Academic literature on the topic 'Morphine'

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Journal articles on the topic "Morphine"

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Ninkovic, Jana, and Sabita Roy. "Chronic morphine modulates actin polymerization leading to inhibition of Fc-gamma receptor mediated phagocytosis (111.29)." Journal of Immunology 186, no. 1_Supplement (April 1, 2011): 111.29. http://dx.doi.org/10.4049/jimmunol.186.supp.111.29.

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Abstract Morphine has been known to modulate innate immune functions, by inhibiting macrophage phagocytosis. However, mechanisms by which morphine inhibits macrophage phagocytic ability remain to be explained. Our results indicate that chronic morphine treatment in vitro and in vivo inhibited Fcγ receptor mediated phagocytosis in murine macrophages by inhibiting actin polymerization. Using fluorescence microscopy and fluorometry, we showed that chronic morphine treatment led to inhibition of actin polymerization resulting in impaired internalization of opsonized dextran beads. Chronic morphine treatment inhibited activation of Rac1-GTPase, therefore inhibiting formation of lamellipodia and membrane ruffling. Morphine’s inhibition of Rac1-GTPase activation was abolished in J774 macrophages transfected with constitutively active Rac1. In addition, chronic morphine treatment led to an increase in intracellular cAMP, which resulted in inhibition of actin polymerization through a PKA dependant pathway. DB-cAMP, by increasing intracellular cAMP, led to suppression of actin polymerization while H89 treatment induced inhibition of PKA and abolished morphine’s inhibitory effect implicating cAMP as the key effector in morphine’s modulation of actin. Together these data indicate that chronic morphine by increasing cAMP, activating PKA which inhibits Rac1 GTP-ase, leads to inhibition of actin polymerization and phagocytosis.
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Bouaziz, Herve, Chuanyao Tong, Young Yoon, David D. Hood, and James C. Eisenach. "Intravenous Opioids Stimulate Norepinephrine and Acetylcholine Release in Spinal Cord Dorsal Horn." Anesthesiology 84, no. 1 (January 1, 1996): 143–54. http://dx.doi.org/10.1097/00000542-199601000-00017.

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Background Opioids produce analgesia by direct effects as well as by activating neural pathways that release nonopioid transmitters. This study tested whether systematically administered opioids activate descending spinal noradrenergic and cholinergic pathways. Methods The effect of intravenous morphine on cerebrospinal fluid and dorsal horn microdialysate concentrations of norepinephrine and acetylcholine was examined in 20 sheep. Animals received either intravenous morphine or fentanyl alone, or morphine plus intravenous naloxone or intrathecal idazoxan. Results Intravenous morphine (0, 0.5, 1 mg/kg, intravenous) produced dose-dependent increases in cerebrospinal fluid norepinephrine and acetylcholine, but not epinephrine or dopamine. Morphine's effect was blocked by intravenous naloxone and by intrathecal idazoxan. In microdialysis experiments, intravenous morphine increased the concentration of norepinephrine and acetylcholine, but not epinephrine or dopamine, in the dorsal horn. In contrast, intravenous morphine exerted no effect on any of these monoamines in the ventral horn. Intravenous naloxone and cervical cord transection each blocked morphine's effect on dorsal horn norepinephrine. Conclusions These results support functional studies that indicate that systematically administered opioids cause spinal norepinephrine and acetylcholine release by a naloxone-sensitive mechanism. Idazoxan blockade of morphine's effects on cerebrospinal fluid norepinephrine was unexpected, and suggests that both norepinephrine and acetylcholine release in the spinal cord may be regulated by alpha 2-adrenoceptors. Microdialysis experiments suggest increased norepinephrine and acetylcholine levels in cerebrospinal fluid resulted from intravenous morphine-induced activation of bulbospinal pathways.
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Møllendal, Harald, David Balcells, Odile Eisenstein, Linda Syversen, and Michal Rachel Suissa. "Conformational complexity of morphine and morphinum in the gas phase and in water. A DFT and MP2 study." RSC Adv. 4, no. 47 (2014): 24729–35. http://dx.doi.org/10.1039/c4ra02992e.

