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Relevant bibliographies by topics / Homocysteine

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Academic literature on the topic 'Homocysteine'

Author: Grafiati

Published: 4 June 2021

Last updated: 9 March 2023

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Journal articles on the topic "Homocysteine"

1

Khajuria, Annu, and Donald S. Houston. "Induction of monocyte tissue factor expression by homocysteine: a possible mechanism for thrombosis." Blood 96, no. 3 (August 1, 2000): 966–72. http://dx.doi.org/10.1182/blood.v96.3.966.

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Abstract Moderately elevated plasma homocysteine levels are an important independent risk factor for arterial and venous thrombosis and for atherosclerosis. Some investigators have proposed that homocysteine's effects result from oxidant injury to the vascular endothelium or from an alteration in endothelial function. However, homocysteine may have other cellular targets. We now report that homocysteine, at physiologically relevant concentrations, induces the expression of tissue factor by monocytes. In response to homocysteine, monocytes express procoagulant activity in a dose-dependent and a time-dependent manner. This activity is attributable to tissue factor because it was dependent on factor VII and blocked by anti-tissue factor antibodies. Tissue factor mRNA levels were also increased in monocytes after homocysteine treatment. The effect was found to be specific because analogues of homocysteine (homocystine and homocysteine thiolactone) did not mimic homocysteine's activity, nor did other thiol compounds (cysteine, 2-mercaptoethanol, dithiothreitol). On the other hand, methionine, the metabolic precursor of homocysteine, was active though less potent than homocysteine. Catalase and superoxide dismutase (scavengers of H2O2 and O2− Radicals, respectively) were unable to block the expression of tissue factor induced by homocysteine, as was a 5-fold excess of the reducing agent 2-mercaptoethanol. We conclude that the induction of tissue factor expression by circulating monocytes is a plausible mechanism by which homocysteine may induce thrombosis and that a nonspecific redox process is not involved.

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Khajuria, Annu, and Donald S. Houston. "Induction of monocyte tissue factor expression by homocysteine: a possible mechanism for thrombosis." Blood 96, no. 3 (August 1, 2000): 966–72. http://dx.doi.org/10.1182/blood.v96.3.966.015k12_966_972.

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Moderately elevated plasma homocysteine levels are an important independent risk factor for arterial and venous thrombosis and for atherosclerosis. Some investigators have proposed that homocysteine's effects result from oxidant injury to the vascular endothelium or from an alteration in endothelial function. However, homocysteine may have other cellular targets. We now report that homocysteine, at physiologically relevant concentrations, induces the expression of tissue factor by monocytes. In response to homocysteine, monocytes express procoagulant activity in a dose-dependent and a time-dependent manner. This activity is attributable to tissue factor because it was dependent on factor VII and blocked by anti-tissue factor antibodies. Tissue factor mRNA levels were also increased in monocytes after homocysteine treatment. The effect was found to be specific because analogues of homocysteine (homocystine and homocysteine thiolactone) did not mimic homocysteine's activity, nor did other thiol compounds (cysteine, 2-mercaptoethanol, dithiothreitol). On the other hand, methionine, the metabolic precursor of homocysteine, was active though less potent than homocysteine. Catalase and superoxide dismutase (scavengers of H2O2 and O2− Radicals, respectively) were unable to block the expression of tissue factor induced by homocysteine, as was a 5-fold excess of the reducing agent 2-mercaptoethanol. We conclude that the induction of tissue factor expression by circulating monocytes is a plausible mechanism by which homocysteine may induce thrombosis and that a nonspecific redox process is not involved.

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Zaw, K., M. T. Hasan, B. Bhowmick, P. B. Khanna, and E. A. Freeman. "Homocysteine and stroke." Reviews in Clinical Gerontology 17, no. 1 (February 2007): 33–38. http://dx.doi.org/10.1017/s0959259807002316.

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Interest in homocysteine's role in vascular disease was stimulated by the paper of McCully (1969) in which, based on autopsy evidence of extensive arterial thrombosis in two children with elevated plasma homocysteine concentrations and homocystinuria, he proposed that elevated plasma homocysteine (hyperhomocysteinaemia) can cause atherosclerotic vascular disease. A meta-analysis of subsequent prospective observational studies concluded that elevated homocysteine is indeed a modest independent predictor of ischaemic heart disease and stroke risk in healthy populations with a 25% reduction in serum homocysteine concentration, a reduction of approximately 3 micromol per litre (μmol/l) being associated with a 19% lower risk of stroke (odds ratio, 0.81; 95% confidence interval (CI), 0.69 – 0.95). In the nationally representative sample of US adults, elevated homocysteine concentration was independently associated with an increased likelihood of non-fatal stroke in both black and white adults. In this article, the current concepts relating homocysteine to ischaemic stroke are reviewed.

