Relevant bibliographies by topics / MAO B

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Academic literature on the topic 'MAO B'

Author: Grafiati
Published: 4 June 2021
Last updated: 25 April 2022

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Journal articles on the topic "MAO B"

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Hubálek, Frantisek, Claudia Binda, Ashraf Khalil, et al. "Demonstration of Isoleucine 199 as a Structural Determinant for the Selective Inhibition of Human Monoamine Oxidase B by Specific Reversible Inhibitors." Journal of Biological Chemistry 280, no. 16 (2005): 15761–66. http://dx.doi.org/10.1074/jbc.m500949200.

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Several reversible inhibitors selective for human monoamine oxidase B (MAO B) that do not inhibit MAO A have been described in the literature. The following compounds: 8-(3-chlorostyryl)caffeine, 1,4-diphenyl-2-butene, andtrans,trans-farnesol are shown to inhibit competitively human, horse, rat, and mouse MAO B withKivalues in the low micromolar range but are without effect on either bovine or sheep MAO B or human MAO A. In contrast, the reversible competitive inhibitor isatin binds to all known MAO B and MAO A with similar affinities. Sequence alignments and the crystal structures of human MAO B in complex with 1,4-diphenyl-2-butene or withtrans,trans-farnesol provide molecular insights into these specificities. These inhibitors span the substrate and entrance cavities with the side chain of Ile-199 rotated out of its normal conformation suggesting that Ile-199 is gating the substrate cavity. Ile-199 is conserved in all known MAO B sequences except bovine MAO B, which has Phe in this position (the sequence of sheep MAO B is unknown). Phe is conserved in the analogous position in MAO A sequences. The human MAO B I199F mutant protein of MAO B binds to isatin (Ki= 3 μm) but not to the three inhibitors listed above. The crystal structure of this mutant demonstrates that the side chain of Phe-199 interferes with the binding of those compounds. This suggests that the Ile-199 “gate” is a determinant for the specificity of these MAO B inhibitors and provides a molecular basis for the development of MAO B-specific reversible inhibitors without interference with MAO A function in neurotransmitter metabolism.
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Chaurasiya, Narayan, Jianping Zhao, Pankaj Pandey, Robert Doerksen, Ilias Muhammad, and Babu Tekwani. "Selective Inhibition of Human Monoamine Oxidase B by Acacetin 7-Methyl Ether Isolated from Turnera diffusa (Damiana)." Molecules 24, no. 4 (2019): 810. http://dx.doi.org/10.3390/molecules24040810.

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The investigation of the constituents that were isolated from Turnera diffusa (damiana) for their inhibitory activities against recombinant human monoamine oxidases (MAO-A and MAO-B) in vitro identified acacetin 7-methyl ether as a potent selective inhibitor of MAO-B (IC50 = 198 nM). Acacetin 7-methyl ether (also known as 5-hydroxy-4′, 7-dimethoxyflavone) is a naturally occurring flavone that is present in many plants and vegetables. Acacetin 7-methyl ether was four-fold less potent as an inhibitor of MAO-B when compared to acacetin (IC50 = 50 nM). However, acacetin 7-methyl ether was >500-fold selective against MAO-B over MAO-A as compared to only two-fold selectivity shown by acacetin. Even though the IC50 for inhibition of MAO-B by acacetin 7-methyl ether was ~four-fold higher than that of the standard drug deprenyl (i.e., SelegilineTM or ZelaparTM, a selective MAO-B inhibitor), acacetin 7-methyl ether’s selectivity for MAO-B over MAO-A inhibition was greater than that of deprenyl (>500- vs. 450-fold). The binding of acacetin 7-methyl ether to MAO-B was reversible and time-independent, as revealed by enzyme-inhibitor complex equilibrium dialysis assays. The investigation on the enzyme inhibition-kinetics analysis with varying concentrations of acacetin 7-methyl ether and the substrate (kynuramine) suggested a competitive mechanism of inhibition of MAO-B by acacetin 7-methyl ether with Ki value of 45 nM. The docking scores and binding-free energies of acacetin 7-methyl ether to the X-ray crystal structures of MAO-A and MAO-B confirmed the selectivity of binding of this molecule to MAO-B over MAO-A. In addition, molecular dynamics results also revealed that acacetin 7-methyl ether formed a stable and strong complex with MAO-B. The selective inhibition of MAO-B suggests further investigations on acacetin 7-methyl as a potential new drug lead for the treatment of neurodegenerative disorders, including Parkinson’s disease.
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Cho, Hyun-U., Sunpil Kim, Jeongeun Sim, et al. "Redefining differential roles of MAO-A in dopamine degradation and MAO-B in tonic GABA synthesis." Experimental & Molecular Medicine 53, no. 7 (2021): 1148–58. http://dx.doi.org/10.1038/s12276-021-00646-3.

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AbstractMonoamine oxidase (MAO) is believed to mediate the degradation of monoamine neurotransmitters, including dopamine, in the brain. Between the two types of MAO, MAO-B has been believed to be involved in dopamine degradation, which supports the idea that the therapeutic efficacy of MAO-B inhibitors in Parkinson’s disease can be attributed to an increase in extracellular dopamine concentration. However, this belief has been controversial. Here, by utilizing in vivo phasic and basal electrochemical monitoring of extracellular dopamine with fast-scan cyclic voltammetry and multiple-cyclic square wave voltammetry and ex vivo fluorescence imaging of dopamine with GRABDA2m, we demonstrate that MAO-A, but not MAO-B, mainly contributes to striatal dopamine degradation. In contrast, our whole-cell patch-clamp results demonstrated that MAO-B, but not MAO-A, was responsible for astrocytic GABA-mediated tonic inhibitory currents in the rat striatum. We conclude that, in contrast to the traditional belief, MAO-A and MAO-B have profoundly different roles: MAO-A regulates dopamine levels, whereas MAO-B controls tonic GABA levels.
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Chaurasiya, Narayan D., Francisco León, Yuanqing Ding, et al. "Interactions of Desmethoxyyangonin, a Secondary Metabolite fromRenealmia alpinia, with Human Monoamine Oxidase-A and Oxidase-B." Evidence-Based Complementary and Alternative Medicine 2017 (2017): 1–10. http://dx.doi.org/10.1155/2017/4018724.

