Relevant bibliographies by topics / Agoniste - Antagoniste

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Academic literature on the topic 'Agoniste - Antagoniste'

Author: Grafiati
Published: 4 June 2021
Last updated: 6 February 2022

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Journal articles on the topic "Agoniste - Antagoniste"

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Carpenter, A., J. Duchateau, and K. Hainaut. "Signification Fonctionnelle de la Coactivation Agoniste-Antagoniste Dans Les Mouvements Rapides de Flexion Plantaire." Archives of Physiology and Biochemistry 103, no. 3 (January 1, 1995): C133. http://dx.doi.org/10.3109/13813459509037341.

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Schwartz, Jean-Charles, Jeanne-Marie Lecomte, and Christian Caussé. "Efficacité anticataplectique de pitolisant, nouvel antagoniste/agoniste inverse du récepteur H3 de l’histamine chez des patients narcoleptiques." Médecine du Sommeil 14, no. 1 (March 2017): 48. http://dx.doi.org/10.1016/j.msom.2017.01.091.

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Pai, Howard Huaihan, Tom Pickles, Mira Keyes, Stuart Jones, Rachel E. McDonald, Mary Lesperance, and Eric Berthelet. "Randomized study evaluating testosterone recovery using short-versus long-acting luteinizing hormone releasing hormone agonists." Canadian Urological Association Journal 5, no. 3 (April 4, 2013): 173. http://dx.doi.org/10.5489/cuaj.639.

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Introduction: We sought to compare the rate of return of testosteronelevels and sexual function in men with prostate cancerreceiving longer acting, 3-month preparation of luteinizing hormone-releasing hormone agonist (L-LHRH-A) versus shorter acting,1-month preparation of luteinizing hormone-releasing hormoneagonist (S-LHRH-A).Methods and Materials: Men with low to intermediate risk localizedprostate cancer were randomized to either L-LHRH-A (2-3 monthduration LHRH-A) or S-LHRH-A (6-1 month duration LHRH-A) ofandrogen suppression therapy (AST) and prostate brachytherapyusing iodine-125 radioisotopes. Serum total testosterone levels andPSA were recorded every 2 months for 2 years.Results: A planned target sample size of 100 was not achieveddue to insufficient accrual. A total of 55 patients were randomizedand 46 were used for analysis. The median time to recovery oftestosterone to baseline levels (calculated from end of AST) was 8and 4 months in the L-LHRH-A and S-LHRH-A arms, respectively(p = 0.268). The median time to testosterone recovery to lower limitof reference range was 4 and 2 months respectively (p = 0.087).Interpretation: This randomized study, which failed to reachaccrual target, showed a trend towards more rapid recovery oftestosterone levels using shorter acting LHRH-A. Another randomizedstudy would be required to validate these findings. Currently,there is insufficient evidence to recommend the use of shorteracting LHRH-A as a means of providing more rapid recovery oftestosterone levels.Introduction : Nous avons voulu comparer la vitesse de retourdes taux de testostérone et de la fonction sexuelle chez des hommesatteints d’un cancer de la prostate recevant un agoniste de laLHRH à longue durée d’action pendant 3 mois ou un agoniste dela LHRH à courte durée d’action pendant 1 mois.Matériel et méthodologie : Des hommes atteints d’un cancer dela prostate localisé avec risque faible à intermédiaire ont été randomiséspour recevoir soit un agoniste de la LHRH à longue duréed’action (2 doses trimestrielles) soit un antagoniste de la LHRHà courte durée d’action (6 doses mensuelles) comme traitementantiandrogène et une brachythérapie prostatique avec des radioisotopesde l’iode 125. Les taux sériques de testostérone totale etd’APS ont été notés tous les 2 mois pendant 2 ans.Résultats : L’échantillon prévu au départ de 100 patients n’apu être obtenu en raison d’un recrutement insuffisant. Au total,55 patients ont été randomisés et 46 ont été inclus dans les analyses.L’intervalle médian de retour à des taux normaux de testostérone(calculés à partir de la fin du traitement antiandrogène) étaitde 8 et 4 mois dans les groupes sous agoniste de la LHRH à longueet à courte durée d’action, respectivement (p = 0,268). L’intervallemédian requis pour que les taux de testostérone atteignent la limiteinférieure des valeurs de référence était de 4 et 2 mois, respectivement(p = 0,087).Interprétation : Cette étude randomisée, où on n’a pas réussi àobtenir le nombre de patients voulu, a montré une tendance vers unretour plus rapide des taux de testostérone avec un traitement paragoniste de la LHRH à courte durée d’action. Une autre étude randomiséeserait nécessaire pour valider ces résultats. Actuellement,on ne dispose pas de suffisamment de données pour recommanderun agoniste de la LHRH à courte durée d’action comme moyenpour ramener les taux de testostérone plus rapidement à la normale.
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Schlezinger, Jennifer J., Wendy Heiger-Bernays, and Thomas F. Webster. "Predicting the Activation of the Androgen Receptor by Mixtures of Ligands Using Generalized Concentration Addition." Toxicological Sciences 177, no. 2 (July 8, 2020): 466–75. http://dx.doi.org/10.1093/toxsci/kfaa108.

