Relevant bibliographies by topics / DOPA

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Academic literature on the topic 'DOPA'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 August 2024

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Journal articles on the topic "DOPA"

1

Eldrup, Ebbe, and Erik A. Richter. "DOPA, dopamine, and DOPAC concentrations in the rat gastrointestinal tract decrease during fasting." American Journal of Physiology-Endocrinology and Metabolism 279, no. 4 (October 1, 2000): E815—E822. http://dx.doi.org/10.1152/ajpendo.2000.279.4.e815.

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The aim of the present study was to test the hypothesis that 3,4-dihydroxyphenylalanine (DOPA) and dopamine (DA) in the gastrointestinal tract are to a large extent of exogenous origin and derived from food. Tissue concentrations of norepinephrine (NE), epinephrine (Epi), DA, DOPA, and 3,4-dihydroxyphenylacetic acid (DOPAC), as measured by reverse-phase HPLC with electrochemical detection, were studied in fed and 4-day-fasted Wistar rats as well as in sympathectomized and adrenodemedullated rats. Sympathectomy and adrenal demedullectomy decreased tissue concentrations of NE and Epi, respectively, but had no effect on the level of tissue DOPA. Large amounts of DOPA and DA were present in the gastrointestinal tract. Fasting decreased DOPA and DA in the stomach and DOPA concentrations in the quadriceps muscle but no concentrations in other organs. DOPAC in the heart decreased both in response to sympathectomy and to fasting, whereas DOPAC decreased in plasma after fasting and in skeletal muscle after sympathectomy. We conclude that the food content of DOPA and DA is of major importance for the metabolism of DA and, thus, for the dopamine-sulfate content in the gastrointestinal tract and in plasma. The decrease in muscle DOPA after fasting may be explained by less insulin being available during fasting for stimulation of DOPA uptake in the muscle depot. DOPAC in the organism seems to be of a dual origin, derived partly from DA in the food and partly from DA synthesized in sympathetic nerves.
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Eldrup, Ebbe, Svend Erik Møller, JAN Andreasen, and Niels Juel Christensen. "Effects of Ordinary Meals on Plasma Concentrations of 3,4-Dihydroxyphenylalanine, Dopamine Sulphate and 3,4-Dihydroxyphenylacetic Acid." Clinical Science 92, no. 4 (April 1, 1997): 423–30. http://dx.doi.org/10.1042/cs0920423.

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1. Plasma concentrations of 3,4-dihydroxyphenylalanine (DOPA), dopamine sulphate (DA-S), and 3,4-dihydroxyphenylacetic acid (DOPAC) in humans have been claimed to be indexes of sympathetic nervous activity, but the source and significance of plasma DOPA, DOPAC and DA-S have not been completely elucidated. 2. The effects of ordinary meals on plasma concentrations of total dopamine, mainly DA-S, DOPAC and DOPA were studied in seven healthy subjects. Venous blood was collected every hour for 25 h, while subjects were either fasting or received three meals at 9.00 hours, 13.00 hours and 18.00 hours. Catecholamines and metabolites were determined by reverse-phase HPLC with electrochemical detection. Neutral amino acids were measured by ionexchange chromatography with photometric detection. 3. The food contained relatively little DOPA as compared with phenylalanine, tyrosine, isoleucine and tryptophan. The content of DA and DA-S varied considerably, with the greatest amount in the evening meal of open sandwiches. 4. Plasma DOPA decreased significantly after the meals at 13.00 hours and 18.00 hours, whereas concentrations of the other amino acids increased as expected. 5. Plasma DA-S increased significantly after meals and especially after the evening meal. Increments in DA-S above basal values after a meal were closely related to the content of DOPA+DA+DA-S in the meal. Plasma DOPAC increased significantly after the evening meal. 6. The decrease in plasma DOPA observed after a meal was probably due to uptake of DOPA by muscle tissue. Changes in plasma DA-S and DOPAC during this 25-h study reflected to a large extent the content of DOPA, DA and DA-S in the meals.
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Okada, Maki, Ryuji Nakao, Rie Hosoi, Ming-Rong Zhang, Toshimitsu Fukumura, Kazutoshi Suzuki, and Osamu Inoue. "Microdialysis with Radiometric Monitoring of L-[β-11C]DOPA to Assess Dopaminergic Metabolism: Effect of Inhibitors of L-Amino Acid Decarboxylase, Monoamine Oxidase, and Catechol-O-Methyltransferase on Rat Striatal Dialysate." Journal of Cerebral Blood Flow & Metabolism 31, no. 1 (April 21, 2010): 124–31. http://dx.doi.org/10.1038/jcbfm.2010.58.

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The catecholamine, dopamine (DA), is synthesized from 3,4-dihydroxy-L-phenylalanine (L-DOPA) by aromatic L-amino acid decarboxylase (AADC). Dopamine metabolism is regulated by monoamine oxidase (MAO) and catechol- O-methyltransferase (COMT). To measure dopaminergic metabolism, we used microdialysis with radiometric detection to monitor L-[β-11C]DOPA metabolites in the extracellular space of the rat striatum. We also evaluated the effects of AADC, MAO, and COMT inhibitors on metabolite profiles. The major early species measured after administration of L-[β-11C]DOPA were [11C]3,4-dihydroxyphenylacetic acid ([11C]DOPAC) and [11C]homovanillic acid ([11C]HVA) in a 1:1 ratio, which shifted toward [11C]HVA with time. An AADC inhibitor increased the uptake of L-[β-11C]DOPA and L-3- O-methyl-[11C]DOPA and delayed the accumulation of [11C]DOPAC and [11C]HVA. The MAO and COMT inhibitors increased the production of [11C]3-methoxytyramine and [11C]DOPAC, respectively. These results reflect the L-DOPA metabolic pathway, suggesting that this method may be useful for assessing dopaminergic metabolism.
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Soares-da-Silva, P., M. Pestana, and M. H. Fernandes. "Involvement of tubular sodium in the formation of dopamine in the human renal cortex." Journal of the American Society of Nephrology 3, no. 9 (March 1993): 1591–99. http://dx.doi.org/10.1681/asn.v391591.