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Renealmia alpinia(Zingiberaceae), a medicinal plant of tropical rainforests, is used to treat snakebites and other injuries and also as a febrifuge, analgesic, antiemetic, antiulcer, and anticonvulsant. The dichloromethane extract ofR. alpinialeaves showed potent inhibition of human monoamine oxidases- (MAOs-) A and B. Phytochemical studies yielded six known compounds, including pinostrobin1, 4′-methyl ether sakuranetin2, sakuranetin3, pinostrobin chalcone4, yashabushidiol A5, and desmethoxyyangonin6. Compound6displayed about 30-fold higher affinity for MAO-B than MAO-A, with Ki values of 31 and 922 nM, respectively. Kinetic analysis of inhibition and equilibrium-dialysis dissociation assay of the enzyme-inhibitor complex showed reversible binding of desmethoxyyangonin6with MAO-A and MAO-B. The binding interactions of compound6in the active site of the MAO-A and MAO-B isoenzymes, investigated through molecular modeling algorithms, confirmed preferential binding of desmethoxyyangonin6with MAO-B compared to MAO-A. Selective reversible inhibitors of MAO-B, like desmethoxyyangonin6,may have important therapeutic significance for the treatment of neurodegenerative disorders, such as Parkinson’s disease and Alzheimer’s disease.
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Billett, E. E., and R. J. Mayer. "Monoclonal antibodies to monoamine oxidase B and another mitochondrial protein from human liver." Biochemical Journal 235, no. 1 (1986): 257–63. http://dx.doi.org/10.1042/bj2350257.

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A monoclonal antibody has been generated to human liver monoamine oxidase (MAO) B by fusion of mouse myeloma cells with spleen cells from a mouse immunized with a mixture of semi-purified MAO A and MAO B. The antibody, 3F12/G10, an immunoglobulin G1, reacts with its antigen in cryostat sections of human liver, showing an intracellular particulate distribution as demonstrated by immunoperoxidase staining. The antibody indirectly precipitates [3H]pargyline-labelled human MAO B both from liver and platelet extracts but fails to precipitate MAO A from liver extracts. The antibody does not recognise rat liver MAO B, showing that the determinant is not universally expressed on MAO B. The antibody has no effect on the catalytic activity of MAO B. Other monoclonal antibodies were generated but they are directed to a protein with a subunit Mr of 54 000, a contaminant of the MAO preparation. One of these antibodies, A8/C2, an IgG2a, reacts with the same protein in both rat and human liver extracts.
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Ottawa, M., and N. Miyashita. "Interaction between PET tracer and the specific residues around the gate of the open form of Monoamine Oxidase B (MAO-B)." Journal of Physics: Conference Series 2207, no. 1 (2022): 012025. http://dx.doi.org/10.1088/1742-6596/2207/1/012025.

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Abstract Monoamine Oxidase B (MAO-B) is the enzyme that metabolizes a monoamine neurotransmitter. Recently, a PET tracer targeting MAO-B, SMBT-1, has been developed as the biomarker of neurodegenerative diseases. However, the detailed binding mode of SMBT-1 has not been clear. To clarify the binding mode of SMBT-1 on MAO-B, we performed the molecular dynamics (MD) simulations of MAO-B in the outer mitochondrial membrane and the complex of MAO-B to SMBT-1, and the docking simulation of MAO-B with SMBT-1. We found that the Leu88, Leu171, Ile199, and Tyr326 around the substrate-binding site interact with SMBT-1. These hydrophobic residues mainly support the two aromatic rings of the center of SMBT-1, making the stable binding of SMBT-1.
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Tan, Yu-Yan, Peter Jenner, and Sheng-Di Chen. "Monoamine Oxidase-B Inhibitors for the Treatment of Parkinson’s Disease: Past, Present, and Future." Journal of Parkinson's Disease 12, no. 2 (2022): 477–93. http://dx.doi.org/10.3233/jpd-212976.

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Monoamine oxidase-B (MAO-B) inhibitors are commonly used for the symptomatic treatment of Parkinson’s disease (PD). MAO-B inhibitor monotherapy has been shown to be effective and safe for the treatment of early-stage PD, while MAO-B inhibitors as adjuvant drugs have been widely applied for the treatment of the advanced stages of the illness. MAO-B inhibitors can effectively improve patients’ motor and non-motor symptoms, reduce “OFF” time, and may potentially prevent/delay disease progression. In this review, we discuss the effects of MAO-B inhibitors on motor and non-motor symptoms in PD patients, their mechanism of action, and the future development of MAO-B inhibitor therapy.
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Thorpe, L. W., K. N. Westlund, L. M. Kochersperger, C. W. Abell, and R. M. Denney. "Immunocytochemical localization of monoamine oxidases A and B in human peripheral tissues and brain." Journal of Histochemistry & Cytochemistry 35, no. 1 (1987): 23–32. http://dx.doi.org/10.1177/35.1.3025289.

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Monoamine oxidases (MAO; EC 1.4.3.4.) A and B occur in the outer mitochondrial membrane and oxidize a number of important biogenic and xenobiotic amines. Monoclonal antibodies specific for human MAO A or B and immunocytochemical techniques were used to visualize the respective enzymes in human placenta, platelets, lymphocytes, liver, brain, and a human hepatoma cell line. MAO A was observed in the syncytiotrophoblast layer of term placenta, liver, and a subset of neurons in brain, but was not observed in platelets or lymphocytes, which are known to lack type A enzyme. MAO B was observed in platelets, lymphocytes, and liver, but not in placenta, which contains little or no MAO B. MAO B was also observed in a subset of neurons in the brain that was distinct from that which contained MAO A. MAO A and MAO B were also observed in some glia. Unlike most tissues examined, liver cells appeared to contain both forms of the enzyme. These studies show that MAO A and MAO B can be specifically visualized by immunocytochemical means in a variety of human cells and tissues and can provide a graphic demonstration of the high degree of cell specificity of expression of the two forms of the enzyme.
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Çeçen, Muhammed, Jong Min Oh, Zeynep Özdemir, et al. "Design, Synthesis, and Biological Evaluation of Pyridazinones Containing the (2-Fluorophenyl) Piperazine Moiety as Selective MAO-B Inhibitors." Molecules 25, no. 22 (2020): 5371. http://dx.doi.org/10.3390/molecules25225371.