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Abstract Concentration/dose addition is widely used for compounds that act by similar mechanisms. But it cannot make predictions for mixtures of full and partial agonists for effect levels above that of the least efficacious component. As partial agonists are common, we developed generalized concentration addition, which has been successfully applied to systems in which ligands compete for a single binding site. Here, we applied a pharmacodynamic model for a homodimer receptor system with 2 binding sites, the androgen receptor, that acts according to the classic homodimer activation model: Each cytoplasmic monomer protein binds ligand, undergoes a conformational change that relieves inhibition of dimerization, and binds to DNA response elements as a dimer. We generated individual dose-response data for full (dihydroxytestosterone, BMS564929) and partial (TFM-4AS-1) agonists and a competitive antagonist (MDV3100) using reporter data generated in the MDA-kb2 cell line. We used the Schild method to estimate the binding affinity of MDV3100. Data for individual compounds fit the homodimer pharmacodynamic model well. In the presence of a full agonist, the partial agonist had agonistic effects at low effect levels and antagonistic effects at high levels, as predicted by pharmacological theory. The generalized concentration addition model fits the empirical mixtures data—full/full agonist, full/partial agonist, and full agonist/antagonist—as well or better than relative potency factors or effect summation. The ability of generalized concentration addition to predict the activity of mixtures of different types of androgen receptor ligands is important as a number of environmental compounds act as partial androgen receptor agonists or antagonists.
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Krenz, Wulf D., Don Nguyen, Nivia L. Pérez-Acevedo, and Allen I. Selverston. "Group I, II, and III mGluR Compounds Affect Rhythm Generation in the Gastric Circuit of the Crustacean Stomatogastric Ganglion." Journal of Neurophysiology 83, no. 3 (March 1, 2000): 1188–201. http://dx.doi.org/10.1152/jn.2000.83.3.1188.

