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Relevant bibliographies by topics / Acetyl Morphine

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Academic literature on the topic 'Acetyl Morphine'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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Journal articles on the topic "Acetyl Morphine"

1

Nagamatsu, K., K. Suzuki, R. Teshima, H. Ikebuchi, and T. Terao. "Morphine enhances the phosphorylation of a 58 kDa protein in mouse brain membranes." Biochemical Journal 257, no. 1 (January 1, 1989): 165–71. http://dx.doi.org/10.1042/bj2570165.

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Morphine and [D-Ala2,D-Leu5]enkephalinamide enhance the phosphorylation of a 58 kDa protein in mouse brain synaptosomal membranes. The enhancement of phosphorylation was inhibited by naloxone, an antagonist of morphine. The phosphorylated 58 kDa protein was retained on wheat-germ-agglutinin-agarose and morphinone-Affi-Gel 401 columns and biospecifically eluted out from the columns with N-acetyl-D-glucosamine and naloxone respectively. These results suggest a strong possibility that the opiate-binding protein undergoes phosphorylation by endogenous protein kinase. Since the molecular mass of a mu-type opioid receptor in mouse brain is suggested to be 58 kDa, coincident with those of rat brain and neuroblastoma x glioma hybrid cells, it is conceivable that the phosphorylated 58 kDa protein is a mu-type receptor.

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2

Welters, Ingeborg D., Axel Menzebach, Yannick Goumon, Patrick Cadet, Thilo Menges, Thomas K. Hughes, Gunter Hempelmann, and George B. Stefano. "Morphine Inhibits NF-κB Nuclear Binding in Human Neutrophils and Monocytes by a Nitric Oxide–dependent Mechanism." Anesthesiology 92, no. 6 (June 1, 2000): 1677–84. http://dx.doi.org/10.1097/00000542-200006000-00027.

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Background The transcription factor NF-kappaB plays a pivotal role in gene expression of inflammatory mediators such as cytokines or adhesion molecules. NF-kappaB-mediated transcriptional activation of these genes is inhibited by nitric oxide (NO) in a variety of cells, including monocytes. Morphine mediates NO release in a naloxone antagonizable manner in monocytes and neutrophils. Methods The influence of morphine on NF-kappaB activation was investigated in a whole-blood flow cytometric assay. A specific antibody against the p65 subunit of NF-kappaB was used and detected by fluoresceine-isothiocyanate-labeled anti-immunoglobulin G. Nuclei were stained with propidium iodide. Leukocyte subpopulations were evaluated by gating on neutrophils and monocytes. The median fluorescence channel was determined. Different morphine concentrations (50 nm, 50 microm, 1 mm) and incubation intervals (10-150 min) were used. Results Morphine inhibits lipopolysaccharide-induced NF-kappaB nuclear binding in human blood neutrophils and monocytes in a time-, concentration-, and naloxone-sensitive-dependent manner. Similar effects were achieved with the NO donor S-nitroso-N-acetyl-pencillamine and the antioxidant N-acetyl-cysteine. The NO synthase inhibitors Nomega-nitro-l-arginine-methyl-esther and Nomega-nitro-l-arginine completely abolished the morphine-induced attenuation of NF-kappaB nuclear binding, demonstrating that the inhibitory action is mediated by NO release. Conclusion Morphine causes immunosuppression, at least in part, via the NO-stimulated depression of NF-kappaB nuclear binding.

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3

Pang, Wei-wu, Martin S. Mok, Ming-Chou Ku, and Min-Ho Huang. "Patient-Controlled Analgesia with Morphine Plus Lysine Acetyl Salicylate." Anesthesia & Analgesia 89, no. 4 (October 1999): 995. http://dx.doi.org/10.1213/00000539-199910000-00032.

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Pang, Wei-wu, Martin S. Mok, Ming-Chou Ku, and Min-Ho Huang. "Patient-Controlled Analgesia with Morphine Plus Lysine Acetyl Salicylate." Anesthesia & Analgesia 89, no. 4 (October 1999): 995. http://dx.doi.org/10.1097/00000539-199910000-00032.

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5

Jones, A. W., A. Holmgren, and F. C. Kugelberg. "Driving Under the Influence of Opiates: Concentration Relationships Between Morphine, Codeine, 6-Acetyl Morphine, and Ethyl Morphine in Blood." Journal of Analytical Toxicology 32, no. 4 (May 1, 2008): 265–72. http://dx.doi.org/10.1093/jat/32.4.265.

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6

Capuano, Ben, Ian T. Crosby, Edward J. Lloyd, Juliette E. Neve, and David A. Taylor. "Aminimides as Potential CNS-Acting Agents. III. Design, Synthesis, and Receptor Binding of Aminimide Analogues of Dopamine, Serotonin, Morphine, and Nicotine." Australian Journal of Chemistry 61, no. 6 (2008): 422. http://dx.doi.org/10.1071/ch08060.

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A series of aminimide derivatives of centrally acting agents, namely dopamine, serotonin, morphine and nicotine, were designed on the basis of the physicochemical properties of the aminimide functional group and synthesized to investigate their central nervous system (CNS) receptor affinity. The target compounds were readily prepared from an appropriate tertiary amine by N-acylation of a hydrazinium salt intermediate using acetic anhydride or acetyl chloride. The aminimides were tested for in vitro affinity at the dopaminergic D4, serotonergic 5-HT2A, opiate (μ, κ, and non-selective) and nicotinic acetylcholine receptors and were found to possess mixed affinities for the aforementioned receptor systems.