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Lubec, Barbara, Klaus Arbeiter, Harald Hoeger, and Gert Lubec. "Increased Cyclin Dependent Kinase in Aortic Tissue of Rats Fed Homocysteine." Thrombosis and Haemostasis 75, no. 04 (1996): 542–45. http://dx.doi.org/10.1055/s-0038-1650317.

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Summary Background. Hyperhomocyst(e)inemia is strongly associated with occlusive arterial disease. Several mechanisms for the development of vascular lesions have been described. A direct effect of homocysteine on proliferation of smooth muscle cells and collagen expression was proposed recently. These observations led us to examine the effect of homocysteine on cyclin dependent kinase, the starter of mitosis and reflecting proliferation. Methods and results. Thirty Him: OF A rats were divided into three groups. Ten animals were fed for a period of six weeks 50 mg/kg body wt per day homocysteine, ten the same dose of homocysteic acid and ten remained untreated controls. At the end of the experiment we determined aortic cyclin dependent kinase, phosphokinases A and C, aortic homocyst(e)ine and aortic hydroxyproline. Aortic cyclin dependent kinase was significantly (p = 0.0001) elevated in the homocysteine treated group (mean 120 ± 15) compared with the homocysteic acid treated group (mean 71 ± 11) or the untreated group (mean 72 ± 10 fmol/mg aortic tissue). Aortic homocyst(e)ine was significantly higher in homocysteine treated animals (p = 0.0002) strongly correlating with cyclin dependent kinase (r squared = 0.85, p = 0.0001) and with aortic hydroxyproline (r squared = 0.66, p = 0.0001), which in turn was significantly (p = 0.0001) increased in the homocysteine treated group. Phosphokinases A and C determined to rule out nonspecific effects on kinases were not increased by administered homocysteine. Conclusions. Our findings indicate that homocysteine stimulates aortic cyclin dependent kinase with the possible consequence of proliferation of aortic cells. Aortic collagen accumulation could be explained by either the homocysteine-effect on collagen synthesis described in literature, or secondarily, by increased proliferation of collagen producing aortic cells.

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Jiang, Xiaohua, Xiao-feng Yang, Eugen Brailoiu, Hieronim Jakubowski, Andrew I. Schafer, William Durante, and Hong Wang. "Regulation of Homocysteine Transport in Vascular Cells." Blood 108, no. 11 (November 16, 2006): 3926. http://dx.doi.org/10.1182/blood.v108.11.3926.3926.

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Abstract Increased levels of plasma homocysteine is an independent risk factor for cardiovascular disease and has cell-type distinct proatherosclerotic effects on vascular cells. In this study, we characterized L- homocysteine transport in cultured human aortic endothelial and aortic smooth muscle cells. L-homocysteine was transported into vascular cells in a time-dependent fashion. L-homocysteine transport activity was about 2-fold higher in aortic smooth muscle cells. In addition, L-homocysteine transport in both cell types was mediated by sodium-dependent and independent carrier systems. Competition studies revealed that the neutral amino acids cysteine, glycine, serine, tyrosine, alanine, leucine, and methionine, and inhibitors of the cysteine transport systems inhibited L-homocysteine uptake in both cell types, but the inhibition was greater in endothelial cells. Eadie-Hofstee plots demonstrated that L-Hcy transport in endothelial cells had a Michaelis constant (Km) of 79mM and a maximum transport velocity (Vmax) of 873 pmol/mg protein/min. In contrast, homocysteine transport in aortic smooth muscle cells had a lower affinity (Km=212mM) but a higher transport capacity (Vmax=4192 pmol/mg protein/min). Interestingly, increases in pH (pH 6.5–8.2) only inhibited L-homocysteine uptake in endothelial cells. Moreover, L-homocysteine transport in endothelial cells was partially inhibited by lysosomal inhibitors. Our studies indicate that L-homocysteine shares transporter systems with cysteine and can be inhibited for transport by multiple neutral amino acids in vascular cells, and that L-homocysteine transport involves lysosomal transport in endothelial cells. The specific lysosomic feature of L-homocystein transport in endothelial cells may contribute to cell type specific growth inhibitory effects and therefore play a role in homocysteine atherogenic potential.