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We have studied the effects of group I, II, and III metabotropic glutamate receptor (mGluR) agonists on rhythm generation by the gastric circuit of the stomatogastric ganglion (STG) of the Caribbean spiny lobster Panulirus argus. All mGluR agonists and some antagonists we tested in this study had clear and distinct effects on gastric rhythm generation when superfused over combined oscillating or blocked silent STG preparations. A consistent difference between group I agonists and group II and III agonists was that group I agonists acted excitatory. The group I-specific agonists l-quisqualic acid and ( S)-3,5-dihydroxyphenylglycine, as well as the nonspecific agonist (1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid accelerated ongoing rhythms and could induce gastric rhythms in silent preparations. The group II agonist (2S,1′S,2′S)-2-(carboxycyclopropyl)glycine (L-CCG-I) and the group III agonist l(+)-2-amino-4-phosphonobutyric acid (l-AP4) slowed down or completely blocked ongoing gastric rhythms and were without detectable effect on silent preparations. The action of L-CCG-I was blocked partially by the group-II-specific antagonist, (RS)-1-amino-5-phosphonoindan-1-carboxylic acid [(RS)APICA], and the group-III-specific antagonist (RS)-α-methyl-4-phosphonophenylglycine completely blocked the action of l-AP4. Besides its antagonistic action, the group-II-specific antagonist (RS)APICA had a remarkably strong apparent inverse agonist action when applied alone on oscillating preparations. The action of all drugs was dose dependent and reversible, although recovery was not always complete. In our experiments, the effects of none of the mGluR-specific agonists were antagonized or amplified by the N-methyl-d-aspartate (NMDA)-receptor-specific antagonistd(−)-2-amino-5-phosphonopentanoic acid, excluding the contamination of responses to mGluR agonists by nonspecific cross-reactivity with NMDA receptors. Picrotoxin did not prevent the inhibitory action of L-CCG-I and l-AP4. We conclude that mGluRs, probably similar to those belonging to groups I, II, and III described in mammals, may play a role as modulators of gastric circuit rhythm generation in vivo.
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Lecendreux, Michel, Giuseppe Plazzi, Patricia Franco, Philippe Robert, Thierry Duvauchelle, and Jeanne-Marie Lecomte. "Tolérance et pharmacocinétique de pitolisant (Wakix®), un antagoniste/agoniste inverse du récepteur à histamine H3, chez 24 enfants narcoleptiques." Médecine du Sommeil 14, no. 1 (March 2017): 10. http://dx.doi.org/10.1016/j.msom.2017.01.129.

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Grider, J. R., and G. M. Makhlouf. "Identification of opioid receptors on gastric muscle cells by selective receptor protection." American Journal of Physiology-Gastrointestinal and Liver Physiology 260, no. 1 (January 1, 1991): G103—G107. http://dx.doi.org/10.1152/ajpgi.1991.260.1.g103.

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Opioid receptors on isolated gastric smooth muscle cells were characterized pharmacologically by a technique in which synthetic selective opioid agonists and antagonists were used to protect and thus enrich a specific receptor type while all other receptors were inactivated by N-ethylamaleimide. Treatment of the cells with the selective mu-receptor agonist DAGO or antagonist CTAP preserved only the response to DAGO; treatment with the selective delta-receptor agonist DPDPE or antagonist naltrindole preserved only the response to DPPE; and treatment with the selective kappa-receptor agonist U50,488H or antagonist nor-binaltorphimine preserved only the response to U50,488H. The results established the presence of distinct kappa-, delta-, and mu-opioid receptors capable of mediating contraction of isolated gastric muscle cells. The pattern of interaction of endogenous opioid peptides with protected receptors implied that dynorphin-(1-13) and Met-enkephalin were selective agonists for kappa- and delta-opioid receptors, respectively, and Leu-enkephalin a preferential agonist of mu-opioid receptors. The results were confirmed by a reverse approach in which opioid receptors were inactivated by site-directed irreversible antagonists. beta-Funaltrexamine, a mu-selective antagonist, abolished the response to mu-receptor agonists, whereas beta-chlornaltrexamine, a mu- and kappa-selective antagonist, abolished the response to mu-receptor agonists and partially inhibited the response to kappa-receptor agonists.
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Sakkiah, Sugunadevi, Chandrabose Selvaraj, Wenjing Guo, Jie Liu, Weigong Ge, Tucker A. Patterson, and Huixiao Hong. "Elucidation of Agonist and Antagonist Dynamic Binding Patterns in ER-α by Integration of Molecular Docking, Molecular Dynamics Simulations and Quantum Mechanical Calculations." International Journal of Molecular Sciences 22, no. 17 (August 29, 2021): 9371. http://dx.doi.org/10.3390/ijms22179371.