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Zhang, Li, Jingjing Meng, Yuguang Ban, Richa Jalodia, Irina Chupikova, Irina Fernandez, Nivis Brito, et al. "Morphine tolerance is attenuated in germfree mice and reversed by probiotics, implicating the role of gut microbiome." Proceedings of the National Academy of Sciences 116, no. 27 (June 17, 2019): 13523–32. http://dx.doi.org/10.1073/pnas.1901182116.

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Prolonged exposure to opioids results in analgesic tolerance, drug overdose, and death. The mechanism underlying morphine analgesic tolerance still remains unresolved. We show that morphine analgesic tolerance was significantly attenuated in germfree (GF) and in pan-antibiotic−treated mice. Reconstitution of GF mice with naïve fecal microbiota reinstated morphine analgesic tolerance. We further demonstrated that tolerance was associated with microbial dysbiosis with selective depletion in Bifidobacteria and Lactobacillaeae. Probiotics, enriched with these bacterial communities, attenuated analgesic tolerance in morphine-treated mice. These results suggest that probiotic therapy during morphine administration may be a promising, safe, and inexpensive treatment to prolong morphine’s efficacy and attenuate analgesic tolerance. We hypothesize a vicious cycle of chronic morphine tolerance: morphine-induced gut dysbiosis leads to gut barrier disruption and bacterial translocation, initiating local gut inflammation through TLR2/4 activation, resulting in the activation of proinflammatory cytokines, which drives morphine tolerance.
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Bimonte, Sabrina, Antonio Barbieri, Domenica Rea, Giuseppe Palma, Antonio Luciano, Arturo Cuomo, Claudio Arra, and Francesco Izzo. "Morphine Promotes Tumor Angiogenesis and Increases Breast Cancer Progression." BioMed Research International 2015 (2015): 1–8. http://dx.doi.org/10.1155/2015/161508.

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Morphine is considered a highly potent analgesic agent used to relieve suffering of patients with cancer. Severalin vitroandin vivostudies showed that morphine also modulates angiogenesis and regulates tumour cell growth. Unfortunately, the results obtained by these studies are still contradictory. In order to better dissect the role of morphine in cancer cell growth and angiogenesis we performedin vitrostudies on ER-negative human breast carcinoma cells, MDA.MB231 andin vivostudies on heterotopic mouse model of human triple negative breast cancer, TNBC. We demonstrated that morphinein vitroenhanced the proliferation and inhibited the apoptosis of MDA.MB231 cells.In vivostudies performed on xenograft mouse model of TNBC revealed that tumours of mice treated with morphine were larger than those observed in other groups. Moreover, morphine was able to enhance the neoangiogenesis. Our data showed that morphine at clinical relevant doses promotes angiogenesis and increases breast cancer progression.
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Bosshart, MD, Herbert. "Morphine and cancer progression: Hydrogen peroxide points to need for more research." Journal of Opioid Management 7, no. 2 (January 15, 2018): 93–96. http://dx.doi.org/10.5055/jom.2011.0051.

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Background: Morphine is widely used in the management of intractable cancer pain. However, conflicting views exist on two suspected nonanalgesic properties of morphine: suppression of immune function and inhibition of cancer progression.Methods: In vitro measurement of the tumor growth-inhibiting signaling molecule, hydrogen peroxide (H2O2), released from the cultured acute monocytic leukemia cell line, THP-1, in the presence or absence of morphine.Results: Morphine at concentrations of 10−8 M significantly reduced H2O2 release from THP-1 cells.Conclusions: These results provide a proof of concept for morphine’s ability to inhibit H2O2 production and release in a leukemia cell system and point to a possible and as yet unrecognized tumor-promoting effect of morphine. More research is needed to systematically examine this suspected morphine-associated tumor-promoting effect.
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Bruce, N. C., C. J. Wilmot, K. N. Jordan, L. D. G. Stephens, and C. R. Lowe. "Microbial degradation of the morphine alkaloids. Purification and characterization of morphine dehydrogenase from Pseudomonas putida M10." Biochemical Journal 274, no. 3 (March 15, 1991): 875–80. http://dx.doi.org/10.1042/bj2740875.