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This study has examined the influence of sodium (0, 20, 40, 80, 120, and 160 mM) and ouabain (100, 500, and 1,000 microM), an inhibitor of the enzyme Na(+)-K+ ATPase, on the synthesis of dopamine in slices of human renal cortex loaded with exogenous L-dihydroxyphenylalanine (L-DOPA). The deamination of newly formed dopamine into 3,4-dihydroxyphenylacetic acid (DOPAC) was also examined. The formation of dopamine and its deamination to DOPAC in slices and homogenates of human renal cortex closely depended on the concentration of L-DOPA added to the medium; in homogenates of renal cortex, the production of dopamine was found to be 74% of that occurring in the renal medulla. Decarboxylation of L-DOPA was found saturable at 1,000 microM L-DOPA, which had Vmax and Km values for L-amino acid decarboxylase activity of, respectively, 5.8 +/- 0.6 nmol/mg of protein per hour and 62 +/- 8 microM. The accumulation of newly formed dopamine and DOPAC in kidney slices loaded with L-DOPA (50 and 100 microM) was found to be partially dependent on the concentration of sodium in the medium; at 0 mM sodium, the synthesis of dopamine from L-DOPA was found to be half of that occurring at 160 mM sodium. A similar picture could be observed for DOPAC. The fractional rate of accumulation (k; mM sodium-1) at 50 and 100 microM L-DOPA was, respectively, 0.0016 +/- 0.0002 and 0.0016 +/- 0.0005 for dopamine and 0.0018 +/- 0.0002 and 0.0021 +/- 0.0005 for DOPAC.(ABSTRACT TRUNCATED AT 250 WORDS)
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Buu, N. T., and C. Lussier. "Origin of dopamine in the rat adrenal cortex." American Journal of Physiology-Renal Physiology 258, no. 2 (February 1, 1990): F287—F291. http://dx.doi.org/10.1152/ajprenal.1990.258.2.f287.

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The hypothesis that dopamine (DA) is involved in the control of aldosterone secretion is given some support by the finding of DA in the adrenal cortex of several species, but the source of this DA is not known. This study showed that the administration of L-dopa to intact rats or medullectomized rats caused a significant DA increase in the adrenal cortex. The DA increase in the cortex was more pronounced than in the medulla, coincident with higher L-dopa uptake by the cortical tissue. Tyrosine administration raised DA levels only in the medulla. Sympathectomy of the rat by 6-hydroxydopamine treatment did not affect DA basal levels in the cortex or the DA increase in this tissue after L-dopa injection. 3,4-Dihydroxyphenylacetic acid (DOPAC) is detectable in the adrenal cortex but not in the adrenal medulla, and DOPAC levels increased significantly after L-dopa, which indicates monoamine oxidase (MAO) activity within the adrenal cortex. Because 6-hydroxydopamine pretreatment did not alter DOPAC levels, cortical MAO may be located outside catecholaminergic neurons. The results established circulating L-dopa as a precursor for DA in the adrenal cortex of the rat. They also showed that tyrosine hydroxylase activity is absent from the adrenal cortex of this species.
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Armando, I., S. Nowicki, J. Aguirre, and M. Barontini. "A decreased tubular uptake of dopa results in defective renal dopamine production in aged rats." American Journal of Physiology-Renal Physiology 268, no. 6 (June 1, 1995): F1087—F1092. http://dx.doi.org/10.1152/ajprenal.1995.268.6.f1087.

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A major proportion of urinary dopamine derives from the renal decarboxylation of circulating dopa. This study evaluates the effects of aging on renal production of dopamine using 3- and 12-mo-old male Wistar rats. Urinary excretion of Na+, norepinephrine (NE), 3,4-dihydroxyphenylglycol, and dopa were similar in the two groups. Urinary dopamine and 3,4-dihydroxyphenylacetic acid (DOPAC) were lower in older animals (dopamine, 20 +/- 6 vs. 47 +/- 7 nmol/24 h, P < 0.001; DOPAC, 142 +/- 36 vs. 304 +/- 56 nmol/24 h, P < 0.03). Urinary 3-O-methyldopa (OM-dopa) was higher in 12-mo-old rats (6.2 +/- 2.0 vs. 3.3 +/- 0.20 nmol/24 h, P < 0.03). Levels of dopa and NE in renal cortex from 12-mo-old rats were higher (P < 0.001) than in younger animals. Dopamine content in renal cortex from 3-mo-old rats was 295 +/- 64 pmol/g, whereas it was undetectable in 12-mo-old animals. Aromatic-L-amino-acid decarboxylase and monoamine oxidase activities were higher (P < 0.001) in renal cortex from 12-mo-old animals. Catechol-O-methyltransferase activity was similar in both groups. The uptake of dopa by the luminal membrane was explored using brush-border membrane vesicles. The Na(+)-gradient-driven (100 mM) uptake of dopa into vesicles from 3-mo-old animals showed at 10 s an overshoot threefold greater than the equilibrium uptake. The overshoot was blunted in 12-mo-old rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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Lavoie, Mark P., Meg Palmatier, Frank T. Gentile, Faith A. Kaplan, Deborah M. Fiore, Tyrone F. Hazlett, William J. Bell, and Thomas R. Flanagan. "Two PC 12 Pheochromocytoma Lines Sealed in Hollow Fiber-Based Capsules Tonically Release L-Dopa In Vitro." Cell Transplantation 2, no. 2 (March 1993): 163–73. http://dx.doi.org/10.1177/096368979300200209.