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Estrogen receptor alpha (ERα) is a ligand-dependent transcriptional factor in the nuclear receptor superfamily. Many structures of ERα bound with agonists and antagonists have been determined. However, the dynamic binding patterns of agonists and antagonists in the binding site of ERα remains unclear. Therefore, we performed molecular docking, molecular dynamics (MD) simulations, and quantum mechanical calculations to elucidate agonist and antagonist dynamic binding patterns in ERα. 17β-estradiol (E2) and 4-hydroxytamoxifen (OHT) were docked in the ligand binding pockets of the agonist and antagonist bound ERα. The best complex conformations from molecular docking were subjected to 100 nanosecond MD simulations. Hierarchical clustering was conducted to group the structures in the trajectory from MD simulations. The representative structure from each cluster was selected to calculate the binding interaction energy value for elucidation of the dynamic binding patterns of agonists and antagonists in the binding site of ERα. The binding interaction energy analysis revealed that OHT binds ERα more tightly in the antagonist conformer, while E2 prefers the agonist conformer. The results may help identify ERα antagonists as drug candidates and facilitate risk assessment of chemicals through ER-mediated responses.
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Wilson, Kristy J., Christopher P. Mill, Richard M. Gallo, Elizabeth M. Cameron, Henry VanBrocklin, Jeffrey Settleman, and David J. Riese. "The Q43L mutant of neuregulin 2β is a pan-ErbB receptor antagonist." Biochemical Journal 443, no. 1 (March 14, 2012): 133–44. http://dx.doi.org/10.1042/bj20110921.

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The ErbB4 receptor tyrosine kinase possesses both tumour suppressor and oncogenic activities. Thus pharmacological agents are needed to help elucidate ErbB4 functions. However, limitations of existing ErbB4 agonists and antagonists have led us to seek novel ErbB4 antagonists. The Q43L mutant of the ErbB4 agonist NRG2β (neuregulin 2β) stimulates ErbB4 tyrosine phosphorylation, yet fails to stimulate ErbB4 coupling to cell proliferation. Thus in the present paper we hypothesize that NRG2β/Q43L may be an ErbB4 antagonist. NRG2β/Q43L competitively antagonizes agonist stimulation of ErbB4 coupling to cell proliferation. NRG2β/Q43L stimulates less ErbB4 tyrosine phosphorylation than does NRG2β. In addition, NRG2β stimulation of cell proliferation requires PI3K (phosphoinositide 3-kinase) activity and NRG2β stimulates greater Akt phosphorylation than does NRG2β/Q43L. Moreover, EGFR [EGF (epidermal growth factor) receptor] kinase activity (but not that of ErbB4) is critical for coupling ErbB4 to proliferation. Experiments utilizing ErbB4 splicing isoforms and mutants suggest that NRG2β and NRG2β/Q43L may differentially stimulate ErbB4 coupling to the transcriptional co-regulator YAP (Yes-associated protein). Finally, NRG2β/Q43L competitively antagonizes agonist stimulation of EGFR and ErbB2/ErbB3, indicating that NRG2β/Q43L is a pan-ErbB antagonist. Thus we postulate that NRG2β/Q43L and other antagonistic ligands stimulate ErbB tyrosine phosphorylation on a set of residues distinct from that stimulated by agonists, thus suggesting a novel mechanism of ErbB receptor regulation. Moreover, NRG2β/Q43L and related ligand-based antagonists establish a paradigm for the discovery of anti-ErbB therapeutics.
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Fong, Tung Ming, Ruey-Ruey C. Huang, Hong Yu, Dennis Underwood, Margaret A. Cascieri, Catherine D. Strader, and Christopher J. Swain. "Mutational analysis of neurokinin receptor function." Canadian Journal of Physiology and Pharmacology 73, no. 7 (July 1, 1995): 860–65. http://dx.doi.org/10.1139/y95-118.

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The interactions of the NK1 receptor with peptide agonists or nonpeptide antagonists have been investigated by site-directed mutagenesis and computer modeling. At least 10 residues in the extracellular and transmembrane regions of the receptor are required for the binding of many peptide agonists. The C-terminal amide of peptide agonists is likely to be bound near Asn-85. Residues likely to be involved in the subsequent receptor activation include Glu-78 and Tyr-205. The binding site for nonpeptide antagonists can be defined by at least five residues in transmembrane helices 4–7, and primary contacts between key residues and quinuclidine antagonists have been assigned based on CP-96,345 and its analogs. Analyses of the wild-type and mutant NK1 and NK2 receptors, intact and truncated peptides, and various antagonists suggest that the agonist and antagonist binding sites overlap spatially, even though agonists and antagonists do not interact with the same set of residues on the receptor. Mapping the ligand binding site not only allows us to better understand the ligand–receptor interaction and antagonism but also leads to a refined three-dimensional model of the NK1 receptor.Key words: receptor, substance P, agonist, antagonist, mutagenesis.
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Dissertations / Theses on the topic "Agoniste - Antagoniste"