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The NADP(+)-dependent morphine dehydrogenase that catalyses the oxidation of morphine to morphinone was detected in glucose-grown cells of Pseudomonas putida M10. A rapid and reliable purification procedure involving two consecutive affinity chromatography steps on immobilized dyes was developed for purifying the enzyme 1216-fold to electrophoretic homogeneity from P. putida M10. Morphine dehydrogenase was found to be a monomer of Mr 32,000 and highly specific with regard to substrates, oxidizing only the C-6 hydroxy group of morphine and codeine. The pH optimum of morphine dehydrogenase was 9.5, and at pH 6.5 in the presence of NADPH the enzyme catalyses the reduction of codeinone to codeine. The Km values for morphine and codeine were 0.46 mM and 0.044 mM respectively. The enzyme was inhibited by thiol-blocking reagents and the metal-complexing reagents 1,10-phenanthroline and 2,2′-dipyridyl, suggesting that a metal centre may be necessary for activity of the enzyme.
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Tai, Yueh-Hua, Ru-Yin Tsai, Shinn-Long Lin, Chun-Chang Yeh, Jhi-Joung Wang, Pao-Luh Tao, and Chih-Shung Wong. "Amitriptyline Suppresses Neuroinflammation-dependent Interleukin-10-p38 Mitogen-activated Protein Kinase-Heme Oxygenase-1 Signaling Pathway in Chronic Morphine-infused Rats." Anesthesiology 110, no. 6 (June 1, 2009): 1379–89. http://dx.doi.org/10.1097/aln.0b013e31819fccd5.

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Background This study explores the underlying mechanism of the antiinflammatory effect of amitriptyline in chronic morphine-infused rats. Methods Male Wistar rats were implanted with two intrathecal catheters. One catheter was for the continuous infusion of saline, amitriptyline (15 microg/h), morphine (15 microg/h), p38 mitogen-activated protein kinase inhibitor SB203580 (0.5 microg/h), morphine plus amitriptyline, or morphine plus amitriptyline plus SB203580 for 5 days. The other catheter was used for daily intrathecal injection of anti-interleukin-10 (IL-10) antibody or heme oxygenase-1 inhibitor zinc protoporphyrin for 5 days. Results Amitriptyline/morphine coinfusion upregulated IL-10 protein expression in microglia; this was not observed in morphine-infused rats. Anti-IL-10 antibody effectively neutralized the amitriptyline-induced IL-10 expression in chronic morphine-infused rats. In addition, coinfusion of amitriptyline restored the antinociceptive effect of morphine (a 4.8-fold right-shift of the morphine dose-response curve compared to a 77.8-fold right-shift in its absence), and the injection of anti-IL-10 antibody or coinfusion of SB203580 partially reversed the effect of amitriptyline on the antinociceptive effect of morphine in morphine-infused rats (a 17.9-fold and 15.1-fold right-shift in morphine dose-response curves). Anti-IL-10 antibody and SB203580 significantly inhibited the amitriptyline-induced p38 mitogen-activated protein kinase and heme oxygenase-1 expression and the associated antiinflammatory effect of amitriptyline. Daily injection of zinc protoporphyrin also demonstrated that it reverses the effect of amitriptyline in morphine's antinociception and antiinflammation in chronic morphine-infused rats. Conclusions These results suggest that the antiinflammatory effect of amitriptyline on morphine tolerance, probably acting by increasing IL-10 expression, is mediated by p38 mitogen-activated protein kinase heme oxygenase-1 signal transduction cascade.
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Kutchy, Naseer A., Amelia Palermo, Rong Ma, Zhong Li, Alexandria Ulanov, Shannon Callen, Gary Siuzdak, Sabita Roy, Shilpa Buch, and Guoku Hu. "Changes in Plasma Metabolic Signature upon Acute and Chronic Morphine Administration in Morphine-Tolerant Mice." Metabolites 13, no. 3 (March 16, 2023): 434. http://dx.doi.org/10.3390/metabo13030434.