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Twelve pyridazinones (T1–T12) containing the (2-fluorophenyl) piperazine moiety were designed, synthesized, and evaluated for monoamine oxidase (MAO) -A and -B inhibitory activities. T6 was found to be the most potent MAO-B inhibitor with an IC50 value of 0.013 µM, followed by T3 (IC50 = 0.039 µM). Inhibitory potency for MAO-B was more enhanced by meta bromo substitution (T6) than by para bromo substitution (T7). For para substitution, inhibitory potencies for MAO-B were as follows: -Cl (T3) > -N(CH3)2 (T12) > -OCH3 (T9) > Br (T7) > F (T5) > -CH3 (T11) > -H (T1). T6 and T3 efficiently inhibited MAO-A with IC50 values of 1.57 and 4.19 µM and had the highest selectivity indices (SIs) for MAO-B (120.8 and 107.4, respectively). T3 and T6 were found to be reversible and competitive inhibitors of MAO-B with Ki values of 0.014 and 0.0071, respectively. Moreover, T6 was less toxic to healthy fibroblast cells (L929) than T3. Molecular docking simulations with MAO binding sites returned higher docking scores for T6 and T3 with MAO-B than with MAO-A. These results suggest that T3 and T6 are selective, reversible, and competitive inhibitors of MAO-B and should be considered lead candidates for the treatment of neurodegenerative disorders like Alzheimer’s disease.
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Chaurasiya, Narayan D., Haining Liu, Robert J. Doerksen, N. P. Dhammika Nanayakkara, Larry A. Walker, and Babu L. Tekwani. "Enantioselective Interactions of Anti-Infective 8-Aminoquinoline Therapeutics with Human Monoamine Oxidases A and B." Pharmaceuticals 14, no. 5 (2021): 398. http://dx.doi.org/10.3390/ph14050398.

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8-Aminoquinolines (8-AQs) are an important class of anti-infective therapeutics. The monoamine oxidases (MAOs) play a key role in metabolism of 8-AQs. A major role for MAO-A in metabolism of primaquine (PQ), the prototypical 8-AQ antimalarial, has been demonstrated. These investigations were further extended to characterize the enantioselective interactions of PQ and NPC1161 (8-[(4-amino-1-methylbutyl) amino]-5-[3, 4-dichlorophenoxy]-6-methoxy-4-methylquinoline) with human MAO-A and -B. NPC1161B, the (R)-(−) enantiomer with outstanding potential for malaria radical cure, treatment of visceral leishmaniasis and pneumocystis pneumonia infections is poised for clinical development. PQ showed moderate inhibition of human MAO-A and -B. Racemic PQ and (R)-(−)-PQ both showed marginally greater (1.2- and 1.6-fold, respectively) inhibition of MAO-A as compared to MAO-B. However, (S)-(+)-PQ showed a reverse selectivity with greater inhibition of MAO-B than MAO-A. Racemic NPC1161 was a strong inhibitor of MAOs with 3.7-fold selectivity against MAO-B compared to MAO-A. The (S)-(+) enantiomer (NPC1161A) was a better inhibitor of MAO-A and -B compared to the (R)-(−) enantiomer (NPC1161B), with more than 10-fold selectivity for inhibition of MAO-B over MAO-A. The enantioselective interaction of NPC1161 and strong binding of NPC1161A with MAO-B was further confirmed by enzyme-inhibitor binding and computational docking analyses. Differential interactions of PQ and NPC1161 enantiomers with human MAOs may contribute to the enantioselective pharmacodynamics and toxicity of anti-infective 8-AQs therapeutics.
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Dissertations / Theses on the topic "MAO B"

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Gretton, Heather Margaret. "Platelet monoamine oxidase type B (MAO-B) activity in psychopathy." Thesis, University of British Columbia, 1991. http://hdl.handle.net/2429/30619.

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Studies of platelet MAO-B activity have revealed a link between low platelet activity and psychiatric syndromes characterized by an inability to control impulses and to anticipate future consequences of behavior (Oreland, 1980; Gottfries, von Knorring, & Oreland, 1980). These characteristics are fundamental to the construct of psychopathy, and we might therefore expect that psychopathy is associated with low MAO activity. Indeed, some investigators have suggested that low platelet MAO-B activity is a potential marker for vulnerability to psychopathy (Schalling, Asberg, Edman, & Oreland, 1987). However, no study to date has directly examined the association between platelet MAO activity and psychometrically-sound indices of psychopathy. The present study measured platelet MAO-B activity in a sample of 54 male offenders, assessed with the Psychopathy Checklist-Revised (PCL-R; Hare, 1991). PCL-R scores were not significantly related to level of platelet MAO activity. The results are discussed in terms of methodological issues involved in conducting biochemical research.<br>Arts, Faculty of<br>Psychology, Department of<br>Graduate
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Anna, Gabriela da Silva Sant. "Efeito de 2-aril(heteroaril)-4,5-diidro-1h-imidazóis sobre a atividade da enzima monoamina oxidase in vitro." Universidade Federal de Santa Maria, 2008. http://repositorio.ufsm.br/handle/1/11095.