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7

Tasker, R. A. R., and K. Nakatsu. "Metabolism and disposition of 3,6-dibutanoylmorphine in rat brain." Canadian Journal of Physiology and Pharmacology 64, no. 9 (September 1, 1986): 1160–63. http://dx.doi.org/10.1139/y86-197.

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In previous studies from this laboratory it was found that dibutanoylmorphine (DBM) was more potent than morphine as an analgesic in rats and that it was less active than acetyl esters of morphine on behaviour. As DBM is a morphine prodrug, the aim of this work was to determine if rat brain homogenates were capable of deacylating DBM and monobutanoylmorphine (MBM) and to determine relative proportions of parent drug to metabolites in the brain in vivo. In 10% (w/v) brain homogenates, DBM was eliminated with a half-life of about 70 min (corrected for dilution), while MBM was eliminated 10 times as quickly. DBM and its metabolites were found in both blood and brain as early as 1 min after i.v. administration of DBM. After 5 min, the predominant form in blood was MBM and in brain it was DBM. Thus, rat brain possesses the capacity to metabolize DBM by deesterification and the parent drug, MBM, and morphine were found in blood and brain in vivo.

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8

Papoutsis, I., and S. Athanaselis. "Error in the Article: "Driving Under the Influence of Opiates: Concentration Relationships Between Morphine, Codeine, 6-Acetyl Morphine, and Ethyl Morphine in Blood"." Journal of Analytical Toxicology 32, no. 5 (June 1, 2008): 392. http://dx.doi.org/10.1093/jat/32.5.392.

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9

Raphael, Jon H., Stephen M. Palfrey, Arasu Rayen, Jane L. Southall, and Maurad H. Labib. "Stability and Analgesic Efficacy of Di-acetyl Morphine (Diamorphine) Compared with Morphine in Implanted Intrathecal Pumps In Vivo." Neuromodulation: Technology at the Neural Interface 7, no. 3 (June 24, 2004): 197–200. http://dx.doi.org/10.1111/j.1094-7159.2004.04205.x.

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10

Hideg, Kálmán, József Csekö, H. Olga Hankovszky, and Pál Sohár. "Further syntheses with nitroxide α,β-unsaturated aldehydes and allylic bromides." Canadian Journal of Chemistry 64, no. 8 (August 1, 1986): 1482–90. http://dx.doi.org/10.1139/v86-244.

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The enhanced reactivity of nitroxide allylic bromides is used for preparation of spin-labelled analogues of biologically active compounds (morphine, Nalorphine, barbituric acid, choline and acetyl choline). Nitroxide α,β-unsaturated aldehydes are reacted with phosphoranes to give nitroxide polyenes. The nitroxides are reduced to diamagnetic N-hydroxy hydrochloride salts, which can be converted in the presence of base to N-acetoxy derivatives.

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Dissertations / Theses on the topic "Acetyl Morphine"

1

Al, Najjar Ahmed Omer. "Enhancement of Sensitivity in Capillary Electrophoresis: Forensic and Pharmaceutical Applications." Ohio University / OhioLINK, 2004. http://www.ohiolink.edu/etd/view.cgi?ohiou1107276943.

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Book chapters on the topic "Acetyl Morphine"

1

Taber, Douglass F. "The Magnus Synthesis of ( ± )-Codeine." In Organic Synthesis. Oxford University Press, 2013. http://dx.doi.org/10.1093/oso/9780199965724.003.0088.

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Although there have been many synthetic approaches to morphine and its methyl ether codeine 3, the pentacyclic structure of these Papaver alkaloids continues to intrigue organic chemists. Philip Magnus of the University of Texas devised (J. Am. Chem. Soc . 2009, 131, 16045) an elegant route to 3 based on the conversion of 1 to 2 by way of an intramolecular Michael addition. The starting point for the synthesis was the commercial bromoaldehyde 4. Coupling with 5 delivered the substituted biphenyl 6, which was carried on to the mixed bromo acetal 8. On exposure to fluoride ion, 8 was desilylated, and the intermediate phenoxide cyclized with impressive facility to give 1. Exposure of 1 to nitromethane delivered the tetracyclic 2. This reaction apparently was initiated by Henry addition of the nitromethane to the aldehyde. The intramolecular Michael addition of the intermediate Henry adduct then proceeded to give the desired cis diastereomer of the newly formed ring. Finally, loss of water gave 2. Conjugate reduction of the nitroalkene 2 led to 9 with remarkable diastereocontrol. Exposure of 9 to LiAlH4 converted the nitro group to the amine and the enone to the allylic alcohol. On exposure to acid, the hemiacetal was hydrolyzed. The liberated aldehyde underwent reductive amination with the free amine, while at the same time ionic cyclization closed the ether ring. N-acylation completed the conversion to 10. The ether 10 had previously been converted to codeine and then, in a single demethylation step, to morphine. In that synthesis, the alkene of 10 was directly epoxidized. The resulting “up” epoxide reacted only sluggishly with phenylselenide anion, and the relative configuration of the resulting allylic alcohol had to be inverted by oxidation followed by reduction. In the current synthesis, exposure of the alkene 10 to dibromohydantoin under aqueous conditions to form the bromohydrin effected concomitant arene bromination, to give, after base treatment, the “down” epoxide 12. Phenylselenide opening of the epoxide was then facile, and the product allylic alcohol had the correct relative configuration for codeine and morphine. The extra Br was of no consequence, as it was removed by the final LiAlH4 reduction.

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