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Morphine administration causes system-level metabolic changes. Here, we show that morphine-tolerant mice exhibited distinct plasma metabolic signatures upon acute and chronic administration. We utilized a mouse model of morphine tolerance by exposing mice to increasing doses of the drug over 4 days. We collected plasma samples from mice undergoing acute or chronic morphine or saline injections and analyzed them using targeted GC–MS-based metabolomics to profile approximately 80 metabolites involved in the central carbon, amino acid, nucleotide, and lipid metabolism. Our findings reveal distinct alterations in plasma metabolite concentrations in response to acute or chronic morphine intake, and these changes were linked to the development of tolerance to morphine’s analgesic effects. We identified several metabolites that had been differentially affected by acute versus chronic morphine use, suggesting that metabolic changes may be mitigated by prolonged exposure to the drug. Morphine-tolerant mice showed a restoration of amino acid and glycolytic metabolites. Additionally, we conducted reconstructed metabolic network analysis on the first 30 VIP-ranked metabolites from the PLSDA of the saline, acute, and morphine-tolerant mice groups, which uncovered four interaction networks involving the amino acid metabolism, the TCA cycle, the glutamine-phenylalanine-tyrosine pathway, and glycolysis. These pathways were responsible for the metabolic differences observed following distinct morphine administration regimens. Overall, this study provides a valuable resource for future investigations into the role of metabolites in morphine-induced analgesia and associated effects following acute or chronic use in mice.
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Fecho, K., K. A. Maslonek, M. E. Coussons-Read, L. A. Dykstra, and D. T. Lysle. "Macrophage-derived nitric oxide is involved in the depressed concanavalin A responsiveness of splenic lymphocytes from rats administered morphine in vivo." Journal of Immunology 152, no. 12 (June 15, 1994): 5845–52. http://dx.doi.org/10.4049/jimmunol.152.12.5845.

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Abstract The present study examined the role of macrophage-derived nitric oxide in the suppressive effect of in vivo morphine administration on Con A-stimulated proliferation of splenic lymphocytes in rats. The results showed that concentrations of nitrite are significantly greater in Con A-stimulated splenocyte cultures from morphine-treated rats than in cultures from saline-treated rats, and that the depletion of macrophages from splenocyte cultures abolishes the suppressive effect of morphine on Con A-stimulated proliferation. Moreover, the addition of NG-monomethyl-L-arginine (NMMA) to Con A-stimulated splenocyte cultures attenuates the suppressive effect of morphine on mitogenic responsiveness. The addition of excess L-arginine to splenocyte cultures containing NMMA reverses the effect of NMMA and restores morphine's suppressive effect on Con A-stimulated proliferation, but the addition of D-arginine to splenocyte cultures containing NMMA does not restore the suppressive effect of morphine. Taken together, these findings demonstrate that the suppressive effect of in vivo morphine administration on Con A-stimulated proliferation of splenic lymphocytes involves macrophage-derived nitric oxide.
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Dissertations / Theses on the topic "Morphine"

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Sokolowska, Marta Siegel Shepard. "Pharmacological cues, morphine tolerance, and morphine withdrawal /." *McMaster only, 2004.

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Chapman, David John. "Analysis and pharmacokinetics of morphine and morphine-6-glucuronide." Thesis, University of Surrey, 1990. http://epubs.surrey.ac.uk/843031/.

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The behaviour of morphine and morphine glucuronides has been defined in an attempt to overcome the confusion surrounding the pharmacokinetics of morphine and the potential contribution of the active metabolite morphine-6-glucuronide (M6G), to the clinical effects observed after morphine treatment. Differential RIAs for the quantitation of morphine, M6G, and morphine-3-glucuronide (M3G) in a range of biological fluids have been developed. A specific M6G antiserum, suitable for use in an immunoassay, has been successfully raised. Pharmacokinetic parameters for morphine and M6G have been established in volunteers treated with morphine. Similar quantities of morphine and M6G were. observed after intravenous dosing. Bioavailabilities of enteral morphine preparations ranged between 19% and 24%. There was little difference between these routes with respect to the relative quantities of morphine and M6G measured, with quantities of M6G exceeding those of morphine by up to 7-fold. Data obtained following intravenous morphine, or M6G revealed similar elimination half-lives for both compounds. M6G was less widely distributed and not significantly bound by plasma proteins. Significant biliary concentrations of morphine and morphine glucuronides suggested the presence of an enterohepatic circulation, but no secondary plasma peaks or prolonged elimination half-lives were apparent. After systemic administration, significantly less M6G than morphine entered the central nervous system (CNS). In rats, the mean brain:serum ratios for morphine and M6G were 0.4:1 and 0.2:1 respectively. A mean cerebrospinal fluid (CSF):plasma morphine ratio of 0.9:1 was found in patients receiving intravenous morphine; no M6G was detected in the CSF. After oral morphine, mean CSF:plasma ratios were 0.6:1 and 0.3:1 for morphine and M6G respectively. A similar rate of disappearance from the CNS was observed for both morphine and M6G. Following intravenous M6G, the mean M6G CSF:plasma ratio was 0.1:1. Morphine was absent from the CSF and plasma indicating that the clinical effects observed are due to M6G alone.
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Hedegaard, Villesen Hanne. "Pharmacokinetic aspects of morphine, morphine-6-glucuronide and oxycodone /." Cph. : Department of Pharmacology and Pharmacotherapy, The Danish University of Pharmaceutical Sciences, 2006. http://www.farma.ku.dk/index.php/Hanne-Hedegaard-Villesen/3439/0/.