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior<br>Monoamine oxidase (MAO) is a flavin adenine dinucleotide (FAD)-containing enzyme attached to the mitochondrial outer membrane of neurons, glia, and other cells. Its roles include regulation of the levels of biogenic and xenobiotic amines in the brain and peripheral tissues by catalyzing their oxidative deamination. On the basis of their substrate and inhibitor specificities, two isoforms of MAO have been described (A and B). Due to their role in the metabolism of catecholamines neurotransmitters, MAO-A and MAO-B have long been of pharmacological interest. Accordingly, and reversible and irreversible inhibitors of MAO-A and MAO-B have been used in the clinics to treat neurological disorders including depression and Parkinson´s disease. Since the demonstration that I2- imidazoline sites are associated with mitochondrial membranes 15 years ago, several studies have provided evidence that these sites represent regions on MAOs. In line with this view, it has been demonstrated that imidazoline derivatives inhibit MAO activity. This effect has been attributed to a high affinity I2 binding site on MAO-B (I2B) and to a similar lower affinity site on MAO-A (I2A). This study investigated the effect of 4,5-dihydro-1H-imidazole-2-substituted compounds on MAO activity in vitro by spectrophotometric and fluorimetric methods using kynuramine as substrate. Among the compounds that inhibited MAO-A (3c-e, 3j), compound 3d was 73-fold more selective towards MAO-A than MAO-B. Among the compounds that selectively inhibited MAO-B (3g-I, 3k, 3o), imidazoline 3g was shown to be potent with Ki value of 5,3 μM. Some of compounds that selectively bind to I2-sites, such as 3l (benazoline), 3n (2-BFI), and 3p (BU224) showed good inhibitory activity especially against MAO-B. Imidazolines inhibited MAO-A and MAO-B activities in liver with less selectively than in rat brain. The compounds 3d and 3g reversibly inhibited MAO, and kinetics studies showed that compound 3d and 3g inhibited MAO in a mixed manner (decreased Vmax and increased Km values). These results confirm that imidazolines inhibit MAO activity and suggest a relationship between I2 binding site and modulation of central MAO<br>A monoamina oxidase (MAO) é uma enzima que contém o dinucleotídeo adenina-flavina (FAD) e que está presente na membrana externa da mitocôndria de células neuronais, glia e outras células. Seu papel inclui a regulação dos níveis de aminas biogênicas e xenobióticas no cérebro e em tecidos periféricos pela desaminação oxidativa. Com base na especificidade a substrato e inibidores, são descritas duas isoformas da MAO (A e B). Devido aos seus papéis no metabolismo das catecolaminas neurotransmissoras, a MAO-A e a MAO-B são consideradas farmacologicamente interessantes, e inibidores reversíveis e irreversíveis destas isoformas são usados clinicamente para tratar doenças neurológicas incluindo depressão e doença de Parkinson. Nos últimos 15 anos, desde a demonstração que sítios I2 estão associados com frações da membrana mitocondrial, muitos estudos provem evidências de que estes sítios representam regiões da MAO. Além disso, alguns estudos têm demonstrado que derivados imidazolínicos são capazes de inibir a atividade da MAO. Este efeito tem sido atribuído a sítios I2 de alta afinidade na MAO-B (I2B) e a um sítio similar de baixa afinidade na MAO-A (I2A). Assim, este estudo teve como objetivo investigar o efeito in vitro de compostos 4,5-diidro-1H-imidazol-2-substituídos sobre a atividade da enzima monoamina oxidase através de métodos espectrofotométricos e fluorimétricos usando quinuramina como substrato. Entre os compostos estudados que inibiram preferencialmente a MAO-A (3c-e, 3j) apenas o composto 3d foi seletivo, apresentando um Ki para a MAO-A de aproximadamente 73 vezes menor do que seu Ki para MAO-B. Entre os compostos obtidos que seletivamente inibiram MAO-B (3g-l, 3K, 3o), apenas a imidazolina 3g mostrou ser potente, com valores de Ki de 5,3 μM. Alguns compostos que exercem ligação potente e seletiva à sítios I2, como o 3l (benazolina), 3n (2-BFI) e 3p (BU224) mostraram boa atividade inibitória especialmente contra MAO-B. Em fígado de ratos, as imidazolinas inibiram com menos seletividade a MAO-A e MAO-B quando comparado com cérebro de ratos. Os compostos 3d e 3g inibiram a MAO de maneira reversível e apresentaram inibição de natureza mista (diminuindo o valor de Vmáx e aumentando o valor de Km) sobre a enzima MAO. Estes resultados confirmam que drogas imidazolinas podem inibir a atividade da MAO e sugerem uma relação entre sítios I2 e a modulação da atividade da enzima.
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Canto, Vanessa Petry do. "Estudo computacional das monoaminoxidases A e B com substratos e inibidores." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2014. http://hdl.handle.net/10183/97873.