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Bellier, Bruno. "Hétérogénéité fonctionnelle du récepteur CCK2 à la cholecystokinine : conception, étude de nouveaux outils pharmacologiques et perspectives thérapeutiques associées." Paris 5, 2000. http://www.theses.fr/2000PA05P605.

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ANSAR, M'HAMMED. "Agonistes et antagonistes de l'acide gamma-aminobutyrique au niveau du recepteur gaba-b : etudes chimique et pharmacologique." Lille 2, 1995. http://www.theses.fr/1995LIL2P251.

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Sachon, Emmanuelle. "Etude de l'interaction entre le récepteur NK-1 et la substance P, par photomarquage et spectrométrie de masse maldi-tof." Paris 6, 2003. http://www.theses.fr/2003PA066298.

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Maingot, Mathieu. "Conception et synthèse de ligands peptidomimétiques du récepteur de la ghréline." Thesis, Montpellier, 2015. http://www.theses.fr/2015MONTS110.

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La ghréline est une hormone de 28 acides aminés, synthétisée principalement par l'estomac. D'abord identifiée comme un sécretagogue de l'hormone de croissance, elle joue également un rôle central dans la prise alimentaire, la glycémie ainsi que dans certains processus liés à l'addiction. Ces effets sont médiés par un récepteur couplé aux protéines G : le GHS-R1a (Growth Hormone Secretagogue Receptor). Ce récepteur possède une activité constitutive élevée et un réseau de signalisation intra-cellulaire relativement complexe via l'activation de β-arrestines et de différentes isoformes de protéines G (Gq, Gi/o, G12/13). Compte tenu de ces multiples effets, les ligands du GHS-R1a présentent un intérêt thérapeutique certain.Cette thèse est consacrée au développement d'antagonistes et d'agonistes inverses du hGHS-R1a, dont la structure est basée sur le motif 1,2,4-triazole 3,4,5-trisubstitué. Grâce à une étude successive des différents substituants de cette plateforme peptido-mimétique nous avons identifié des antagonistes d'affinités nanomolaires ainsi que des agonistes inverses possédant une efficacité significative. Ces composés paraissent donc être des candidats intéressants pour des études in vivo sur des modèles de prise alimentaire ou d'addiction. D'autre part, une étude pharmacologique sophistiquée, menée sur nos composés, a démontré qu'il est possible d'obtenir des ligands biaisés sur la base du motif triazole. Ces résultats fournissent de nouvelles informations sur la sélectivité fonctionnelle du GHS-R1a. Ainsi, associés à des études in vivo complémentaires, ces données pourraient être précieuses pour la conception de nouveaux médicaments possédant des effets secondaires limités
Ghrelin is a hormone of 28 amino acids, mostly synthesized in the stomach. Firstly identified as a growth hormone secretagogue, this peptide is also involved in food intake, blood glucose and in some processes related to addiction. Ghrelin effects are mediated by a G protein-coupled receptor: GHS-R1a (Growth Hormone Secretagogue Receptor). This receptor has a high constitutive activity and a complex intra-cellular signaling network via the activation of β-arrestin and different isoforms of G protein (Gq, Gi / o, G12 / 13). Given these multiple effects, ligands of GHS-R1a have a therapeutic interest.This thesis is devoted to the development of antagonists and inverse agonists of hGHS-R1a whose structure is based on the 3,4,5-trisubstituted 1,2,4-triazole scaffold. Thanks to a successive study of the various substituents of the peptidomimetic platform we identified antagonists with nanomolar affinity and inverse agonists with a significant efficiency. These compounds appear to be attractive candidates for in vivo studies on food intake or addiction models. On the other hand, a sophisticated pharmacological study, conducted on our compounds, has demonstrated that it is possible to obtain biased ligands based on the triazole motif. These results provide new informations about the functional selectivity of GHS-R1a. Thus, these data, combined with additional in vivo studies, could be useful for the design of new drugs with limited side effects
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Édouard, Pascal. "Adaptations de la force musculaire des muscles rotateurs médiaux et latéraux dans la stabilisation dynamique de l' articulation scapulo-humérale : applications à des situations pathologiques et sportives." Thesis, Saint-Etienne, 2011. http://www.theses.fr/2011STET010T/document.

