources required to quantify Hcy using currently accepted instrumental analysis methods. As part of the continuing effort to develop a quick, reliable, inexpensive, and user-friendly test to quantify Hcy at the point of care, we have designed a series of novel colorimetric and fluorescent chemical probes based on bridged viologen structures. The absorbance at 540 nm for the para-bridged bis-nitrile viologen probe (pCN) was found to be proportional to the concentration of Hcy analyte, with LOD = 2.17 μM and LOQ = 6.10 μM where unhealthy Hcy plasma concentrations are > 15 μM. The mechanism of reactivity between pCN and Hcy encompasses a dynamic set of reactions which involve pimerization of radical probe species and thioether adduct formation of pCN with Hcy. Preliminary results with fluorometric analogs of the bridged viologen probes are also presented.
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20

Semmler, 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.

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Background: Impaired homocysteine metabolism is associated with a number of vasculopathies including extracranial aneurysms. We analyzed the possible association of nine genetic variants of homocysteine metabolism with the occurrence of intracranial aneurysms. Methods: Caucasian patients (n = 255) treated at two German hospitals for intracranial aneurysms and local controls (n = 348) were genotyped for the following polymorphisms: methionine synthase (MTR) c.2756A→G, methylenetetrahydrofolate reductase (MTHFR) c.677C→T, MTHFR c.1298A→C, cystathionine β-synthase (CBS) c.844_855ins68, CBS c.833T→C, dihydrofolate reductase (DHFR) c.594 + 59del19bp, glutathione S-transferase Ω-1 (GSTO1) c.428C→A, reduced folate carrier 1 (RFC1) c.80G→A and transcobalamin 2 (Tc2) c.776C→G. Results: The G-allele of the missense polymorphism Tc2 c.777C→G was found to be underrepresented in patients, suggesting that this variant may protect from the formation of cerebral aneurysms [odds ratio per two risk alleles (OR) 0.48; 95% confidence interval (CI) 0.30–0.77; p = 0.002]. We obtained borderline results for the G-allele of RFC1 c.80G→A (OR 1.64; 95% CI 1.01–2.65; p = 0.051) and the insertion allele of DHFR c.594 + 59del19bp (OR 1.61; 95% CI 1.00–2.60; p = 0.059), which were found to be overrepresented in patients. Conclusion: Polymorphisms of homocysteine metabolism are possible risk factors for the formation of intracranial aneurysms.
Dieser Beitrag ist mit Zustimmung des Rechteinhabers aufgrund einer (DFG-geförderten) Allianz- bzw. Nationallizenz frei zugänglich.
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21

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.

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22

Sung, 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.

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23

Chan, 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.

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24

Yeung, 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.

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25

Chow, 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.

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26

Doshi, 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.

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27

Christie, 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.

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The focus of this thesis was to investigate the non-essential, sulphur-containing amino acid homocysteine (HCY); elevations in plasma HCY have been associated with several pathological states in the elderly; age-associated reductions in vitamins, essential for the metabolism of HCY, are common and this situation is exacerbated during Alzheimer’s disease (AD).  Primary culture preparations of hippocampal tissue were utilised to investigate intracellular signalling and Ca2+ homeostasis, which were monitored using the Ca2+ fluorescent dye Fluo-4.  In the present study hippocampal slices were prepared from adult rats.  In Fluo 4 Ca2+ imaging studies, HCY (10, 100 µM and 1 mM) added acutely, caused rises in intracellular Ca2+ and decreased NMDA-induced Ca2+ responses.  Pharmacological investigations confirmed that the primary Ca2+ influx following addition of HCY (1 mM) was not mediated via NMDA, group I mGluRs, glycine or GABA receptors, voltage-gated Ca2+ channels (VGCCs) or intracellular stores (ER).  Results with specific antagonists indicate that HCY may have a partial interaction with NMDA receptors and intracellular stores; additionally, experiments revealed that HCY may antagonise the glycine co-agonist binding site on the NMDA receptor and may depend of HCY dose or competition with other glycine site modulators.  Acute application of HCY in slices (10 µM - 1 mM) in vitro caused a dose-response effect with lower concentrations impairing and higher doses enhancing LTP.  With different systemic routes and longer durations (with two concentrations: 20 and 200 mg/kg) basic transmission and LTP were altered in a bi-directional as well as concentration- and time-dependent manner, suggestive of diverse and complex targets for HCY.  Overall, the observed HCY-induced functional alterations amid lack of severe toxicity in vitro and ex vivo in healthy cells suggest a possible contribution in aged or diseased tissues, making this an extremely important consideration for future research as well as for dietary considerations in the elderly.
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28

Weaving, Gary Ronald. "Measurement and clinic applications of homocysteine and methylated arginines." Thesis, University of Sussex, 2010. http://sro.sussex.ac.uk/id/eprint/2495/.