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A monoaminoxidase (MAO) é uma enzima importante, que pode atuar como alvo terapêutico. Inibidores da MAO-A apresentam atividade no tratamento de distúrbios de humor, enquanto os inibidores seletivos da MAO-B tem uso, especialmente, no tratamento da Doença de Parkinson. O conhecimento das interações ENZIMA-INIBIDOR é importante no planejamento de fármacos. Nesse contexto, foram realizados estudos das enzimas MAO-A e MAO-B com diferentes ligantes, através da combinação das metodologias de docking, Dinâmica Molecular e Ensemble Docking. Foram escolhidos os ligantes derivados da 1,4-naftoquinona (1,4-NQ), lapachol, menadiona, norlapachol, A2, B2 e C2, os inibidores comerciais clorgilina (MAO-A) e selegilina (MAO-B) e os substratos naturais serotonina (MAO-A) e dopamina (MAO-B). Os resultados do docking mostraram interação de todos os ligantes com algum dos resíduos da "gaiola aromática" (FAD, Tyr407/Tyr444 para MAO-A, Tyr398/Tyr435 para MAO-B), uma importante região catalítica da MAO. Além disso, a seletividade observada experimentalmente da menadiona com a MAO-B também foi observada no docking. Através da DM, foi possível observar algumas diferenças conformacionais entre as estruturas da MAO-A e MAO-B, que podem explicar a seletividade entre as duas isoformas, como por exemplo, distâncias entre resíduos do sítio ativo e ligações de hidrogênio. A partir do Ensemble Docking, foi verificado que a conformação do receptor influencia significativamente o escore das interações ENZIMA+LIGANTE para ligantes volumosos.<br>Monoamine oxidase (MAO) is an important enzyme that acts as therapeutic target. MAO-A inhibitors show pharmacological activity in the treatment of mood disorders, whereas MAO-B inhibitors are used especially in treatment of Parkinson's Disease. Knowledge of enzyme-inhibitor interactions is important in drug design. Therefore, studies of MAO-A and MAO-B enzymes with different ligands were performed by combining docking, Molecular Dynamics and Ensemble Docking methodologies. Ligands derived from 1,4-naphthoquinone, lapachol, menadione, nor-lapachol, A2, B2, C2, commercial inhibitors clorgyline (MAO-A) and selegiline (MAO-B) and the natural substrates serotonin (MAO-A) and dopamine (MAO-B) were chosen. The docking results shows interactions of all ligands with some residue of the "aromatic cage” (FAD cofactor, Tyr407/Tyr444 for MAO-A and Tyr398/Tyr435 for MAO-B), an important catalytic region of MAO. Furthermore, the experimentally observed selectivity of menadione with MAO-B was also observed by Docking. In Molecular Dynamics results, conformational differences were observed between MAO-A and MAO-B structures, which could explain the selectivity observed between isoforms, e.g. distances between residues of the active site and hydrogen bonds. Ensemble Docking results shows that the conformation of the receptor significantly influence the score of ENZYME+LIGAND interactions for bulky ligands.
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Wargelius, Hanna-Linn. "The Relation between Serotonergic Biomarkers and Behaviour : – studies on human primates, non-human primates and transgenic mice." Doctoral thesis, Uppsala universitet, Farmakologi, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-151870.

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Rationale: The serotonergic system is involved in the modulation of emotion and plays an important role for personality and vulnerability for psychiatric disorders. In the papers included in this thesis, we investigate three biological factors that have been studied in relation to psychiatric symptoms: Platelet monoamine oxidase B (MAO-B) activity, and variations in the MAO-A and the serotonin transporter (5HTT) genes. We also study intensity dependent auditory evoked potentials (IAEP) as an intermediate phenotype for serotonergic capacity. Platelet MAO-B has been shown to be a biological marker for the properties of monoamine systems, with low activity being associated with vulnerability for high scores of sensation seeking, monotony avoidance, and impulsiveness, as well as for susceptibility for alcoholism. Functional polymorphisms in the promoter of the genes encoding MAO-A and the serotonin transporter result in high- or low- activity alleles that have been associated with numerous psychiatric symptoms. One hypothesis for the shaping of personality is that these genotype variants have prenatal effects on the wiring of the brain. Thus, exploring how the development of the brain is affected by different prenatal serotonin levels is relevant in this context. Observations: (i) Platelet MAOB activity was associated with monoamine metabolites in cerebrospinal fluid from cisterna magna in monkeys, as well as with voluntary alcohol intake, alcohol-induced aggression, and alcohol sensitivity. (ii) The long 5HTTLPR allele was associated with increased IAEP. (iii) The functional MAOA and 5HTT polymorphisms were associated with symptoms of ADHD-related traits in a population based sample of Swedish adolescents. Associations of these candidate genes with ADHD scores were strenghtened when the platelet MAOB activity was combined with genotype. (iv) Our pilot data showed that treatment of pregnant mice with 5HTT blocking antidepressives resulted in more serotonergic cellbodies in lateral wings of dorsal raphe in the offspring, when compared to saline treatment. Conclusions: Our studies support the notion that platelet MAOB activity and IAEP are endophenotypes for monoaminergic capacity and related behaviours. The functional candidate polymorphisms in MAOA and 5HTT were linked to behaviour, however, the cause-relationship is unclear and the explanation for the associations need to be further investigated, possibly with focus on prenatal effects of the polymorphisms.
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Senini, Vincent Wally James. "MAO-B inhibitors protect against lipopolysaccharide-mediated epithelial barrier loss and cytokine release." Thesis, University of British Columbia, 2011. http://hdl.handle.net/2429/36429.

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Epithelial tissues play a critical role in maintaining systemic health by establishing a functional barrier that separates the external environment from the host to provide an innate defense against environmental insult. Epithelial barrier disruption is suspected to play a central role in the onset of chronic inflammatory disease, although, fundamental knowledge of the underlying pathogenesis remains poorly understood. Thus, identifying factors that mediate epithelial barrier loss is clinically relevant as it will open the possibility that novel interventional strategies may be developed to mitigate early disease-associated signaling events. Lipopolysaccharide (LPS) is a Gram-negative bacterial virulence factor implicated in periodontal disease onset. Amphiregulin (AR) is a ligand for the epidermal growth factor receptor (EGFR) and downstream mediator of tumor necrosis factor-alpha (TNF-α) (Chokki et al., 2006) that is normally sequestered at cell-cell contacts in stable epithelial barriers. AR and corresponding signaling components modulating the EGFR pathway are altered in a rat model of periodontal disease that exhibited concomitant altered barrier architecture (Fujita et al., 2011; Firth et al., 2011). Treatment of this model with monoamine oxidase (MAO) inhibitors ameliorated disease indices (Ekuni et al., 2009). This study employs an in vitro histiotypic model of epithelium to provide evidence that LPS-reduced epithelial barrier function associated with chronic inflammatory disease may be mediated by altered AR and TNF-α secretion. MAO-B inhibition by (−)-deprenyl enhanced barrier model transepithelial electrical resistance (TER), prevented LPS-, AR- and H₂O₂-induced reduction in TER and attenuated LPS-induced AR and TNF-α secretion and H₂O₂-induced AR secretion. Furthermore, immunostaining of barrier model cultures showed that markers of cell-cell junctions were altered by LPS challenge and treatment of the model with (−)-deprenyl protects against this disruption. This study addresses the underlying mechanism by which (−)-deprenyl protects against bacterial virulence factor-induced epithelial barrier disruption and points to a significant role for AR as a central mediator of barrier integrity. Ultimately, this project aims to provide in vitro evidence for the efficacy of (−)-deprenyl treatment of LPS-induced epithelial barrier disruption, which may promote development of enhanced MAO-B inhibitors and lead to an effective clinical treatment for disease-associated epithelial barrier loss.
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Pazini, Andreia Martini. "SELEGILINA REVERTE A PIORA DA MEMÓRIA INUZIDA POR Aβ25-35 EM CAMUNDONGOS: ENVOLVIMENTO DA ATIVIDADE DA MAO-B". Universidade Federal de Santa Maria, 2013. http://repositorio.ufsm.br/handle/1/8996.