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Nieman, Kristin M., Matthew J. Rowling, Timothy A. Garrow, and Kevin L. Schalinske. "Modulation of Methyl Group Metabolism by Streptozotocin-induced Diabetes and All-trans-retinoic Acid." Journal of Biological Chemistry 279, no. 44 (August 30, 2004): 45708–12. http://dx.doi.org/10.1074/jbc.m408664200.

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The hepatic enzyme glycineN-methyltransferase (GNMT) plays a major role in the control of methyl group and homocysteine metabolism. Because disruption of these vital pathways is associated with numerous pathologies, understanding GNMT control is important for evaluating methyl group regulation. Recently, gluconeogenic conditions have been shown to modulate homocysteine metabolism and treatment with glucocorticoids and/or all-trans-retinoic acid (RA)-induced active GNMT protein, thereby leading to methyl group loss. This study was conducted to determine the effect of diabetes, alone and in combination with RA, on GNMT regulation. Diabetes and RA increased GNMT activity 87 and 148%, respectively. Moreover, the induction of GNMT activity by diabetes and RA was reflected in its abundance. Cell culture studies demonstrated that pretreatment with insulin prevented GNMT induction by both RA and dexamethasone. There was a significant decline in homocysteine concentrations in diabetic rats, owing in part to a 38% increase in the abundance of the transsulfuration enzyme cystathionine β-synthase; treatment of diabetic rats with RA prevented cystathionine β-synthase induction. A diabetic state also increased the activity of the folate-independent homocysteine remethylation enzyme betaine-homocysteineS-methyltransferase, whereas the activity of the folate-dependent enzyme methionine synthase was diminished 52%. In contrast, RA treatment attenuated the streptozotocin-mediated increase in betaine-homocysteineS-methyltransferase, whereas methionine synthase activity remained diminished. These results indicate that both a diabetic condition and RA treatment have marked effects on the metabolism of methyl groups and homocysteine, a finding that may have significant implications for diabetics and their potential sensitivity to retinoids.

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Yilmaz, Vural Taner, Erkan Coban, Ali Berkant Avci, Fatih Yilmaz, and Ramazan Cetinkaya. "Levels of Plasma Homocysteine in Obese Women Subjects Homocysteine and Obesity." Turkish Nephrology Dialysis Transplantation 23, no. 2 (May 6, 2014): 91–94. http://dx.doi.org/10.5262/tndt.2014.1002.03.

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Razygraev, A. V. "Homocysteine peroxidase activity in rat blood plasma: stoichiometry and enzymatic character of the reaction." Biomeditsinskaya Khimiya 59, no. 6 (2013): 636–43. http://dx.doi.org/10.18097/pbmc20135906636.

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Recently it was shown that the presence of rat blood plasma (as well as of erythrocyte hemolysate) in the reaction mixture containing 43 mM Tris-HCl-buffer (pH 8.5), 0.29 mM EDTA, 19.2 mM sodium azide, 1 mM DL-homocysteine (Hcy), and 198 mM hydrogen peroxide (incubation at 37°C) results in a significant acceleration of the decrease in Hcy concentration caused by addition of H O . In this paper, we present data indicating that the observed activity is the homocysteine:H O -oxidoreductase (homocysteine peroxidase) activity. It has been found that the level of H O -dependent Hcy decrease observed in the presence of blood plasma corresponds to homocysteine:H O -oxidoreductase reaction stoichiometry of 2:1 (mole ratio). The activity observed belongs to the protein fraction isolated by saturation with ammonium sulfate to 50%; the specific activity in this protein fraction is significantly higher than that in the whole plasma. The results confirm the hypothesis that the reaction between Hcy and H O at the presence of plasma is catalyzed by the protein component of plasma and this is the homocysteine peroxidase reaction. This activity is not associated with serum albumin, which is known to function as thiol peroxidase, and probably belongs to extracellular glutathione peroxidase (Gpx3).

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Leung, Sin Bond, Huina Zhang, Chi Wai Lau, Yu Huang, and Zhixiu Lin. "Salidroside Improves Homocysteine-Induced Endothelial Dysfunction by Reducing Oxidative Stress." Evidence-Based Complementary and Alternative Medicine 2013 (2013): 1–8. http://dx.doi.org/10.1155/2013/679635.