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Doduy, Marie. "Douleur et morphine." Paris 5, 1998. http://www.theses.fr/1998PA05P142.

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Klepstad, Pål. "Morphine for cancer pain." Doctoral thesis, Norwegian University of Science and Technology, Norwegian University of Science and Technology, 2002. http://urn.kb.se/resolve?urn=urn:nbn:no:ntnu:diva-1983.

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The objectives of the present study were:

I. To assess the effect from start of morphine treatment to cancer pain patients in respect to time needed for dose-finding, dose needed for pain control and adverse symptoms.

II. To assess the effects from start of morphine treatment to cancer pain patients on health related quality of life.

III. To compare the efficacy of start of morphine treatment with sustained vs. immediate release morphine.

IV. To investigate the relationship between serum concentrations of morphine, M6G and M3G and subjective symptoms during start of therapy and after long-term morphine administration.

V. To assess the feasibility of a Norwegian translation of the Brief Pain Inventory questionnaire.


Paper II reprinted with kind permission of Elsevier, sciencedirect.com
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Rutter, Dag Allenson. "The Pharmacogenetics of Morphine Metabolism." Thesis, Imperial College London, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.503842.

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Ellwood, Charles W. "A synthetic approach to morphine." Thesis, University of Southampton, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.252649.

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Lacy, Christopher. "The syntheses of morphine glycosides." Thesis, University of Bath, 1995. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.760686.

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Walker, Edward Hugh. "Strategic engineering of morphine dehydrogenase." Thesis, University of Cambridge, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.624817.

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French, Christopher E. "Biotransformations of the morphine alkaloids." Thesis, University of Cambridge, 1994. https://www.repository.cam.ac.uk/handle/1810/272997.

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Books on the topic "Morphine"

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Olive, M. Foster. Morphine. New York, NY: Chelsea House, 2011.

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Busse, Gregory D. Morphine. Philadelphia: Chelsea House Publishers, 2005.

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Bulgakov, Mikhail Afanasʹevich. Morphine. [Paris]: Gallimard, 2012.

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Vogel, Mikael. Morphine. Berlin: Frank, 2014.

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Parat, Marie-Odile, ed. Morphine and Metastasis. Dordrecht: Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-5678-6.

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Parat, Marie-Odile. Morphine and metastasis. Dordrecht: Springer, 2013.

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Courtney, Carol-Ann. Morphine and dolly mixtures. London: Penguin, 1991.

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Robinette, G. W. Did Lin Zexu make morphine? Valparaiso, Chile: Graffiti Militante Press, 2008.

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Dohoo, Susan. Pharmacokinetics of parentral morphine sulphate and oral sustained release morphine sulphate in dogs. Charlottetown: University of Prince Edward Island, 1991.

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Dohoo, Susan. Pharmacokinetics of parentral morphine sulphate and oral sustained release morphine sulphate in dogs. Ottawa: National Library of Canada, 1991.

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Book chapters on the topic "Morphine"

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Egan, Terrance M. "Morphine." In Abnormal States of Brain and Mind, 79–80. Boston, MA: Birkhäuser Boston, 1989. http://dx.doi.org/10.1007/978-1-4899-6768-8_35.