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Conselho Nacional de Desenvolvimento Científico e Tecnológico<br>Alzheimer s disease (AD) is biochemically characterized by the occurrence of extracellular deposits of amyloid beta peptide (Aβ) and intracellular deposits of the hyperphosphorylated tau protein, which are causally related to the pathological hallmarks senile plaques and neurofibrillary tangles. Monoamine oxidase B (MAO-B) activity, an enzyme involved in the oxidation of biogenic monoamines, is particularly high around the senile plaques and increased in AD patients in middle to late clinical stages of the disease. Selegiline, a selective and irreversible MAO-B inhibitor, improves learning and memory in AD patients. Notwithstanding, its mechanism of action is still not completely known. The current study aimed to investigate whether selegiline improves the Aβ25-35 induced cognitive deficit in the object recognition task in mice. In addition, we investigated whether selegiline alters MAO-B and MAO-A activities in the hippocampus, perirhinal and remaining cerebral cortices of Aβ25-35-injected mice. Acute (1 and 10 mg/kg, p.o., immediately post-training) and subchronic (10 mg/kg, p.o., seven days after Aβ25-35 injection and immediately post-training) administration of selegiline reversed the cognitive impairment induced by Aβ25-35 (3 nmol, i.c.v.). Acute administration of selegiline (1 mg/kg, p.o.) in combination with Aβ25-35 (3 nmol) decreased MAO-B activity in the perirhinal and remaining cerebral cortices. Acute administration of selegiline (10 mg/kg, p.o.) decreased MAO-B activity in hippocampus, perirhinal and remaining cerebral cortices, regardless of Aβ25-35 or Aβ35-25 treatment. MAO-A activity was not altered by selegiline or Aβ25-35. In summary, the current findings further support a role for MAO-B in the cognitive deficits observed in AD.<br>A doença de Alzheimer (DA) é bioquimicamente caracterizada por depósitos extracelulares de peptídeo beta amiloide (Aβ) e de proteína tau hiperfosforilada, que são causalmente relacionadas com as características patológicas, placas neuríticas e emaranhados neurofibrilares. A atividade da monoamina oxidase B (MAO-B), uma enzima envolvida na oxidação de monoaminas biogênicas, é particularmente elevada ao redor das placas senis e aumenta nos pacientes com DA em estágios clínicos de moderado a grave. A selegilina, um inibidor seletivo e irreversível da MAO-B, é relatada por melhorar a memória e o aprendizado em pacientes com DA. Porém, seu mecanismo de ação ainda não é completamente conhecido. O presente estudo teve como objetivo investigar se a selegilina melhora o déficit cognitivo induzido por Aβ25-35. na tarefa de reconhecimento de objetos em camundongos. Além disso, investigou-se a atividade da MAO-A e da MAO-B no hipocampo, no córtex cerebral e no córtex perirrinal de camundongos injetados com Aβ25-35 e com selegilina. Administração aguda (1 e 10 mg/kg, p.o., imediatamente pós-treino) e subcrônica (10 mg/kg, p.o., por sete dias depois da injeção do Aβ25-35 e imediatamente pós-treino) de selegilina preveniu o prejuízo da memória induzido pelo Aβ25-35 (3 nmol, icv). A administração aguda de selegilina (1 mg/kg, p.o.) em combinação com Aβ25-35 (3 nmol) diminuiu a atividade da MAO-B no córtex perirrinal e córtex cerebral. A administração aguda de selegilina (10 mg/kg, p.o.) diminuiu a atividade da MAO-B no hipocampo, no córtex cerebral e no córtex perirrinal independentemente da presença de Aβ25-35. A atividade da MAO-A não foi alterada pelo tratamento com selegilina ou Aβ25-35 em nenhuma das estruturas estudadas. Em resumo, os dados atuais suportam um papel adicional para a MAO-B no déficit cognitivo observado na DA.
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Palmer, Sonya Lenette Jr. "The Investigation of the Active Sites of Monoamine Oxidase (MAO) A and B and the Study of MAO-A Mediated Neurotoxicity Using 4-Substituted Tetrahydropyridines." Diss., Virginia Tech, 1998. http://hdl.handle.net/10919/30611.