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Homocysteine is an amino acid formed by the metabolism of methionine. Increased plasma homocysteine concentrations are associated with cardiovascular disease, and it has been suggested that homocysteine lowering therapy may reduce cardiovascular risk. Plasma homocysteine measurements are frequently requested by clinicians investigating patients with vascular disease. A mechanism for homocysteine causing vascular disease has not yet been proven, but one possibility is that an elevated plasma homocysteine concentration may lead to the accumulation of asymmetric dimethylarginine (ADMA), a naturally occurring amino acid that inhibits nitric oxide synthase, resulting in impaired nitric oxide production, and therefore vascular dysfuntion. The aim of this project was to develop analytical methods suitable for the measurement of homocysteine and related metabolites in a routine clinical laboratory, and two methods have been established; i) for homocysteine, cysteine and methionine and ii) for asymmetric dimethylarginine, symmetric dimethylarginine (SDMA, a sterioisomer of ADMA), monomethylarginine (MMA) and arginine. A novel feature of the method for ADMA is that the use of unique daughter ions allows the determination of both ADMA and SDMA without the need to separate the isomers chromatographically. In addition, the synthesis and application of isotopically labelled SDMA, for use as an internal standard, is described for the first time. When the methods were applied to the analysis of routine clinical samples no association was detected between plasma total homocysteine and plasma ADMA concentrations. Measurements were also performed on samples from patients enrolled in a clinical trial investigating the progression of vascular dysfuntion, as measured by carotid-femoral pulse wave velocity (CF-PWV), in chronic kidney disease. Again no association could be found between plasma total homocysteine and plasma ADMA concentrations. In addition plasma total homocysteine was not a determinant of CF-PWV. These findings do not support the hypothesis that hyperhomocysteinaemia causes vascular disease by increasing ADMA concentrations.
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29

Skipsey, Mark. "Cloning and characterisation of S-adenosyl-L-homocysteine hydrolase." Thesis, University of Leicester, 1996. http://hdl.handle.net/2381/35350.

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This thesis concerns S-adenosyl-L-homocysteine hydrolase (SHH), the enzyme responsible for the reversible hydrolysis of S-adenosyl-L-homocysteine (SAH) to adenosine and homocysteine. SAH is formed as a direct product of transmethylation reactions involving S-adenosyl-L-methionine (SAM) and is known to be a potent inhibitor of most SAM mediated methyltransfer reactions. An Asparagus officinalis cDNA showing strong homology to previously cloned SHH cDNAs was identified by the random sequencing of cDNAs from a library enriched for wound induced clones. PCR primers were designed which allowed the amplification of a region of the SHH gene from any plant species tested to date. The alignment of sequences from both cloned PCR products, A. officinalis cDNAs, and previously isolated SHH clones, highlights the high level of sequence homology retained between divergent species as well as the presence of an extra polypeptide motif in the amino acid sequence of SHH genes from photosynthetic species. Northern analysis using RNA isolated from asparagus suggested SHH is transcriptionally upregulated from its constitutive low level by a wound stimulus. An Arabidopsis thaliana genomic SHH clone was isolated and used in promoter/reporter gene fusion studies to facilitate a detailed study of the temporal and spatial expression pattern of the SHH gene. Data obtained from this study corroborated evidence obtained from northern, western and enzyme activity analysis, suggesting SHH was expressed in all plant organs. Perturbation of SHH gene expression was also attempted within transgenic plants to try and further elucidate biochemical pathways requiring SHH enzyme activity.
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30

Oyesanya, Olufemi. "Mechanistic Studies on the Electrochemistry of Glutathione and Homocysteine." VCU Scholars Compass, 2008. http://scholarscompass.vcu.edu/etd/1583.