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Hyperhomocysteinemia is associated with an increased risk for cardiovascular diseases through increased oxidative stress. Salidroside is an active ingredient of the root ofRhodiola roseawith documented antioxidative, antihypoxia and neuroprotective properties. However, the vascular benefits of salidroside against endothelial dysfunction have yet to be explored. The present study, therefore, aimed to investigate the protective effect of salidroside on homocysteine-induced endothelial dysfunction. Functional studies on the rat aortas were performed to delineate the vascular effect of salidroside. DHE imaging was used to evaluate the reactive oxygen species (ROS) level in aortic wall and endothelial cells. Western blotting was performed to assess the protein expression associated with oxidative stress and nitric oxide (NO) bioavailability. Exposure to homocysteine attenuated endothelium-dependent relaxations in rat aortas while salidroside pretreatment rescued it. Salidroside inhibited homocystein-induced elevation in the NOX2 expression and ROS overproduction in both aortas and cultured endothelial cells and increased phosphorylation of eNOS which was diminished by homocysteine. The present study shows that salidroside is effective in preserving the NO bioavailability and thus protects against homocysteine-induced impairment of endothelium-dependent relaxations, largely through inhibiting the NOX2 expression and ROS production. Our results indicate a therapeutic potential of salidroside in the management of oxidative-stress-associated cardiovascular dysfunction.

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Szegedi, Sandra S., Carmen C. Castro, Markos Koutmos, and Timothy A. Garrow. "Betaine-HomocysteineS-Methyltransferase-2 Is anS-Methylmethionine-Homocysteine Methyltransferase." Journal of Biological Chemistry 283, no. 14 (January 29, 2008): 8939–45. http://dx.doi.org/10.1074/jbc.m710449200.

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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.

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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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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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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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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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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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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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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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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
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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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Books on the topic "Homocysteine"

1

Bolander-Gouaille, Christina, and Teodoro Bottiglieri. Homocysteine. Paris: Springer Paris, 2007. http://dx.doi.org/10.1007/978-2-287-69375-5.

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Bolander-Gouaille, Christina, and Teodoro Bottiglieri. Homocysteine. Paris: Springer Paris, 2003. http://dx.doi.org/10.1007/978-2-8178-0759-1.

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Bolander-Gouaille, Christina. Focus on Homocysteine. Paris: Springer Paris, 2001. http://dx.doi.org/10.1007/978-2-8178-0741-6.

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Focus in homocysteine. Paris: Springer, 2000.

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Robinson, Killian, ed. Homocysteine and Vascular Disease. Dordrecht: Springer Netherlands, 2000. http://dx.doi.org/10.1007/978-94-017-1789-2.

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Victoria, Colby, ed. Homocysteine: The secret killer. New Canaan, Conn: Keats Pub., 1997.

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Bhargava, Seema. The Clinical Application of Homocysteine. Singapore: Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-10-7632-9.

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Ralph, Carmel, and Jacobsen Donald W. 1939-, eds. Homocysteine in health and disease. Cambridge, UK: Cambridge University Press, 2001.

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Brown, John Charles Woodside. Homocysteine metabolism and copper status. [s.l: The Author], 1993.

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Matzkin, Valerie. Cholesterol and homocysteine in anorexia nervosa. [Guildford]: University of Surrey, 1999.

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Book chapters on the topic "Homocysteine"

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Bolander-Gouaille, Christina, and Teodoro Bottiglieri. "Introduction." In Homocysteine, 11–13. Paris: Springer Paris, 2003. http://dx.doi.org/10.1007/978-2-8178-0759-1_1.

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Bolander-Gouaille, Christina, and Teodoro Bottiglieri. "What is Homocysteine?" In Homocysteine, 15–19. Paris: Springer Paris, 2003. http://dx.doi.org/10.1007/978-2-8178-0759-1_2.

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Bolander-Gouaille, Christina, and Teodoro Bottiglieri. "Homocysteine Metabolism." In Homocysteine, 21–33. Paris: Springer Paris, 2003. http://dx.doi.org/10.1007/978-2-8178-0759-1_3.

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Bolander-Gouaille, Christina, and Teodoro Bottiglieri. "How can Homocysteine be Neurotoxic?" In Homocysteine, 35–57. Paris: Springer Paris, 2003. http://dx.doi.org/10.1007/978-2-8178-0759-1_4.