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The mitochondrial membrane bound flavoenzymes monoamine oxidase A and B (MAO-A and MAO-B) catalyze the a-carbon oxidation of a variety of amines including neurotransmitters such as dopamine and serotonin. Although the primary structures of these enzymes have been established from the corresponding gene sequences, relatively little is known regarding the structural features of the active sites which lead to the selectivities observed with various substrates and inhibitors. In spite of many efforts, these enzymes have not been crystallized. In the absence of X-ray structures, the design, synthesis, and evaluation of biological activity remain the only way to assess a view of the active sites, through SAR and QSAR studies. The excellent MAO-A and/or B substrate and inhibitor properties of various 1,4-disubstituted-1,2,3,6-tetrahydropyridine derivatives offer an interesting opportunity to probe the active sites of MAO-A and MAO-B. In an effort to explore the spatial features of the active sites, we have synthesized series of substituted tetrahydropyridines, evaluated their biological activity with purified MAO-A and MAO-B, and carried out a topological analysis of the MAO active sites using molecular modeling. In addition, the results described in this thesis provide evidence that the MAO-A and MAO-B active sites differ in shape, regions of activity, and areas that tolerate polar interactions. The role of MAO in neurodegenerative processes such as Parkinson's Disease has been recognized for some time. The structurally unique parkinsonian inducing substrate 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is bioactivated to neurotoxic metabolites. The mechanism of neurotoxicity has been studied extensively and it is known that MAO-B catalyzes the conversion of MPTP to the 2,3-dihydro-1-methyl-4-phenylpyridinium species (MPDP+) which undergoes further oxidation to the neurotoxic metabolite 1-methyl-4-phenyl pyridnium (MPP+). However, the role of MAO-A in mediating a neurotoxic response, has not been fully defined due to the lack of selective MAO-A substrates. In this thesis, we have investigated the neurotoxic potential of several tetrahydropyridines in C57Bl/6 mice and the ability of selective inhibitors to protect against the expression of MAO mediated neurotoxicity.<br>Ph. D.
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Poesch, Axel [Verfasser]. "Auswirkungen der pharmakologischen MAO-B-Inhibition auf die murine Herzfunktion bei Doxorubicin-induzierter Kardiomyopathie / Axel Poesch." Greifswald : Universitätsbibliothek Greifswald, 2014. http://d-nb.info/1054017840/34.

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Aliyu, S. U. "Biochemical pharmacology of acute ethanol intoxication and activation of MAO-B : Behavioural, physiological and biochemical implications." Thesis, Cardiff University, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.384146.

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Mao, Lujia [Verfasser], Todd B. [Gutachter] Marder, and Kálmán J. [Gutachter] Szabó. "Transition Metal-Catalyzed Construction of Benzyl/Allyl sp3 and Vinyl/Allenyl sp2 C-B Bonds / Lujia Mao ; Gutachter: Todd B. Marder, Kálmán J. Szabó." Würzburg : Universität Würzburg, 2018. http://d-nb.info/116957288X/34.

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Books on the topic "MAO B"

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guan, Shanghai bo wu, and Shanghai bo wu guan, eds. Hai fan liu zong: Helan Nihanke juan zeng Ming Qing mao yi ci / Shanghai bo wu guan = Traces of the trade : Chinese export porcelain donated by Henk B. Nieuwenhuys / Shanghai Museum. Shanghai shu hua chu ban she, 2009.

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Andrew, Davies. B. Monkey. Miramax Books, 1997.

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Andrew, Davies. B. Monkey. Lime Tree, 1992.

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Andrew, Davies. B. Monkey. Minerva, 1993.

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The man who deciphered Linear B: The story of Michael Ventris. Thames & Hudson, 2002.

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Un-jin, Yi, Chʻoe Sŏg-wŏn, and Wang Haijuan, eds. Wo de B xing nan you: My boyfriend is type-B. Da tian chu ban you xian gong si, 2005.

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Park, Barbara. Junie B., first grader: One-man band. Random House, 2003.

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ill, Brunkus Denise, ed. Junie B., first grader: One-man band. Random House, 2003.

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DePalo, Anna. The billionaire in penthouse B. Silhouette Books, 2008.

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Heinold, Wolfgang Ehrhardt. B"ucher und Buchh"andler: Was man vom Einzelhandel mit B"uchern wissen sollte. 2nd ed. Decker & M"uller, 1990.

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Book chapters on the topic "MAO B"

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Morgan, Michael M., MacDonald J. Christie, Thomas Steckler, et al. "MAO-B Inhibitor." In Encyclopedia of Psychopharmacology. Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_949.

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Gerlach, M., P. Riederer, and P. A. Fischer. "MAO-B-Hemmer." In Neuro-Psychopharmaka. Springer Vienna, 1992. http://dx.doi.org/10.1007/978-3-7091-3330-9_6.

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Saura Marti, J., R. Kettler, M. Prada, and J. G. Richards. "Molecular neuroanatomy of MAO-A and MAO-B." In Amine Oxidases and Their Impact on Neurobiology. Springer Vienna, 1990. http://dx.doi.org/10.1007/978-3-7091-9113-2_5.

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Polymeropoulos, E. E. "l-Deprenyl: A Unique MAO-B Inhibitor." In Inhibitors of Monoamine Oxidase B. Birkhäuser Basel, 1993. http://dx.doi.org/10.1007/978-3-0348-6348-3_5.

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Gerlach, M., P. Riederer, and M. B. H. Youdim. "The Mode of Action of MAO-B Inhibitors." In Inhibitors of Monoamine Oxidase B. Birkhäuser Basel, 1993. http://dx.doi.org/10.1007/978-3-0348-6348-3_9.

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Gaál, J., and I. Hermecz. "Medicinal Chemistry of Present and Future MAO-B Inhibitors." In Inhibitors of Monoamine Oxidase B. Birkhäuser Basel, 1993. http://dx.doi.org/10.1007/978-3-0348-6348-3_4.

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Wessel, K. "MAO-B Inhibitors in Neurological Disorders with Special Reference to Selegiline." In Inhibitors of Monoamine Oxidase B. Birkhäuser Basel, 1993. http://dx.doi.org/10.1007/978-3-0348-6348-3_13.

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LeWitt, P. A. "Neuroprotective Effects of MAO-B Inhibition: Clinical Studies in Parkinson’s Disease." In Inhibitors of Monoamine Oxidase B. Birkhäuser Basel, 1993. http://dx.doi.org/10.1007/978-3-0348-6348-3_15.

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Da Prada, M., G. Zürcher, and R. Kettler. "Therapieoptimierung mit Madopar HBS und MAO B-Hemmer." In L-Dopa-Substitution der Parkinson-Krankheit. Springer Vienna, 1985. http://dx.doi.org/10.1007/978-3-7091-8822-4_13.