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This research work has investigated the electrochemistry of glutathione (GSH)and homocysteine (HCSH) in order to develop sensors for these biological thiols.Ru(bpy)33+ and IrCl62− have been used as mediators for the electrooxidation of GSH andHCSH because direct oxidation of these thiols is slow at most conventional electrodes.The electrochemical detection of GSH and HCSH has been pursued because of their biological roles. Concerted proton electron transfer (CPET) and stepwise proton electron transfer(PT/ET) pathways have been observed in the electrooxidation of GSH and HCSH.Oxidation of GSH by Ru(bpy)33+ carried out in deuterated and undeuterated buffered (pH= pD = 5.0) and unbuffered solutions (pH = pD 5.0−9.0) indicates a CPET pathway. AtpH 7.0 buffered solution, the involvement of the buffer was obvious, with rate increasing as the buffer concentration increases − an indication of a general base catalysis. The oxidation of GSH by IrCl62− follows through CPET at pH 7.0 when the optimum concentration of the buffer is established. The plot of the rate vs. buffer concentration gave a curvature at lower buffer concentration and then a plateau at higher concentration,which implies a change in the rate determining step as the buffer concentration increases.At lower buffer concentration, proton transfer was seen to be the rate determining step asthe reduction current increases upon scan rate increase. In the oxidation of HCSH by IrCl62−, CPET was observed at pH = pD values of7.0 and 8.0, whereas PT/ET was seen at pH = pD values of 9.0 and 10. Increase in the buffer concentration at pH 7.0 revealed the contribution of the buffer, in that, the oxidation proceeds more efficiently, seeing that the catalytic peak current shifts more negatively and the peak broadness diminishes. Increase in the temperature for the electrooxidation of HCSH resulted in increase in the rate.
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Chan, 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.

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32

Chaudhry, 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.

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Background: Preeclampsia, small for gestational age (SGA), placental abruption, and fetal death are pregnancy complications linked to the utero-placental vasculature with serious consequences for maternal and infant well-being. Elevated homocysteine, a marker of cardiovascular disease risk, is postulated to play a role in placenta-mediated complications, but epidemiologic studies have reported inconsistent findings. The two primary objectives of this thesis were to 1: comprehensively investigate the association of homocysteine with placenta-mediated complications and examine modifying effects of pre-specified factors on this association, and 2: comprehensively investigate determinants of maternal homocysteine during pregnancy. Methods: A systematic review and meta-analysis of prospective studies was conducted to address thesis objective 1. The Ottawa and Kingston (OaK) Birth Cohort, a prospective cohort study that recruited pregnant women between 2002 and 2009, was used to address thesis objectives 1 and 2. Homocysteine concentration was measured between 12 and 20 weeks gestation. Analyses based on the OaK Birth Cohort consisted of multivariable regressions using restricted cubic splines to model associations with continuously distributed variables. Results: Objective 1: In an analysis of 7587 participants, a significant association between homocysteine concentration and a composite outcome of any placenta-mediated complication was observed (odds ratio (OR) for a 5 µmol/L increase: 1.63, 95% Confidence Interval (CI) 1.23-2.16) and SGA (OR 1.76, 95% CI 1.25-2.46), with potential modifying effects of the methylene tetrahydrofolate reductase (MTHFR) 677C>T variant (SGA) and high-risk pregnancy (preeclampsia). In the systematic review identifying 30 prospective cohort or nested case-control studies, a random effects meta-analysis of pooled mean differences in homocysteine between cases and controls in 28 studies revealed significantly higher means for SGA: 0.35 µmol/L (95% CI 0.19 to 0.51, I2=33%); and preeclampsia: 0.87 µmol/L (95% CI 0.52 to 1.21, I2=92%). Significant sources of heterogeneity were study region (SGA and preeclampsia), adjusting for covariates (preeclampsia), folate status (preeclampsia), and severity (preeclampsia). Objective 2: In 7587 OaK participants, factors related to favourable health status were associated with lower maternal homocysteine concentrations. Folic acid supplementation during pregnancy of >1 mg/day did not substantially increase serum folate concentration. Conclusion: This thesis suggests an independent effect of slightly higher homocysteine concentration in the early to mid-second trimester on the risk of any placenta-mediated complication, SGA, and preeclampsia. Modifying effects explain some of the variability in previous studies. Favourable preconception health status was associated with lower maternal homocysteine.
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33

Malaguarnera, Giulia Anna. "Diabetic retinopathy and Type 3 Diabetes Role of Homocysteine." Doctoral thesis, Università di Catania, 2015. http://hdl.handle.net/10761/3950.