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Bolander-Gouaille, Christina, and Teodoro Bottiglieri. "Why do Homocysteine Levels increase?" In Homocysteine, 59–108. Paris: Springer Paris, 2003. http://dx.doi.org/10.1007/978-2-8178-0759-1_5.

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Bolander-Gouaille, Christina, and Teodoro Bottiglieri. "Neuropsychiatric Conditions associated with Hyperhomocysteinemia." In Homocysteine, 109–49. Paris: Springer Paris, 2003. http://dx.doi.org/10.1007/978-2-8178-0759-1_6.

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Bolander-Gouaille, Christina, and Teodoro Bottiglieri. "Clinical Impact of Enzyme Defects." In Homocysteine, 151–61. Paris: Springer Paris, 2003. http://dx.doi.org/10.1007/978-2-8178-0759-1_7.

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Bolander-Gouaille, Christina, and Teodoro Bottiglieri. "When and how to check Homocysteine Levels?" In Homocysteine, 163–69. Paris: Springer Paris, 2003. http://dx.doi.org/10.1007/978-2-8178-0759-1_8.

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Bolander-Gouaille, Christina, and Teodoro Bottiglieri. "How to interpret the Test Results and how to handle Hyperhomocysteinemia?" In Homocysteine, 171–82. Paris: Springer Paris, 2003. http://dx.doi.org/10.1007/978-2-8178-0759-1_9.

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Bolander-Gouaille, Christina, and Teodoro Bottiglieri. "Introduction." In Homocysteine, 11–13. Paris: Springer Paris, 2007. http://dx.doi.org/10.1007/978-2-287-69375-5_1.

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Conference papers on the topic "Homocysteine"

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Jiráček, Jiří, Michaela Collinsová, Ivan Rosenberg, Hana Netušilová, Miloš Buděšínský, and Timothy A. Garrow. "New inhibitors of human betaine-homocysteine S-methyltransferase." In IXth Conference Biologically Active Peptides. Prague: Institute of Organic Chemistry and Biochemistry, Academy of Sciences of the Czech Republic, 2005. http://dx.doi.org/10.1135/css200508033.

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Timlin, Homa. "162 Homocysteine level in patients with lupus nephritis." In 13th International Congress on Systemic Lupus Erythematosus (LUPUS 2019), San Francisco, California, USA, April 5–8, 2019, Abstract Presentations. Lupus Foundation of America, 2019. http://dx.doi.org/10.1136/lupus-2019-lsm.162.

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Goldbart, AD, A. Broydes, S. Greenberg-Dotan, and A. Tal. "Homocysteine in Children with Obstructive Sleep Apnea Syndrome." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a1751.

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Pirildar, T., N. Turgan, E. Tunc, T. Turk, D. Ozmen, G. Keser, O. Bayindir, and E. Doganavsargil. "FRI0206 Plasma homocysteine levels in patients with systemic sclerosis." In Annual European Congress of Rheumatology, Annals of the rheumatic diseases ARD July 2001. BMJ Publishing Group Ltd and European League Against Rheumatism, 2001. http://dx.doi.org/10.1136/annrheumdis-2001.287.

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"Does the Concurrent Training Affect on Plasma Homocysteine Level?" In International Institute of Chemical, Biological & Environmental Engineering. International Institute of Chemical, Biological & Environmental Engineering, 2015. http://dx.doi.org/10.15242/iicbe.c0615091.

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Alonso, José, Carlos Cabezas, E. Alonso, Santiago Mata, Miguel Rodríguez, and Verónica Díez. "PREFERRED CONFORMERS OF NON-PROTEINOGENIC AMINO ACIDS HOMOSERINE AND HOMOCYSTEINE." In 71st International Symposium on Molecular Spectroscopy. Urbana, Illinois: University of Illinois at Urbana-Champaign, 2016. http://dx.doi.org/10.15278/isms.2016.wc06.

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Massarotti, M., C. Maioli, A. Bestetti, R. Coppola, S. Leviti, and B. Marasini. "FRI0197 Prostaglandin e1 infusions and plasma homocysteine in systemic sclerosis." In Annual European Congress of Rheumatology, Annals of the rheumatic diseases ARD July 2001. BMJ Publishing Group Ltd and European League Against Rheumatism, 2001. http://dx.doi.org/10.1136/annrheumdis-2001.278.

