Relevant bibliographies by topics / (E)-8-(3-chlorostyryl)caffeine

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  1. Journal articles
  2. Dissertations / Theses
  3. Book chapters

Academic literature on the topic '(E)-8-(3-chlorostyryl)caffeine'

Author: Grafiati
Published: 4 June 2021
Last updated: 3 February 2022

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Journal articles on the topic "(E)-8-(3-chlorostyryl)caffeine"

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Vlok, Nevil, Sarel F. Malan, Neal Castagnoli, Jacobus J. Bergh, and Jacobus P. Petzer. "Inhibition of monoamine oxidase B by analogues of the adenosine A2A receptor antagonist (E)-8-(3-chlorostyryl)caffeine (CSC)." Bioorganic & Medicinal Chemistry 14, no. 10 (2006): 3512–21. http://dx.doi.org/10.1016/j.bmc.2006.01.011.

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Rivara, Silvia, Giovanni Piersanti, Francesca Bartoccini, et al. "Synthesis of (E)-8-(3-Chlorostyryl)caffeine Analogues Leading to 9-Deazaxanthine Derivatives as Dual A2A Antagonists/MAO-B Inhibitors." Journal of Medicinal Chemistry 56, no. 3 (2013): 1247–61. http://dx.doi.org/10.1021/jm301686s.

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Jacobson, Kenneth A., Olga Nikodijević, William L. Padgett, Carola Gallo-Rodriguez, Michel Maillard, and John W. Daly. "8-(3-Chlorostyryl)caffeine (CSC) is a selective A2 -adenosine antagonist in vitro and in vivo." FEBS Letters 323, no. 1-2 (1993): 141–44. http://dx.doi.org/10.1016/0014-5793(93)81466-d.

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4

Chen, Jiang-Fan, Salome Steyn, Roland Staal, et al. "8-(3-Chlorostyryl)caffeine May Attenuate MPTP Neurotoxicity through Dual Actions of Monoamine Oxidase Inhibition and A2AReceptor Antagonism." Journal of Biological Chemistry 277, no. 39 (2002): 36040–44. http://dx.doi.org/10.1074/jbc.m206830200.

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Gołembiowska, Krystyna, and Anna Dziubina. "Effect of the adenosine A2A receptor antagonist 8-(3-chlorostyryl)caffeine on l-DOPA biotransformation in rat striatum." Brain Research 998, no. 2 (2004): 208–17. http://dx.doi.org/10.1016/j.brainres.2003.11.028.

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Frédérick, Raphaël, Frederic Ooms, Neal Castagnoli Jr, et al. "(E)-8-(3-Chlorostyryl)-1,3,7-trimethylxanthine, a caffeine derivative acting both as antagonist of adenosine A2A receptors and as inhibitor of MAO-B." Acta Crystallographica Section C Crystal Structure Communications 61, no. 9 (2005): o531—o532. http://dx.doi.org/10.1107/s0108270105023140.

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Thümmler, Susanne, and Thomas V. Dunwiddie. "Adenosine Receptor Antagonists Induce Persistent Bursting in the Rat Hippocampal CA3 Region Via an NMDA Receptor-Dependent Mechanism." Journal of Neurophysiology 83, no. 4 (2000): 1787–95. http://dx.doi.org/10.1152/jn.2000.83.4.1787.

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Adenosine receptor antagonists initiate repetitive bursting activity in the CA3 region of hippocampal slices. Although some studies have suggested that this effect is irreversible, this has been difficult to establish because many adenosine antagonists wash out of brain slices extremely slowly. Furthermore the cellular mechanism that underlies persistent bursting is unknown. To resolve these issues, we studied the effects of nonselective (8-p-sulfophenyltheophylline, 8SPT, 50–100 μM), Al-selective (8-cyclopentyl-1,3-dipropylxanthine, 100 nM; xanthine carboxylic acid congener, 200 nM), and A2A-
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8

Xu, H., B. Stein, and B. Liang. "Characterization of a stimulatory adenosine A2a receptor in adult rat ventricular myocyte." American Journal of Physiology-Heart and Circulatory Physiology 270, no. 5 (1996): H1655—H1661. http://dx.doi.org/10.1152/ajpheart.1996.270.5.h1655.

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The expression and function of stimulatory adenosine A2 receptor on the cardiac myocyte is not well defined. The objective of the present study is to characterize the A2a receptor in adult rat cardiac ventricular myocytes. After selection of an optimal lot of collagenase for myocyte isolation and for consistent measurement of adenosine-mediated responses, the A1-receptor pathway was inactivated by pertussis toxin and by the A1-selective antagonist 1,3-dipropyl-8-cyclopentylxanthine. Effects of the adenosine agonist and antagonist or cardiac myocyte contractile amplitude and on adenosine 3',5'-
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9

Macala, Lawrence J., and John P. Hayslett. "Basolateral and apical A1 adenosine receptors mediate sodium transport in cultured renal epithelial (A6) cells." American Journal of Physiology-Renal Physiology 283, no. 6 (2002): F1216—F1225. http://dx.doi.org/10.1152/ajprenal.00085.2002.