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Two PC12 cell-derived lines have been studied following encapsulation into polymer-based hollow fibers with respect to secreted catecholamines and their metabolites. Cellular encapsulation provides a chronic microperfusion environment within which basally secreted PC12 products can be readily measured. Encapsulated PC12 cells grown and held under the conditions specified in this report basally release amounts exceeding their total cellular stores of the dopamine precursor L-DOPA and the electrochemically active dopamine metabolites DOPAC and HVA during 45-min static incubations. Under these same conditions, these cells release less than 0.1% of their total cellular store of dopamine. Depolarizing incubations enhance dopamine secretion eightyfold and enhance secretion of L-DOPA, HVA, and DOPAC about twofold. The relative composition of products basally secreted differs between PC12-derived cell lines, and an inverse relationship exists between basal release of L-DOPA and total cellular store of dopamine. These results further indicate that selected PC12 cell lines are potentially a source of both dopamine and L-DOPA in therapeutic cellular replacement applications.
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Dutton, J., L. G. Copeland, J. R. Playfer, and N. B. Roberts. "Measuring L-dopa in plasma and urine to monitor therapy of elderly patients with Parkinson disease treated with L-dopa and a dopa decarboxylase inhibitor." Clinical Chemistry 39, no. 4 (April 1, 1993): 629–34. http://dx.doi.org/10.1093/clinchem/39.4.629.

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Abstract We have established a method for measuring L-dopa in plasma and urine, including the metabolites dopamine and L-dopac, using separation by ion-pair reversed-phase HPLC and quantification with an electrochemical detector. The assay was applied to the therapeutic monitoring of elderly patients with established Parkinson disease being treated with L-dopa plus a dopa decarboxylase inhibitor. Plasma L-dopa was evaluated in relation to dosage and postdose sampling time in 71 outpatients with Parkinson disease. L-Dopa concentrations were greatest in the patients taking the highest dosages prescribed and decreased significantly with increasing time after postdose sampling. Comparison of plasma L-dopa concentrations with a published therapeutic range established by intravenous administration of L-dopa was helpful in assessing the suitability of each patient's drug dosage, assessing patients' compliance, and avoiding overdosage but was not useful in the overall clinical assessment of progression of disease or of the long-term therapeutic response. Urine measurements confirmed the plasma concentrations but showed no further advantage. The recommended time for sample collection is between 1.5 and 3 h after the first morning dose. Plasma is the preferred matrix but if blood sampling is difficult, particularly from elderly/infirm individuals, an untimed urine collection could be used.
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Abbas, Ghulam, Alfredo E. Cardenas, and Ron Elber. "The Structures of Heterogeneous Membranes and Their Interactions with an Anticancer Peptide: A Molecular Dynamics Study." Life 12, no. 10 (September 22, 2022): 1473. http://dx.doi.org/10.3390/life12101473.

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We conduct molecular dynamics simulations of model heterogeneous membranes and their interactions with a 24-amino acid peptide—NAF-144–67. NAF-144–67 is an anticancer peptide that selectively permeates and kills malignant cells; it does not permeate normal cells. We examine three membranes with different binary mixtures of lipids, DOPC–DOPA, DOPC–DOPS, and DOPC–DOPE, with a single peptide embedded in each as models for the diversity of biological membranes. We illustrate that the peptide organization in the membrane depends on the types of nearby phospholipids and is influenced by the charge and size of the head groups. The present study sheds light on early events of permeation and the mechanisms by which an amphiphilic peptide crosses from an aqueous solution to a hydrophobic membrane. Understanding the translocation mechanism is likely to help the design of new permeants.
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Eisenhofer, G., D. S. Goldstein, R. Stull, H. R. Keiser, T. Sunderland, D. L. Murphy, and I. J. Kopin. "Simultaneous liquid-chromatographic determination of 3,4-dihydroxyphenylglycol, catecholamines, and 3,4-dihydroxyphenylalanine in plasma, and their responses to inhibition of monoamine oxidase." Clinical Chemistry 32, no. 11 (November 1, 1986): 2030–33. http://dx.doi.org/10.1093/clinchem/32.11.2030.

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Abstract This is a reversed-phase liquid-chromatographic method, with electrochemical detection, for simultaneously measuring, in plasma, the concentrations of the catecholamine precursor dihydroxyphenylalanine (DOPA); the endogenous catecholamines norepinephrine, epinephrine, and dopamine; and the deaminated catecholamine metabolites dihydroxyphenylacetic acid (DOPAC) and dihydroxyphenylglycol (DHPG). We used this method to assess effects of monoamine oxidase (EC 1.4.3.4) inhibition in humans. Plasma DHPG concentrations as determined by the present method (mean 826, SEM 61 ng/L) were similar to those found by other methods. Inhibition of monoamine oxidase (by administering deprenyl or tranylcypromine) decreased plasma DHPG by greater than 65%, plasma DOPAC by greater than 50%, and plasma DOPA by about 20%, without consistently affecting norepinephrine or epinephrine. Simultaneous measurement of DOPA, catecholamines, and DHPG may be useful for examining the synthesis, release, and intraneuronal metabolism of norepinephrine. The assay method is rapid, reliable, and simple, and it provides a more comprehensive assessment of noradrenergic nervous function than does measurement only of catecholamines.
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Dissertations / Theses on the topic "DOPA"

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Khan, Ghulam Ahmed. "Enzymatic synthesis of L-DOPA esters." Thesis, University of Reading, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.333598.

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Branden, Stansley. "L-dopa and the Serotonergic System." University of Toledo Health Science Campus / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=mco1429543879.

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Wiese, Claudia Anette Elisabeth. "Metabolismus fluorierter DOPA-Isomere in aggregierenden Hirnzellkulturen /." [S.l.] : [s.n.], 1991. http://e-collection.ethbib.ethz.ch/show?type=diss&nr=9542.