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Homocysteine is a sulphur amino acid converted to methionine to a remethylation pathway and to cysteine via transulphuration patway. Its level in the blood increase with age and are associated with several pathologies: cancer, autoimmune disease, cardiovascular and neurodegenerative disorders. The present thesis has focused on the study of the relationship between elevated levels of homocysteine and the deficiency of his metabolites, focusing on folate, in the severity of diabetic retinopathy (non- proliferative and proliferative). Then it had been investigated whether retinal Hcy is associated with retinal neurodegeneration. Histopathological, molecular, and biochemical abnormalities have commonalities in Diabetes and Alzheimer s Disease (AD), which has lead to AD recently termed as "Type 3 Diabetes". Therefore, the present study has focused to evaluate the role of homocysteine in animal models of Type 2 Diabetes (Goto-Kakizaki (GK) rats) and Alzheimer Disease (TASTPM transgenic mice).
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Crew, 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.

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35

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.

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36

Demuth, 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.

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37

Chu, 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.

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38

Škovierova, 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.

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Astrocytes are multipotent and serve surprisingly large and diverse variety of functions, providing for the overall brain homeostasis, assisting in neurogenesis, determining the microarchitecture of the grey matter, and defending the brain through evolutionary conserved astrogliosis programs. Astrocytes are specifically involved in various neurodegenerative diseases, including Alzheimer’s and Parkinson’s diseases, and various forms of dementia. Homocysteine is a nonessential sulphur-containing amino acid that had been linked with neurodegenerative diseases and aging.
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39

Gao, 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.

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Biomedical Sciences
M.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
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40

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.

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41

Nakano, 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.

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42

VARKADOS, MARGARET. "Synthese d'inhibiteurs specifiques des s-adenosyl-homocysteine hydrolase et nucleosidase." Paris 6, 1989. http://www.theses.fr/1989PA066499.

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Le travail de recherche qui constitue le sujet de cette these d'universite consiste a concevoir et synthetiser des inhibiteurs specifiques tels que les analogues de l'etat de transition ou substrats suicides pour les deux enzmes suivantes: la s-adenosyl-l-homocysteine hydrolase (eucaryotes) et nucleosidase (procaryotes). La s-adenosyl-homocysteine (s. A. H. ) est le produit des reactions de transmethylation qui utilisent la s-adenosyl-methionine comme donneur de methyles. Sa degradation est donc un evenement indispensable a tous les processus de methylation. Les modeles etudies sont des nucleosides derives de l'adenosine qui resultent de modifications structurales au niveau de la base ou du sucre. Les purifications enzymatiques ont ete effectuees ainsi que l'evaluation du pouvoir inhibiteur in vitro de ces modeles
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43

Owen, Laura Jean. "Modulation of the Cardiac Calcium Release Channel by Homocysteine Thiolactone." PDXScholar, 2014. https://pdxscholar.library.pdx.edu/open_access_etds/2071.

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Elevated levels in blood serum (≥10μmol/L) of the amino acid homocysteine is strongly correlated with the incidence of heart failure (HF). We present evidence that the cyclic thioester, homocysteine thiolactone (HTL), a metabolic product of homocysteine, irreversibly modifies proteins that regulate the contractile process in cardiac muscle. Two proteins found in the sarcoplasmic reticulum (SR), the Ca2+ pump (SERCA2), and the ryanodine receptor (RyR2), are responsible for controlling the cytosolic Ca2+ concentration and hence the contractile state of the heart. While both improper Ca2+ handling and elevated homocysteine levels have been considered bio-markers in HF, a direct connection between the two has not previously been made. We show that HTL reacts with lysine residues on RyR2, generating a Nε-homocysteine-protein, which results in carbonyl formation and a change in the Ca2+ sensitivity of RyR2. This is a new molecular mechanism linking elevated levels of Homocysteine, improper Ca2+ handling and heart failure. This work was supported by NIH 1 R41 HL105063-01 to J. Abramson and R. Strongin.
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44

Kitami, 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.

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45

Hyndman, 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.

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46

Thomas, 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.

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47

Karamanoli, 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.

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48

Meiklejohn, 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.

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49

Moat, 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.

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50

Ward, 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.

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