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There are conflicting reports in the literature regarding the adenosine receptor that mediates the increase in sodium transport in the A6 cell. In this study we used specific A1 and A2 adenosine receptor agonists and antagonists, as well as two different subclones of the A6 cell, to determine which adenosine receptor mediates the increase in sodium transport. In the A6S2 subclone, basolateral and apical N 6-cyclohexyladenosine (CHA), a selective A1 receptor agonist, stimulated sodium transport at a threshold concentration <10−7 M, whereas CGS-21680, a selective A2 receptor agonist, had a th
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Merkus, Daphne, David W. Stepp, Deron W. Jones, Yasuhiro Nishikawa, and William M. Chilian. "Adenosine preconditions against endothelin-induced constriction of coronary arterioles." American Journal of Physiology-Heart and Circulatory Physiology 279, no. 6 (2000): H2593—H2597. http://dx.doi.org/10.1152/ajpheart.2000.279.6.h2593.

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Myocardial hypoperfusion is accompanied by concomitant increases in adenosine and endothelin-1 (ET-1) production, but the vasodilatory effect of adenosine prevails over that of ET-1. Therefore, we hypothesized that adenosine-induced or ischemic preconditioning reduces the vasoconstrictive effect of ET-1. Coronary arteriolar diameter in vivo was measured using fluorescence microangiography in anesthetized open-thorax dogs. ET-1 (5 ng · kg−1 · min−1administered intracoronary, n = 10) induced progressive constriction over 45 min [25 ± 6% (SE)]. The constriction was blocked by preconditioning with
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Dissertations / Theses on the topic "(E)-8-(3-chlorostyryl)caffeine"

1

Vlok, Nevil. "Rational approaches towards the design of (E)-8-(3-Chlorostyryl)-caffeine derivatives as novel reversible inhibitors of monoamine oxidase B / Nevil Vlok." Thesis, North-West University, 2005. http://hdl.handle.net/10394/1017.

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Reversible and selective inhibitors of monoamine oxidase B (MAO-B) are under investigation for the treatment and prevention of Parkinson's disease (PD) and Alzheimer's disease. The mechanism-based inactivator of MAO-B, (R)-deprenyl is frequently used in combination with L-dopa as dopamine replacement therapy in PD. In contrast with reversible inhibitors, following treatment with inactivators such as (R)- deprenyl, enzyme activity can only be regained via de novo synthesis of the MAO-B protein. For these reasons, several studies are currently under way to develop safer inhibitors of MAO-B. The
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Okaecwe, Thokozile Audrey Dorcas. "Inhibition of monoamine oxidase by selected 8-[(phenylsulfanyl)methyl]caffeine derivatives / Thokozile Okaecwe." Thesis, North-West University, 2012. http://hdl.handle.net/10394/9187.

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Purpose Monoamine oxidase (MAO) consists of two isoforms, namely MAO-A and MAO-B. Both these isoforms are involved in the oxidation of dopamine. In Parkinson’s disease (PD) therapy, the inhibition of the oxidation of dopamine by MAO may elevate the levels of dopamine in the brain and prevent the generation of toxic by-products such as hydrogen peroxide. MAO-B inhibitors have found application as monotherapy in PD and it has been shown that MAO-B inhibitors may also be useful as adjuvants to L-dopa in PD therapy. For example, an earlier study has shown that the combination of L-dopa with (R)-de
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3

Swanepoel, Abraham Johannes. "The synthesis and evaluation of phenoxymethylcaffeine analogues as inhibitors of monoamine oxidase / Braam Swanepoel." Thesis, North-West University, 2010. http://hdl.handle.net/10394/8428.

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Purpose: Monoamine oxidase (MAO) plays a key role in the treatment of Parkinson‟s disease (PD), since it is the major enzyme responsible for the catabolism of dopamine in the substantia nigra of the brain. Inhibition of MAO-B may conserve dopamine in the brain and provide symptomatic relief. The MAO-B inhibitors that are currently used for the treatment of PD, are associated with a variety of adverse effects (psychotoxic and cardiovascular effects) along with additional disadvantages such as irreversible inhibition of the enzyme. Irreversible inhibition may be considered a disadvantage, since
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Book chapters on the topic "(E)-8-(3-chlorostyryl)caffeine"

1

Lengyel, Zs, I. Boros, T. Márián, et al. "Possible Use of 11C-Labeled 8-(3-Chlorostyryl) Caffeine (CSC) Mapping A2A Adenosine Receptors in the CNS and Myocardium." In Radioactive Isotopes in Clinical Medicine and Research XXIII. Birkhäuser Basel, 1999. http://dx.doi.org/10.1007/978-3-0348-8782-3_62.

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You might also be interested in the extended bibliographies on the topic '(E)-8-(3-chlorostyryl)caffeine' for particular source types:
Journal articles
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