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Nelson, Michelle Amy. "Protein bound 3,4 dihydroxyphenyalanine as a signal for enhanced antioxidant defences /." full text via ADT, 2008. http://erl.canberra.edu.au/public/adt-AUC20081209.125208/index.html.

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Moheimen, Jamil. "Striatal neuropeptides associated with L- DOPA-induced dyskinesia." Thesis, Uppsala universitet, Institutionen för farmaceutisk biovetenskap, 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-209915.

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Abstract Striatal neuropeptides associated with L-DOPA-induced dyskinesia 2012-02-14 Parkinson's disease (PD) is the most common neurodegenerative disease, with approximately 6 million sufferers in the world. The patients are usually diagnosed between the ages 50-70 years and as the disease progress more symptoms may occur. The cause of the disease is unknown, but the characteristic of PD is that it is a selective degeneration of dopaminergic neurons in the substantia nigra, which leads to an absence of dopamine release in striatum. This affects the motor system of the central nervous system, resulting in a movement disorder. It is not until 70% of the dopamine neurons have been lost that the patient will show the first symptoms of the disease. This will thereby complicate the treatment of the disease. When the motor symptoms are established, it is extremely difficult to stop or reverse the disease. The most effective treatment of patients with Parkinson's disease is L-DOPA that is converted to dopamine in the brain. Dopamine agonists have also been used as a treatment alternative in PD in attempts to avoid the motor symptoms. However, everyone who gets Parkinson's disease will eventually be required to start using L-DOPA as the disease worsen and dopamine agonists loses in efficacy. The majority of patients being treated with L- DOPA have disturbing adverse reactions during the treatment as involuntary, abnormal movements, known as dyskinesias may develop. Once you have got dyskinesias it will not disappear and cannot be effectively alleviated, and will therefore often impair the person's daily life. It is therefore a major focus in research to find new treatments focused on L-DOPA induced side-effects. In a previous study several unknown neuropeptides has been detected, which might have a strong correlation between the L-DOPA and dyskinesia. The main purpose of this study is to identify these neuropeptides and locate them in the striatum of high and low dyskinetic rats. This was performed by using MALDI imaging mass spectrometry and the computer program FlexImaging that provides a visualization of peptides and proteins and their distribution in tissue sections. Of the 76 peptide families that were found in rat brains, 33 of them were identified in this study, and some of them proved to be of high interest. From these 33, three neuropeptides; corticoliberin, P3(42) and cholecystokinin-39, were chosen for further investigation. We saw elevated levels of these three in both high and low dyskinetic rats. We were able to verify with antibodies their localization in normal brains in the striatum and hippocampus. In the future, these peptides will be studied in dyskinetic rats to verify if they are significantly elevated in dyskinetic animals. These three peptides together with the other identified peptides are very interesting in hopes to be able to cure or ameliorate L- DOPA-induced dyskinesias.
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DIMOV, MICHEL. "Melanomes malins et 5-s-cysteinyl- dopa urinaire." Strasbourg 1, 1991. http://www.theses.fr/1991STR15033.

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Tison, François. "La L-Dopa endogène : aspects neurochimiques, physiologiques et étude anatomofonctionnelle par immunohistochimie dans le cerveau de rat." Bordeaux 2, 1990. http://www.theses.fr/1990BOR23037.

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Nelson, Michelle Amy, and n/a. "Protein Bound 3,4-Dihydroxyphenylalanine as a Signal for Enhanced Antioxidant Defences." University of Canberra. n/a, 2008. http://erl.canberra.edu.au./public/adt-AUC20081209.125208.

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Protein-bound 3,4-dihydroxyphenylalanine (PB-DOPA), a long-lived, redox-active product of protein oxidation, is capable of functioning as both a pro- and anti-oxidant. A number of in vitro and in vivo studies have demonstrated a toxic, non-toxic or even beneficial effect of free DOPA, however little investigation has examined the physiological activity of PB-DOPA. Furthermore, as free DOPA is currently the major treatment available for Parkinson?s disease, most studies have focused on the effect of DOPA within neurological cells or tissues, although the presence of PB-DOPA in other locations, for example within atherosclerotic plaques, suggests that broader research is needed to fully understand the physiological effects of both free and PB-DOPA. The hypothesis presented in this thesis is that under physiological conditions, when little redox active transition metal is available, PB-DOPA can function as a redox signalling molecule, triggering an enhancement of cellular antioxidant defences, with a potentially specific role in the regulation of defences targeted against protein oxidation. Physiological levels of PB-DOPA are very low, however the level on individual proteins can change to a proportionally large degree during oxidative stress, an appropriate property for a signalling molecule. In addition, remarkably elevated levels occur in some pathologies, including atherosclerosis. As an initial and commonly formed product of protein oxidation, PB-DOPA is well placed for a signalling role, promoting a significant up-regulation of antioxidant defences in the early stages of oxidative stress, before extensive damage has occurred. As an initiator of antioxidant defences, PB-DOPA would be potentially useful as a therapeutic for the treatment of diseases involving oxidative stress or the accumulation of oxidative damage. The main objective of this thesis was, therefore, to examine the effect of PB-DOPA on the cellular antioxidant defence system using monocytic and macrophage-like cells, key cells involved in the formation of atherosclerotic plaques. The incorporation of free DOPA into protein during protein synthesis, a process previously shown to occur both in vitro and in vivo, was used to generate PB-DOPA. Neither free nor PB-DOPA were found to be toxic to monocytic or macrophage-like cells in culture, but rather were both capable of protecting these cells from oxidative stress. Free DOPA was shown to be capable of directly scavenging radicals, a process that was thought to be in part responsible for the protection induced during oxidative stress. The presence of free and PB-DOPA up-regulated the activity of catalase and NAD(P)H:quinone oxidoreductase, two enzymatic antioxidants, however the activity of superoxide dismutase and the concentration of oxidised and reduced glutathione were not affected. Whilst it was thought that PB-DOPA would have a specific effect on the activity of antioxidant defences targeted against protein oxidation, proteolysis and bulk chaperone activity were not affected by a combination of free and PB-DOPA. Oxidatively-induced protein aggregation, however, was inhibited by the presence of free and PB-DOPA, suggesting that a more specific chaperone regulation may be taking place. The regulation of gene and protein expression was thought to be one possible mechanism by which PB-DOPA could function as a signalling molecule. To test this hypothesis, the effect of free and PB-DOPA on transcription factor activation and protein expression were investigated. Free and PB-DOPA did not induce the expression or activation of Nrf2, AP-1 or NFJB, three transcription factors thought to be involved in the expressional regulation of genes involved in the antioxidant defence system. However, the expression of a number of proteins, including antioxidants, chaperones and proteins involved in cell cycle progression, were regulated in monocytic and macrophage-like cells following the administration of free DOPA under conditions that resulted in either a high or low level of PB-DOPA generation. The regulated proteins differed between the two conditions, suggesting that the level of PB-DOPA may be a key factor in determining the specific defences targeted. The results presented in this thesis support the hypothesis that PB-DOPA can function as a signalling molecule, triggering an enhancement of cellular antioxidant defences, with a specific role in the regulation of the chaperone system, a key defence targeted against protein oxidation. This thesis may provide the basis for the potential use of free or PB-DOPA as a therapeutic for diseases known to involve oxidative stress or oxidative damage, however more research will be required to determine if the effects demonstrated in this thesis are also capable of occurring in vivo.
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Nevalainen, Nina, Martin Lundblad, Greg A. Gerhardt, and Ingrid Strömberg. "Striatal Glutamate Release in L-DOPA-Induced Dyskinetic Animals." Umeå universitet, Institutionen för strålningsvetenskaper, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-67595.