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Le but de ce travail est de déterminer les liens éventuels existant entre la force et l’équilibre agoniste / antagoniste des muscles rotateurs médiaux et latéraux de l’articulation scapulohumérale, et la stabilité scapulo-humérale. La première partie de ce travail est un rappel d’anatomie fonctionnelle, de physiologie articulaire et de biomécanique de l’articulation scapulo-humérale, ainsi que des aspects pathologiques en rapport avec la problématique de sa stabilité et de son exploration. La deuxième partie propose une analyse critique de la technique d’exploration de la force musculaire par dynamométrie isocinétique, afin de déterminer un protocole d’évaluation fiable et reproductible. Ainsi, nous choisissons d’utiliser la position d’évaluation la plus reproductible et la plus adaptée pour l’évaluation de sujets pathologiques : la position assise avec 45° d’abduction dans le plan de la scapula avec correction de la gravité. La troisième partie a pour objet de rechercher, à partir d’études cliniques originales, les liens existant entre la force musculaire des rotateurs médiaux et latéraux de l’épaule et l’instabilité antérieure chronique post-traumatique d’une part, et les adaptations de cette force avec certaines sollicitations sportives d’autre part. Bien qu’un déficit de la force musculaire des rotateurs médiaux et latéraux soit associé à l’instabilité antérieure chronique, nos études ne rapportent pas d’association entre le déséquilibre agoniste/antagoniste et l’instabilité antérieure chronique. Dans le cadre de la pratique de sports sollicitant les membres supérieurs, les adaptations de la force, avec une augmentation de la force des muscles rotateurs médiaux et latéraux du côté dominant, sont inconstantes, et surtout, nos résultats ne rapportent aucun déséquilibre agoniste/antagoniste induit par la pratique sportive. En conclusion, notre travail de thèse met en évidence des adaptations de la force musculaire sans perturbation de l’équilibre agoniste/antagoniste des rotateurs médiaux et latéraux de l’articulation scapulo-humérale, associées à l’instabilité scapulo-humérale ou induites par la pratique de sports sollicitant cette articulation. Prenant en compte les limites de notre expérimentation, on peut faire l’hypothèse que les adaptations physiologiques induites par la pratique sportive n’interviendraient pas comme un mécanisme de désadaptation, ou un facteur de risque prédisposant, à l’origine des pathologies de l’articulation scapulo-humérale. Ainsi, notre conclusion serait que l’équilibre agoniste / antagoniste aurait un rôle protecteur de la stabilité articulaire ; la survenue d’un déséquilibre musculaire agoniste / antagoniste serait alors secondaire à une lésion anatomique et marquerait le signe de son évolution longue et/ou péjorative
The aim of this work is to determine the possible links between strength and agonist/antagonist balance of the shoulder internal and external rotators muscle, and the glenohumeral stability. The first part of this work is a reminder of functional anatomy, joint physiology and biomechanics of the glenohumeral joint, and pathological aspects related to the problem of its stability and its exploration. The second part propose a critical analysis of technical exploration of muscular strength by isokinetic dynamometer to determine a reliable and reproducible protocol. We choose to use the more reliable and more suitable position for evaluation of pathological subject: the seated position with 45° of shoulder abduction in the scapular plane, with gravity corrected. The third part is aimed to research, from original clinical studies, the relationship between shoulder internal and external rotators muscle strength and balance, and shoulder instability on the one hand, and adaptations of this strength with sports practice on the other hand. Although a deficit in rotators muscle strength is associated with recurrent anterior instability, our work reporte no association between agonist/antagonist imbalance and recurrent anterior instability. In overhead sports and sports seeking the upper limbs, adaptations of strength, with a rotator strength increase on the dominant side, are inconsistent, and most importantly, our results reporte no agonist/antagonist imbalance induced by the sports practice. In conclusion, this work highlights adaptations in strength and balance of the shoulder internal and external rotators muscle associated with the glenohumeral joint instability, or induced by the sports practice. Tacking into account the limits of our experiment, we can hypothesis that any physiological adaptations induced by sport practice would not intervene as a pathophysiological mechanisms of desadaptation, or not be considered a risk factor predisposing, to glenohumeral joint diseases. Thus, our conclusion is that the agonist/antagonist balance would have a protective role of the joint stability; the occurrence of a muscle agonist / antagonist imbalance may be secondary to an anatomical lesion and mark the sign of its long and/or pejorative evolution
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By, Youlet. "Modulation des récepteurs de l'adénosine par anticorps monoclonaux et ligands synthétiques. : application en physiopathologie humaine." Thesis, Aix-Marseille 2, 2010. http://www.theses.fr/2010AIX20688/document.