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Collinsová, Michaela, Carmen Castro, Timothy Garrow, Vincent Dive, Athanasios Yiotakis, and Jiří Jiráček. "Development of novel inhibitors of Zn-metalloenzyme betaine: Homocysteine S-methyltransferase." In VIIth Conference Biologically Active Peptides. Prague: Institute of Organic Chemistry and Biochemistry, Academy of Sciences of the Czech Republic, 2001. http://dx.doi.org/10.1135/css200104049.

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Asri, Ennesta, Gardenia Akhyar, and Rina Gustia. "Correlation Between Homocysteine and Vitamin B12 Serum Level with Vitiligo Severity." In Proceedings of the 1st EAI International Conference on Medical And Health Research, ICoMHER November 13-14th 2018, Padang, West Sumatera, Indonesia. EAI, 2019. http://dx.doi.org/10.4108/eai.13-11-2018.2283593.

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Cienfuegos, Antonio Alvarez de, Lucia Cantero-Nieto, José Alberto García-Gómez, Jose Luis Callejas-Rubio, Miguel A. González-Gay, and Norberto Ortego. "AB0293 ASSOCIATION OF HOMOCYSTEINE WITH BONE MINERAL DENSITY IN RHEUMATOID ARTHRITIS PATIENTS." In Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.7572.

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Reports on the topic "Homocysteine"

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Rautiola, Davin. Detection of Homocysteine with Bridged Viologen Chemical Probes. Portland State University Library, January 2000. http://dx.doi.org/10.15760/etd.1540.

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Owen, Laura. Modulation of the Cardiac Calcium Release Channel by Homocysteine Thiolactone. Portland State University Library, January 2000. http://dx.doi.org/10.15760/etd.2070.

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Ganapathy, Vadivel. Homocysteine Is an Oncometabolite in Breast Cancer, Which Promotes Tumor Progression and Metastasis. Fort Belvoir, VA: Defense Technical Information Center, September 2014. http://dx.doi.org/10.21236/ada612888.

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Barve, Aabha. Development of an Optical Method for the Detection of Homocysteine as a Disease Biomarker Using Fluorescein-Aldehydes. Portland State University Library, January 2000. http://dx.doi.org/10.15760/etd.2218.

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Kong, Yixuan, Jinghui Zheng, Zhuomiao Ye, Jie Wang, Xiangmei Xu, and Xuan Chen. A comprehensive evaluation of association between homocysteine levels and single nucleotide polymorphisms with hypertension risk : A protocol of systematic review and network meta-analysis. International Platform of Registered Systematic Review and Meta-analysis Protocols, May 2020. http://dx.doi.org/10.37766/inplasy2020.5.0002.

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Singh, Ruchi, Akhiya Nail, and Nirendra Kumar Rai. Effectiveness of Vitamin B12 Supplementation on cognitive, motor & mood instability of Parkinson’s disease patients on levodopa treatment :A Systematic review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, February 2023. http://dx.doi.org/10.37766/inplasy2023.2.0066.

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Abstract:

Review question / Objective: The treatment of choice for patients of Parkinson's disease is levodopa. However, levodopa has been suggested to decrease Vit B12 level in these patients. Thus, the research question for this systematic review is whether vit B 12 supplementation in Parkinson's disease(PD) patients on treatment with levodopa improves vit B12 level effecting the Cognition, Motor functions and Mood instability among them in comparison to PD patients on levodopa treatment who are not supplemented with Vit B12. Condition being studied: Parkinson disease is the progressive degeneration of dopaminergic neurons present within the substantia nigra that can lead to altered movements along with the prevalence of cognitive and mood instability as a result of dopamine(neurotransmitter) deficiency. The most effective treatment for the Parkinson's disease is the administration of levodopa, a dopamine precursor . Long term treatment with levodopa causes an increase in homocysteine levels and tissue deficiency of vitamin B12 and folate may occur. Vitamin B12 supplementation is administered as after management regime, in Parkinson patient on levodopa treatment . This study aims to conduct a systematic review, of studies , randomized control trials investigating the ability of vitamin B12 supplementation to enhances the recovery/reduce the decline, if any, of the symptoms of cognitive, motor, mood impairments associated with Parkinson's disease patient on levodopa treatment.

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Depressed young people have lower vitamin B12 and vitamin D levels than their peers. ACAMH, August 2020. http://dx.doi.org/10.13056/acamh.12905.

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