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L-DOPA-induced dyskinesia is a common side effect developed after chronic treatment with 3,4-dihydroxyphenyl-L-alanine (L-DOPA) in Parkinson's disease. The biological mechanisms behind this side effect are not fully comprehended although involvement of dopaminergic, serotonergic, and glutamatergic systems has been suggested. The present study utilizes in vivo amperometry to investigate the impact from unilateral 6-hydroxydopamine lesions and L-DOPA (4 mg/kg, including benserazide 15 mg/kg) -induced dyskinetic behavior on striatal basal extracellular glutamate concentration and potassium-evoked glutamate release in urethane-anesthetized rats. Recordings were performed before and after local L-DOPA application in the striatum. In addition, effects from the 5-HT1A receptor agonist (2R)-(+)-8-hydroxy-2-(di-n-propylamino)tetralin hydrobromide (8-OHDPAT; 1 mg/kg) was assessed on glutamate release and on dyskinetic behavior. The results revealed a bilateral similar to 30% reduction of basal extracellular glutamate concentration and attenuated potassium-evoked glutamate release after a unilateral dopamine-depletion in L-DOPA naive animals. In dyskinetic subjects, basal glutamate concentration was comparable to normal controls, although potassium-evoked glutamate release was reduced to similar levels as in drug naive dopamine-lesioned animals. Furthermore, acute striatal L-DOPA administration attenuated glutamate release in all groups, except in the dopamine-lesioned striatum of dyskinetic animals. Co-administration of 8-OHDPAT and L-DOPA decreased dyskinesia in dopamine-lesioned animals, but did not affect potassium-evoked glutamate release, which was seen in normal animals. These findings indicate altered glutamate transmission upon dopamine-depletion and dyskinesia.
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Cabral, Kibedi. "Towards optimisation of L-DOPA synthesis in Mucuna pruriens." Thesis, Cardiff University, 2014. http://orca.cf.ac.uk/70680/.

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This study examines the potential for increasing natural L-DOPA drug biosynthesis in Mucuna pruriens by silencing or “knocking down” expression of putative DOPA/tyrosine decarboxylase (Mp-ty/ddc) in situ. Mp-ty/ddc codes for DOPA/tyrosine decarboxylase (Mp-TY/DDC) which converts L-DOPA to dopamine in plants. The hypothesis of the work was that silencing the Mp-ty/ddc gene would result in accumulation of L-DOPA in the plant tissues. This work involved isolation and characterisation of 1.73 kb putative full-length ORF of Mp-ty/ddc. The gene showed 74% homology with TY/DDC protein alignments of other plants in the same taxa, although no enzyme activity was detected when the gene product was heterologously expressed. In addition, a protocol was developed for Agrobacterium mediated transformation of M. pruriens so as to be able to manipulate expression of the DOPA genes in situ. The cotyledonary nodal and hypocotyl tip explants regenerated shoots on M.S media supplemented with 50 μM BA, 0.5 μM NAA and 50 mg l-1 kanamycin selection also the nptII transgene was detected by PCR. The Agrobacteria strains GV3101 harbouring a pGREEN vector and carrying an Mp-ty/ddc antisense were used for the plant transformation experiments. Further work showed that the Mp-ty/ddc gene copy number was 1, the gene expression was highest in roots and stems, followed by seeds and was very low in leaves. On the other hand, L-DOPA-content in seeds was 17-fold higher relative to leaves and 15 fold relative to stems and roots.
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Books on the topic "DOPA"

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Riederer, Peter, and Helga Umek, eds. L-Dopa-Substitution der Parkinson-Krankheit. Vienna: Springer Vienna, 1985. http://dx.doi.org/10.1007/978-3-7091-8822-4.