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Morgan, Michael M., MacDonald J. Christie, Thomas Steckler, Ben J. Harrison, Christos Pantelis, Christof Baltes, Thomas Mueggler, et al. "Morphine." In Encyclopedia of Psychopharmacology, 798. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_1760.

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Wilson, John Fawcett. "Morphine." In The Immunoassay Kit Directory, 1729–32. Dordrecht: Springer Netherlands, 1995. http://dx.doi.org/10.1007/978-94-011-0679-5_68.

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Kong, Ling-Lei, Jin-Hua Wang, and Guan-Hua Du. "Morphine." In Natural Small Molecule Drugs from Plants, 295–302. Singapore: Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-10-8022-7_49.

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de Groot, Anton C. "Morphine." In Monographs In Contact Allergy, 668–70. Boca Raton: CRC Press, 2022. http://dx.doi.org/10.1201/9781003158004-332.

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LaCaille, Lara, Anna Maria Patino-Fernandez, Jane Monaco, Ding Ding, C. Renn Upchurch Sweeney, Colin D. Butler, Colin L. Soskolne, et al. "Endogenous Morphine." In Encyclopedia of Behavioral Medicine, 686. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-1005-9_100557.

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Parat, Marie-Odile. "Morphine and Metastasis: From Bench to Bedside." In Morphine and Metastasis, 1–13. Dordrecht: Springer Netherlands, 2012. http://dx.doi.org/10.1007/978-94-007-5678-6_1.

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Johnson, Katherine N. H., Nurulain Zaveri, and Kalpna Gupta. "Interaction of Naloxone and Estrogen Receptor in Breast Cancer." In Morphine and Metastasis, 15–29. Dordrecht: Springer Netherlands, 2012. http://dx.doi.org/10.1007/978-94-007-5678-6_2.

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Koodie, Lisa, and Sabita Roy. "Morphine and Immunosuppression in the Context of Tumor Growth and Metastasis." In Morphine and Metastasis, 31–46. Dordrecht: Springer Netherlands, 2012. http://dx.doi.org/10.1007/978-94-007-5678-6_3.

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Lennon, Frances E., and Patrick A. Singleton. "Opioid Regulation of Vascular Integrity." In Morphine and Metastasis, 47–61. Dordrecht: Springer Netherlands, 2012. http://dx.doi.org/10.1007/978-94-007-5678-6_4.

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Conference papers on the topic "Morphine"

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Kuznetsov, Pavel E., Anna A. Gracheva, Vladimir A. Zlobin, Georgy V. Nazarov, Nina B. Kuznetsova, and Svetlana M. Rogacheva. "Optical properties of aqueous morphine solutions." In SPIE Proceedings, edited by Valery V. Tuchin. SPIE, 2003. http://dx.doi.org/10.1117/12.518858.

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"Sex differences in tolerance to morphine antinociception in intra-nucleus accumbens administration of morphine in rat." In International Conference on Medicine, Public Health and Biological Sciences. CASRP Publishing Company, Ltd. Uk, 2016. http://dx.doi.org/10.18869/mphbs.2016.58.

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Abdildin, Yerkin, Dinmukhammedali Narbayev, and Dmitriy Viderman. "Statistical Analysis of the Effect of Extended-Release Epidural Morphine Versus Morphine Sulfate on Postoperative Medical Outcomes." In 2023 IEEE International Conference on Smart Information Systems and Technologies (SIST). IEEE, 2023. http://dx.doi.org/10.1109/sist58284.2023.10223514.

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Gonzalez, Julio D. Zuarth, Alexandria K. Ragsdale, Sushobhan Mukhopadhyay, Christopher R. McCurdy, Lance McMahon, and Jenny L. Wilkerson. "Mitragynine Pretreatment Prevents Morphine-Induced Respiratory Depression." In ASPET 2023 Annual Meeting Abstracts. American Society for Pharmacology and Experimental Therapeutics, 2023. http://dx.doi.org/10.1124/jpet.122.261220.

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Png, Wen-Yang, Siew-Ying Mok, Pek-Yee Tang, Satoshi Ogawa, and Ishwar Parhar. "Morphine-induced Cognitive Dysfunction Model in Zebrafish." In 2020 IEEE-EMBS Conference on Biomedical Engineering and Sciences (IECBES). IEEE, 2021. http://dx.doi.org/10.1109/iecbes48179.2021.9398834.