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L’adénosine est un nucléoside ubiquitaire qui exerce un contrôle puissant sur les systèmes nerveux,immunitaire et cardiovasculaire par l’intermédiaire de quatre récepteurs membranaires : A1R, A2AR, A2BR etA3R. L’étude des récepteurs de l’adénosine est nécessaire à la compréhension de physio‐pathologieshumaines non encore élucidées. Pour étudier l’expression des A2AR, nous avons, dans une première étude,produit un anticorps monoclonal, appelé Adonis, d’isotype IgM, . Adonis reconnait un épitope linéaire desept acides aminés sur la partie C‐terminale de la seconde boucle extra‐cellulaire de l’A2AR humain. Adonisrévèle, par Western blotting sur lysats cellulaires, une bande de 45 KDa, correspondant à l’A2AR. Adonis secomporte comme un « agonist‐like » en augmentant la production d’AMPc et en inhibant la proliférationcellulaire via la stimulation des A2AR. Dans une deuxième étude, nous avons utilisé Adonis pour montrerque l’expression des A2AR de cellules mononucléées, qui mime celle des tissus cardiaques, permet dedifférencier certains patients souffrant de syncope neurocardiogénique. Nous avons monté dans unetroisième étude, qu’Adonis induit une « down‐régulation » de l’expression des co‐récepteurs CXCR4 etCCR5 des cellules T via la stimulation des A2AR, et qu’à ce titre il pouvait être un outil thérapeutique dans lesinfections par HIV. Dans une quatrième étude, nous avons évalué les effets anti‐nociceptifs d’Adonis qui,administré par voie intra‐cérébro‐ventriculaire, augmente de manière dose‐dépendante les latencesobtenues avec le test du Hot‐plate et du Tail‐flick chez la souris. Ces effets sont renversés par deuxantagonistes des A2AR mais aussi par un antagoniste des récepteurs aux opioïdes. Ceci suggère que leseffets anti‐nociceptifs d’Adonis sont médiés par la libération d’opioïdes endogènes. En marge de sesétudes, nous avons également testé les propriétés biologiques de nouveaux ligands des A1R dans le cadred’une collaboration entre chimistes et biologistes. Ainsi, nous montrons, dans une cinquième étude, queparmi la trentaine de molécules synthétisées, quatre sont des antagonistes et deux autres des agonistesavec un EC50 de l’ordre du micromolaire pour la production d’AMPc. De tels agonistes des A1R pourraientêtre utiles dans le traitement des douleurs neuropathiques, tandis que les antagonistes le seraient dansl’insuffisance cardiaque ou utilisés comme diurétique. Enfin dans une sixième étude, nous avons testé unemolécule originale, puisque bivalente, possédant un pôle d’activité pour les récepteurs aux opioïdes μ et unautre pour les A1R. Cette molécule est un antagoniste pour les deux récepteurs. Elle pourrait avoir desapplications cliniques dans certaines pathologies comme le choc hypovolémique ou le sevrage aux opiacés
Adenosine interacts on its cell surface receptors, namely A1R, A2AR, A2BR and A3R, to exertphysiological effects on target tissues. Modulation of these adenosine receptors appears to be a currenttopic of research which may bring more comprehensions on human pathophysiology yet to be elucidated.In order to study A2AR expression, we produced, in study 1, a monoclonal antibody anti‐human A2AR, calledAdonis being of IgM, isotype. Adonis recognized a linear epitope of seven amino acids on the C‐terminalpart of the A2AR second extra‐cellular loop. By Western blotting, Adonis reveals a 45 KDa band of A2AR incell lysates. Adonis behaves as an agonist‐like which increases the cAMP production and inhibits cellproliferation through A2AR stimulation. In study 2, we showed that using Adonis, to measure the A2ARexpression of peripheral blood mononuclear cells which mimic those of the cardiac tissue, was able todifferentiate some patients with suspected neurally mediated syncope. We showed, in study 3, that A2ARstimulation by Adonis leads to a down‐regulation of CXCR4 and CCR5 expression on T‐cells, suggesting thatAdonis would be a potential drug to treat HIV infections. In study 4, we showed that intracereboventricularinjection of Adonis increased the Hot‐plate and Tail‐flick test latencies in mice in a dose‐dependent manner.Such increases were prevented by two A2AR antagonists and by an opiate receptor antagonist, suggestingthat the anti‐nociceptive effects of Adonis were mediated, at least in part, by endogenous opioid liberation.The last section focused on biological evaluation of new A1R ligands in collaborative studies betweenchemists and biologists. Indeed we showed, in study 5, that among thirty synthesized molecules, four act asA1R antagonists and two turn out to be A1R agonists with a micromolar EC50 on cAMP production. ThoseA1R agonists would be used in neuropathic pains, whereas other antagonists could be used in cardiacfailure or as diuretic. Finally, in study 6, we tested an original hybrid molecule which was revealed to be abivalent antagonist to μ opiate receptors and A1R. This hybrid compound may have applications in somepathologies such as hypovolemic shock and opiate addiction
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Belkhiria, Chama. "Exploration et analyse de la relation cerveau-muscles squelettiques lors de la préparation et de l’exécution motrice." Thesis, Paris 10, 2016. http://www.theses.fr/2016PA100191.