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2

1934-, Misu Yoshimi, and Goshima Yoshio, eds. Neurobiology of DOPA as a neurotransmitter. Boca Raton, F.L: CRC/Taylor & Francis, 2006.

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Koch, E. Pathogenic problems of phenolase enzymatic oxidation of catecholamines and dopa in humans. Amsterdam: Elsevier, 1988.

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Pialis, Peter. The production of L-dopa from mushroom tyrosinase immobilized on nyulon 6,6. Ottawa: National Library of Canada, 1996.

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Phǣnngān, Thailand Krom Kānpokkhrō̜ng Kō̜ng Wichākān læ. Facts about DOPA: Alleviation of suffering and promotion of the people's well-being. [Bangkok]: Kōng Wichākān læ Phǣnngān, Krom Kānpokkhrō̜ng, 2006.

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1933-, Fahn Stanley, ed. Parlodel® (bromocriptine mesylate) in the early management of Parkinson's disease: Excerpts from Recent developments in Parkinson's disease, volume 2. Florham Park, N.J: Macmillan Healthcare Information, 1987.

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Wong, Clara Lai Fong. Effect of L-DOPA on dopamine synthesis and tyrosine hydroxylase concentration in young adult nigrostriatal neurons. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1991.

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Sacks, Oliver W. Przebudzenia. Poznań: Wydawnictwo Zysk i S-ka, 2011.

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Sacks, Oliver W. Awakenings: Das Buch zum Film = Zeit des Erwachens. Reinbek bei Hamburg: Rowohlt, 1995.

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Sacks, Oliver W. Awakenings. New York: Vintage Books, 2002.

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Book chapters on the topic "DOPA"

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Maxwell, Robert A., and Shohreh B. Eckhardt. "l-Dopa." In Drug Discovery, 179–91. Totowa, NJ: Humana Press, 1990. http://dx.doi.org/10.1007/978-1-4612-0469-5_14.

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Fischer, Gabriele, Annemarie Unger, W. Wolfgang Fleischhacker, Cécile Viollet, Jacques Epelbaum, Daniel Hoyer, Ina Weiner, et al. "l-Dopa." In Encyclopedia of Psychopharmacology, 692. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_955.

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Colzi, A., G. Zürcher, R. Kettler, M. Da Prada, and E. Schneider. "L-Dopa." In Neuro-Psychopharmaka, 29–57. Vienna: Springer Vienna, 1992. http://dx.doi.org/10.1007/978-3-7091-3330-9_3.

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Calabria, Ferdinando, and Orazio Schillaci. "18F-DOPA." In Radiopharmaceuticals, 37–55. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-27779-6_2.

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Furukawa, Yoshiaki, Mark Guttman, Shinichiro Nakamura, and Stephen J. Kish. "Dopa-Responsive Dystonia." In Movement Disorder Emergencies, 319–40. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-60761-835-5_24.

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Brouwers, Adrienne H., Klaas P. Koopmans, Rudi A. J. O. Dierckx, and Philip H. Elsinga. "Dopa PET-CT." In PET-CT Beyond FDG A Quick Guide to Image Interpretation, 161–79. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-93909-2_10.

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States, Lisa J., and Klaus Mohnike. "18F-DOPA PET." In Congenital Hyperinsulinism, 85–93. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-02961-6_7.

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Furukawa, Yoshiaki, Mark Guttman, and Stephen J. Kish. "Dopa-Responsive Dystonia." In Movement Disorder Emergencies, 209–29. Totowa, NJ: Humana Press, 2005. http://dx.doi.org/10.1385/1-59259-902-8:209.

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Metze, Dieter, Tam Nguyen, Birgit Haack, Alexander K. C. Leung, Noriko Miyake, Naomichi Matsumoto, A. J. Larner, et al. "Dopa-responsive Dystonia." In Encyclopedia of Molecular Mechanisms of Disease, 542–43. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_510.

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Metze, Dieter, Tam Nguyen, Birgit Haack, Alexander K. C. Leung, Noriko Miyake, Naomichi Matsumoto, A. J. Larner, et al. "Dystonia, Dopa-responsive." In Encyclopedia of Molecular Mechanisms of Disease, 558. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_9143.

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Conference papers on the topic "DOPA"

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Farah, Pedro Felisberto Nogueira Viana, Felipe dos Santos Souza, Felipe Oliveira Costa, Mariana Bastos Rodrigues dos Santos, and Yasmim Evelyn Lisboa Barbosa. "L-dopa: main drug induced dyskinesia." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.111.

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Introduction: 3,4-dihydroxy-L-phenylalanine (L-dopa) is the gold standard drug for the treatment of Parkinson’s disease (PD). This disease causes degeneration of dopaminergic cells, L-dopa supplies the lack of dopamine, being effective in its treatment. The average time for the onset of this hyperkinetic disorder is usually 6.5 years and the young age at the beginning of the disease. This pathology may present with chorea, dystonia, myoclonus and stereotypes. Diskinesia-inducing L-dopa (LID) remains one of the most challenging unmet needs in the treatment of PD and other neurodegenerative diseases. Methodology: This is an integrative review, using the MedLine, Cochrane and PubMed databases with the descriptors “drug induced”, “dyskinesia” and “L- dopa”. Articles published in the last 10 years; in English; clinical trial articles and original articles were included. Results: The prevalence for the development of LID was 50% for those who started PD at 40-59 years of age, compared to 16% at 70 years of age. The incidence of LID is about 90% after 9 years, but the main cause is related to the dose of levodopa and the duration of the disease. The risk factors for the development of LID are modifiable (levoodopa dose and body weight) and non- modifiable (age, sex, duration, progress and severity of the disease). Conclusion: With this, it can be concluded that doctors who deal with PD need to be aware of the risk factors for LID and know how to manage it.
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Alshehri, Ali, Hani Alshahrani, Abdulrahman Alzahrani, Raed Alharthi, Huirong Fu, Anyi Liu, and Ye Zhu. "DOPA: Detecting Open Ports in Android OS." In 2018 IEEE Conference on Communications and Network Security (CNS). IEEE, 2018. http://dx.doi.org/10.1109/cns.2018.8433207.