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Trauner, Dirk, Johann Mulzer, Jan Bats, Stefanie Porth, and Till Opatz. "Total Synthesis of Morphine- and Hasubanane Alkaloids." In The 1st International Electronic Conference on Synthetic Organic Chemistry. Basel, Switzerland: MDPI, 1997. http://dx.doi.org/10.3390/ecsoc-1-02045.

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Nielsen, T. H., H. K. Nielsen, S. E. Husted, S. L. Hansen, and K. H. Olsen. "PLATELET FUNCTION AND ENDOCRINE STRESS RESPONSE DURING BUPIVACAINE EPIDURAL ANALGESIA. THE EFFECT OF MORPHINE ADDITION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644887.

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Platelet aggregation plays a central role in thromboembolism. Epidural analgesia can diminish the formation of deep venous thrombosis. In a randomized study twenty patients admitted to transartliroscopic meniscectomy were allocated to epidural analgesia with or without morphine epidurally. S-cortisol, s-thromboxane -B2(s-T2 B2) and platelet aggregation were measured before premedication, when epidural block extended from S3to T5, just before skin closure and exsufflation of tne thigh tourniquet, and the last sample was taken ten min after exsufflation. Aggregability was measured in platelet-rich plasma and expressed as the treshold concentration of collagen. Cortisol and T Bp were measured by RIA.S-cortisol decreased duringxanalgesia in the morphine group (p<o.o5), and during operation in both groups (p<o.o5) being significant lower in the morphine group (p<o.o5).S-TxB2 decreased significantly in the morphine group during analgesia, but there was no significant difference in s-TxB2 between the two groups. Treshold concentration of Collagen for aggregation of platelets showed an insignificant increase for both groups during analgesia, but did not differ between the two groups. Removal of the tourniquet did not influence any of the measurements. It is concluded that additionof morphine to bupivaca- ine epidural analgesia further decrease activity of the adrenocortical system, and the combined regime seems to inhibit platelet function in the same manner as monotherapy with local anaesthetics.
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DOSENKO, Victor. "WILL THERE BE HAPPINESS FROM MORPHINE-LIKE PEPTIDES OF MILK?" In Happiness And Contemporary Society : Conference Proceedings Volume. SPOLOM, 2021. http://dx.doi.org/10.31108/7.2021.20.

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The two types of milk are analysed: A2 milk, which is initial, natural and is considered to have no negative impact on human organism, and A1 milk that is a result of mutation and contains β-casein out of which a very active morphine receptor agonist derives. It is analysed how morphine peptides affect the “triangle of happiness” – brain areas responsible for experiencing happiness that are integrated in a Reward System. It is explicated that for experiencing happiness a human being needs social, psychological and other cultural factors that cannot be replaced by a mere consumption of morphinelike peptides with food and nutrients. Keywords: β-casein, β-casomorphine, morphine-like peptides, brain, happiness, Reward System, Anti-Reward System.
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"Aripiprazole effect on prolongation of morphine antinociception effect." In International Conference on Medicine, Public Health and Biological Sciences. CASRP Publishing Company, Ltd. Uk, 2016. http://dx.doi.org/10.18869/mphbs.2016.53.

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Rao, Jie, Xiaotong Gu, Jin Li, Zhichun Zhang, and Feifan Zhou. "Morphine-mediated abnormal neuronal activation boosts mitochondrial fragmentation." In Biophotonics and Immune Responses XVIII, edited by Wei R. Chen. SPIE, 2023. http://dx.doi.org/10.1117/12.2647093.

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Reports on the topic "Morphine"

1

Thomas, Thommey P., Baohua Huang, Ankur Desai, Hong Zong, Xue-Min Cheng, Alina Kotlyar, Pascale R. Leroueil, et al. Plasma-Mediated Release of Morphine from Synthesized Prodrugs. Fort Belvoir, VA: Defense Technical Information Center, January 2013. http://dx.doi.org/10.21236/ada577469.

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Yue, Lei, Guanzhang Mu, Zengmao Lin, and Haolin Sun. Impact of low-dose intrathecal morphine on orthopedic surgery: a protocol of a systematic review and meta-analysis of randomized controlled trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, February 2022. http://dx.doi.org/10.37766/inplasy2022.2.0029.