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Laux, G. "Do MAO-B Inhibitors Have Any Role in the Treatment of Depression?" In Inhibitors of Monoamine Oxidase B. Birkhäuser Basel, 1993. http://dx.doi.org/10.1007/978-3-0348-6348-3_17.

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Conference papers on the topic "MAO B"

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Castillo, Jimmy A., Jannett Hung, M. Rodriguez, E. Bastidas, I. Laboren, and A. Jaimes. "Direct led-fluorescence method for Mao-B inactivation in the treatment of Parkinson's." In SPIE Proceedings, edited by Aristides Marcano O. and Jose Luis Paz. SPIE, 2004. http://dx.doi.org/10.1117/12.590947.

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Kushiyama, Kumiko, Yuya Kikukawa, Tetsuaki Baba, Paul Haimes, and Shinji Sasada. "Mag-B." In ACM SIGGRAPH 2014 Studio. ACM Press, 2014. http://dx.doi.org/10.1145/2619195.2656327.

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Avvenuti, Marco, and Alessio Vecchio. "Adaptability in the B-MAC+ Protocol." In 2008 IEEE International Symposium on Parallel and Distributed Processing with Applications (ISPA). IEEE, 2008. http://dx.doi.org/10.1109/ispa.2008.82.

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Costa, Sidonie Fernandes. "“B-MAT@PLICADA”: A B-LEARNING MATHEMATICS COURSE IN HIGHER EDUCATION." In 10th annual International Conference of Education, Research and Innovation. IATED, 2017. http://dx.doi.org/10.21125/iceri.2017.2497.

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Windhorst, R., S. Odewahn, S. Cohen, et al. "The HST/WFPC2 B-band galaxy counts vs. type for 19≲B≲29 mag." In The ultraviolet universe at low and high redshift. AIP, 1997. http://dx.doi.org/10.1063/1.53796.

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Grøne, Ole. "Advanced MAN-B & amp;W Engine Development." In SAE Government Industry Meeting and Exposition. SAE International, 1985. http://dx.doi.org/10.4271/851220.

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Lucas, Keith. "B-MAC — A Transmission Standard for PAY DBS." In SMPTE Television Conference. IEEE, 1985. http://dx.doi.org/10.5594/m00803.

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Bartholoma¨, Klaus. "TCA: MAN B&W Diesel’s New Turbocharger Generation." In ASME 2003 Internal Combustion Engine Division Spring Technical Conference. ASMEDC, 2003. http://dx.doi.org/10.1115/ices2003-0692.

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MAN B&amp;W Diesel’s proven NA/S and /T9 turbocharger generation has been successfully in the market for approximately 10 years. Early in 2000, MAN B&amp;W Diesel decided to meet the increased demands of the engine manufacturers by developing a new turbocharger generation. The investigations of the two prototype TCA77 turbochargers were already started in the middle of 2001 on the burner rig test bed and afterwards on the engine. This abstract gives an overview about the development targets and shows the TCA turbocharger programme. The design details are explained with special attention to the design features of the compressor, the turbine and the bearing concept. This paper explains MAN B&amp;W’s new containment safety concept applied to the TCA generation and shows the results of the investigations with regard to noise emissions and efficiencies.
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Bonnot-Courtois, Chantal, and Louis-Robert Lafond. "Défense contre la mer à Saint-Malo par réhabilitation de la plage." In Journées Nationales Génie Côtier - Génie Civil. Presses Universitaires de Perpignan, 1994. http://dx.doi.org/10.5150/jngcgc.1994.036-b.

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Bdiri, Sadok, Faouzi Derbel, and Olfa Kanoun. "Wireless sensor nodes using energy harvesting and B-Mac protocol." In 2013 10th International Multi-Conference on Systems, Signals & Devices (SSD). IEEE, 2013. http://dx.doi.org/10.1109/ssd.2013.6564160.

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Reports on the topic "MAO B"

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Aeromagnetic total field map, 64D/4a,b, Saskatchewan. Natural Resources Canada/ESS/Scientific and Technical Publishing Services, 1985. http://dx.doi.org/10.4095/120516.

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Aeromagnetic total field map, 64D/5a,b, Saskatchewan. Natural Resources Canada/ESS/Scientific and Technical Publishing Services, 1985. http://dx.doi.org/10.4095/120518.

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Aeromagnetic total field map, 74A/1a,b, Saskatchewan. Natural Resources Canada/ESS/Scientific and Technical Publishing Services, 1985. http://dx.doi.org/10.4095/120522.

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Aeromagnetic total field map, 74A/8a,b, Saskatchewan. Natural Resources Canada/ESS/Scientific and Technical Publishing Services, 1985. http://dx.doi.org/10.4095/120524.

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Aeromagnetic total field map, 64C/12a,b, Manitoba. Natural Resources Canada/ESS/Scientific and Technical Publishing Services, 1985. http://dx.doi.org/10.4095/120529.

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Aeromagnetic total field map, 64B/11a,b, Manitoba. Natural Resources Canada/ESS/Scientific and Technical Publishing Services, 1985. http://dx.doi.org/10.4095/120538.

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Aeromagnetic total field map, 64B/5a,b, Manitoba. Natural Resources Canada/ESS/Scientific and Technical Publishing Services, 1985. http://dx.doi.org/10.4095/120549.

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Aeromagnetic total field map, 64B/12a,b, Manitoba. Natural Resources Canada/ESS/Scientific and Technical Publishing Services, 1985. http://dx.doi.org/10.4095/120551.

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Aeromagnetic vertical gradient map, Saskatchewan [64D/4a,b]. Natural Resources Canada/ESS/Scientific and Technical Publishing Services, 1985. http://dx.doi.org/10.4095/120556.

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Aeromagnetic vertical gradient map, Saskatchewan [74A/1a,b]. Natural Resources Canada/ESS/Scientific and Technical Publishing Services, 1985. http://dx.doi.org/10.4095/120561.

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