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Black, Kvar C., Zhongqiang Liu, and Phillip B. Messersmith. "DOPA-Mediated Self-Assembled Biocompatible Plasmonic Nanocrystals." In Frontiers in Optics. Washington, D.C.: OSA, 2007. http://dx.doi.org/10.1364/fio.2007.jsua41.

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Gratz, M., S. Hofmann, C. Kuhn, S. Mahner, U. Jeschke, and A. Vattai. "Verminderte Expression der L-DOPA Decarboxylase im Abortgeschehen." In Jahrestagung der Österreichischen Gesellschaft für Gynäkologie und Geburtshilfe (OEGGG) gemeinsam mit der Bayerischen Gesellschaft für Geburtshilfe und Frauenheilkunde e.V (BGGF). Georg Thieme Verlag KG, 2017. http://dx.doi.org/10.1055/s-0037-1602266.

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Kumar, Ratnesh, Abhishek Kumar, and Neeraj Misra. "Interaction of C24 with L-dopa, a biologically active molecule." In 3RD INTERNATIONAL CONFERENCE ON CONDENSED MATTER AND APPLIED PHYSICS (ICC-2019). AIP Publishing, 2020. http://dx.doi.org/10.1063/5.0001450.

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G., Sarahí Rosas, Alberto Reynoso M., Osbaldo Lopez C., Ignacio Cruz V., Rita Osorio D., Iván Díaz, Ana Laura Pesquera, María Elena Bernal, Antonio Manzo, and Nora Kerik Rotenberg. "Compartmental modeling of F-DOPA PET images from Parkinson’s patients." In MEDICAL PHYSICS: Fourteenth Mexican Symposium on Medical Physics. Author(s), 2016. http://dx.doi.org/10.1063/1.4954132.

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Lohr, Christina, and Udo Hahn. "DOPA METER – A Tool Suite for Metrical Document Profiling and Aggregation." In Proceedings of the 2023 Conference on Empirical Methods in Natural Language Processing: System Demonstrations. Stroudsburg, PA, USA: Association for Computational Linguistics, 2023. http://dx.doi.org/10.18653/v1/2023.emnlp-demo.18.

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Silva, Thais Ellen de Ramos, Diego Rodrigues Castelhano, Cintia Anchieta, and Bruna Kuhn de Freitas Silva. "Benefits of using cannabidiol in the treatment of dyskinesias in patients with Parkinson’s." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.301.

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Introduction: Parkinson’s disease (PD) is a neurological, chronic, and progressive disease that causes the death of brain cells, especially in the area responsible for the production of dopamine, which, among other functions, controls body movements. The first signs of PD are usually hand tremors, muscle stiffness, pain, dizziness, sleep disturbances, respiratory and urinary systems. In this context, cannabidiol (CBD) has been a source of research to improve institutional motor disorders. Objectives: Compile scientific evidence on the use of cannabidiol to improve dyskinesias in patients with Parkinson’s. Methodology: This is an integrative literature review, through the selection of scientific articles, available in the virtual databases: PubMed, Scielo, and Google academic, published between the years 2018 to 2021. Results: CBD has a positive effect, bradykinesia, tremors, stiffness and psychotic, mood and sleep disorders, quality of life, its adverse effects are observed with low frequency. In addition, there seems to be a beneficial drug interaction between CBD and levodopa (l-DOPA), the drug of choice for the treatment of this disease. The prolonged use of this drug causes a type of dyskinesia, known as DOPA- induced dyskinesias (LIDs). Thus, modulation of the endocannabinoid system through CBD presents itself as a possible promising therapy for the control of PD and LIDs. Conclusion: Studies induced expressive results regarding the use of CBD to treat PD. However, as there is still no consensus, specific studies are carried out to assess the safety of using CBD in patients with long-term PD and its possible beneficial interaction with antiparkinsonian drugs.
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Zhao, Weirui, Keshun Hu,, Jiaqi Mei, and Lehe Mei. "Biosynthesis of Salvianic Acid from L-Dopa via a Two-Step Process." In The 5th World Congress on New Technologies. Avestia Publishing, 2019. http://dx.doi.org/10.11159/icbb19.142.

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MOURA, G. A., S. M. B. CASTAÑEDA, B. T. SILVA, A. J. DEMUNER, and R. C. S. SOUSA. "EXTRAÇÃO SÓLIDO-LÍQUIDO E ANÁLISE DE L-DOPA EM SEMENTES DE MUCUNA." In XXII Congresso Brasileiro de Engenharia Química. São Paulo: Editora Blucher, 2018. http://dx.doi.org/10.5151/cobeq2018-pt.0683.

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Reports on the topic "DOPA"

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Halley, Charlotte. The Gut-Brain Axis: Assessment of EcNL-DOPA in mice and dogs. Ames (Iowa): Iowa State University, January 2020. http://dx.doi.org/10.31274/cc-20240624-1441.

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Pina-Burón, María Rosa. Doña Mencía. Institut Català d’Arqueologia Clàssica, 2022. http://dx.doi.org/10.51417/figlinae_018.

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Ficha del yacimiento Doña Mencía ubicado a Écija (Sevilla) incluida en el proyecto "Figlinae Hispanae (FIGHISP). Catálogo en red de las alfarerías hispanorromanas y estudio de la comercialización de sus productos".
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Pina-Burón, María Rosa. Tesorillo de Doña Mencía. Institut Català d’Arqueologia Clàssica, 2022. http://dx.doi.org/10.51417/figlinae_032.