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Review question / Objective: Patients undergoing orthopedic surgery usually suffer considerably from peri-operative pain and intrathecal morphine (ITM) has recent been used as an effective analgesia method. The intrathecal morphine dose achieving optimal analgesia for orthopedic surgery while minimizing side effects has not yet been determined. There is currently a lack of literature synthesis in the safety and effects of low-dose ITM on orthopedic surgery. Condition being studied: Low-dose intrathecal morphine on orthopedic surgery. Information sources: We will search the following electronic databases, registries and websites on January 11th 2022, unrestricted by date. Grey literature and non-English studies will not be excluded. English Databases: PubMed, Cochrane library and Web of science. Chinese database: Cnki.net Trial registries: ClinicalTrials.gov.
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Kastin, Abba J. Facilitated Delivery of Endomorphins and Morphine into the CNS. Fort Belvoir, VA: Defense Technical Information Center, March 2001. http://dx.doi.org/10.21236/ada393979.

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Bossone, Carol A., and John P. Hannon. Metabolic Actions of Morphine in Conscious Chronically Instrumented Pigs,. Fort Belvoir, VA: Defense Technical Information Center, January 1991. http://dx.doi.org/10.21236/ada240344.

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Brown, Kelly J. Examination of Acute Sensitivity to Morphine and Morphine Self-Administration Following Physical and Environmental Stressors in Fischer-344 and Lewis Female Rats. Fort Belvoir, VA: Defense Technical Information Center, January 1997. http://dx.doi.org/10.21236/ad1011564.

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WolfvWolf, Anne, Matthias Unterberg, Andrea Witowski, Michael Adamzik, and Alexander Wolf. Efficacy and effectiveness of Oliceridine in acute postoperative pain, a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, January 2023. http://dx.doi.org/10.37766/inplasy2023.1.0063.

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Review question / Objective: Oliceridine is a relatively novel so called bias opioid which is approved for severe opioid requiring pain. Due to its biased agonism, it is said to have fewer side effects than conventional opioids. This systematic review and meta-analysis will analyze the efficacy and effectiveness of oliceridine compared to placebo or morphine in acute postoperative pain for up to 72 hours. This will be the first meta-analysis on this topic. Our aim with this work is to evaluate the clinical utility of this relatively new substance in a broad postoperative context. The lead questions of this systematic review and meta-analysis are: 1. Does Oliceridine demonstrate comparable analgesia to morphine with an improved side effect profile? 2. Does oliceridine demonstrate a superior analgesia compared to placebo with a comparable side effect profile? Transfered to PICOS, the study questions present as follows: Patients: Postoperative (up to 72hours) patients with moderate to severe pain Intervention: Oliceridine (TRV130) Comparison: Morphine and Placebo Outcome: Efficacy (pain reduction), effectiveness (side effects, adverse events) Study: Randomized controlled trials, at least single-blind.
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Lee, Che-Hung, Robert Brown, Elizabeth A. Jajane, and Hsiu-Ying T. Yang. Monoclonal Antibody to an Endogenous Neuropeptide with Putative Morphine-Modulating Activity. Fort Belvoir, VA: Defense Technical Information Center, December 1988. http://dx.doi.org/10.21236/ada205386.

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Polt, Robin. Glycopeptides as Analgesics: Non-Toxic Alternatives to Morphine for Combat Casualty Care. Fort Belvoir, VA: Defense Technical Information Center, December 2013. http://dx.doi.org/10.21236/ada594872.

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Qiu, Yan-Li, Jian Zu, and Yan Luo. Effect of butorphanol on morphine-related pruritus: a meta-analysis of randomized controlled trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, April 2022. http://dx.doi.org/10.37766/inplasy2022.4.0004.

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Mullins, Mary F., and Tori E. Pearce. Two Different Epidural Analgesic Combinations: Morphine vs. Fentanyl/Bupivacaine or Fentanyl/Ropivacaine and Their Post Operative Effects. Fort Belvoir, VA: Defense Technical Information Center, September 2001. http://dx.doi.org/10.21236/ad1012418.

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