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Ficha del yacimiento Tesorillo de Doña Mencía ubicado a Écija (Sevilla) incluida en el proyecto "Figlinae Hispanae (FIGHISP). Catálogo en red de las alfarerías hispanorromanas y estudio de la comercialización de sus productos".
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León, Carlos. Digital Operational Resilience Act (DORA). FNA, July 2023. http://dx.doi.org/10.69701/deff9232.

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One of the key lessons of the 2007-2008 global financial crisis is the importance of financial market infrastructures (FMIs) as a pillar of financial stability. Before, the role of financial market infrastructures, namely the provision of trading, clearing, settling, recording, and compressing services for transactions between financial institutions (FIs) was often taken for granted. This was reflected in FMIs having often been referred to as the financial system’s plumbing, including by the Federal Reserve’s 14th chairman (Bernanke, 2011)—a clear reference to the critical yet concealed importance of FMIs in the safe and efficient functioning of financial markets. Today, it is clear that the failure of an important FMI will almost certainly lead to systemic instability in financial markets. Given this, it is evident that FMIs are critical infrastructures; that is, based on a definition by the European Commission (2008), FMIs can be considered systems that are essential for the maintenance of vital societal functions, health, safety, security, economic or social well-being of people. In light of this importance, it’s perhaps surprising that the literature about financial networks has addressed the importance of FMIs rather recently and sparingly. The archetypical financial network, composed of FIs as elements (the nodes) that are interlinked through different types of relations (e.g., exposures, payments, ownership, common holdings), has been complemented by the introduction of FMIs as an additional layer that provides a medium for FIs to interact. As highlighted in Berndsen, et al. (2018), a network of FIs that does not include FMIs is a logical network—one that displays bilateral relations despite those requiring the intervention of an FMI to exist. And that’s why the plumbing reference is particularly illustrative: when looking at the floor plan of a house, the plumbing is a critical additional layer hidden beneath the first—immediately visible—layer; in a building, carelessly knocking down a wall could have a disastrous effect on the supply of water, electricity, gas, communications within the apartment and even to others above and below–not to mention the effect on the structural integrity of the building. However, there are further layers beneath those containing FIs and FMIs. In fact, a financial network composed of FIs and FMIs is still a logical network, as the connections between FIs and FMIs also require the intervention of other elements to exist. Those elements provide the physical connection that enables the interlinkages among FIs and FMIs, in the form of wired (e.g., cable) or wireless (e.g., radio waves) connections. That is, as stated by Berndsen, et al. (2018), the interdependence of financial markets with physical networks, such as power and communication networks, make those networks critical infrastructures and obvious candidates for examining the stability of financial systems from an operational perspective.
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Jara, Alejandro. Services, Anti-dumping and Other "New Issues" in the WTO Negotiations and Their Relevance for the FTAA. Inter-American Development Bank, September 2002. http://dx.doi.org/10.18235/0012240.

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In the semester following the Doha Ministerial, WTO Members were able to set up the essential elements of the Work Program decided by Ministers at Doha (November 2001), including the negotiations mandated in the declaration.
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Seager, William R. Geologic Map of the Dona Ana 7.5-Minute Quadrangle and Adjacent Areas, Dona Ana County, New Mexico. New Mexico Bureau of Geology and Mineral Resources, 2018. http://dx.doi.org/10.58799/of-gm-267.

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Amiti, Mary, and John Romalis. Will the Doha Round Lead to Preference Erosion? Cambridge, MA: National Bureau of Economic Research, March 2007. http://dx.doi.org/10.3386/w12971.

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Defraigne, Pierre. CANCUN: Un Hito en el Camino hacia la Conclusión de la RONDA DE DOHA. Inter-American Development Bank, August 2003. http://dx.doi.org/10.18235/0007419.

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El porqué de la agenda de dsarrollo de la Ronda de Doha fortalecimiento del sistema de comercio multilateral contra el unilateralismo redacción de los Tratados de Comercio Regionales [RTA] Respaldo de la dinámica de la liberación del comercio y el establecimiento de normas (crecimiento mundial y políticas locales efectivas) La Agenda de Desarrollo de la Ronda de Doha es parte de una agenda global (Monterrey - Joburg ¿ regiones más desarrolladas [MDR¿s]) en busca de coherencia entre: convergencia norte-sur sustentabilidad
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Research Institute (IFPRI), International Food Policy. Assessing the potential cost of a failed Doha Round. Washington, DC: International Food Policy Research Institute, 2017. http://dx.doi.org/10.2499/9780896292499_06.

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Hertel, Thomas, Roman Keeney, Maros Ivanic, and Alan Winters. Why Isn’t the Doha Development Agenda More Poverty Friendly? GTAP Working Paper, April 2007. http://dx.doi.org/10.21642/gtap.wp37.

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The breakdown of the WTO negotiations under the Doha Development Agenda has inspired critics to highlight the lack of effort on the part of rich countries to reform their agricultural policies. In this paper, we focus instead the poverty impacts of developing country tariff cuts – particularly those in agriculture. We argue that the Doha Development Agenda is fundamentally less poverty-friendly than it could be -- in large part due to the absence of tariff cuts on staple food products in developing countries. Such cuts would give the poor access to food at world prices, thereby reducing the cost of living at the poverty line. We also explore the contention that such tariff cuts will hurt the poor working in agriculture. Based on our analysis of the impacts of multilateral trade policy reforms on a sample of fifteen developing countries, we find there is some evidence of poverty increases in agriculture. However, such effects are minimized by ensuring that agricultural tariffs are cut in all developing countries. Overall, the poverty-reducing impact of lower food prices dominates; we conclude that the Doha Development Agenda would be more poverty friendly if it were to include deeper cuts in developing country agricultural tariffs. This contrasts sharply with calls for special products exemptions by many developing country advocates.
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