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Les travaux de cette thèse s’inscrivent à la frontière des neurosciences et de la physiologie musculaire. Trois études se sont articulées de la préparation et l’exécution motrice. La première étude (A) a relié l'activité cérébrale à l'activité musculaire lors de la préparation motrice. Les résultats ont montré que des régions, telles que le cortex moteur primaire et l’aire motrice supplémentaire sont impliquées dans l'activité du muscle fléchisseur (FDS) alors que d’autres régions, telles que les ganglions de la base, les aires fronto-pariétales et le cervelet, sont impliquées dans l'activité du muscle extenseur (EDC). L’étude (B) a exploré le rôle du réseau cérébro-cérébelleux et du réseau striatal lors de l’exécution d’une tâche cognitive et motivationnelle. Les données ont révélé que la partie antérieure du lobule VI droit était activée par l'exécution motrice tandis que sa partie postérieure était spécifiquement activée par les encouragements verbaux. Les mesures de l’interaction psychophysiologique ont permis de faire immerger une boucle de connectivité fermée et formée par le cortex cérébral, le cervelet et les noyaux rouges. La troisième étude (C) concerne l’effet de la consigne réalisée lors de l’exécution motrice sur les paramètres neuromusculaires de FDS et EDC. Les résultats ont montré que la Force Maximale Volontaire, la Pente Maximale de Montée de Force et l’éléctromyographie associée étaient plus élevées (p < 0.05) avec la consigne accompagnée d’encouragement verbal
The present work fits on the border of neurosciences and muscular physiology. Three studies explored the brain and muscle activities following motor preparation and execution. The first study (A) linked brain and muscle activity during motor preparation. The results revealed that regions (e.g primary motor cortex and supplementary motor area) are involved in the activity of the flexor muscle (FDS) while other regions (e.g basal ganglia, fronto-parietal areas and cerebellum) are involved in the activity of the extensor muscle (EDC). The study (B) explored the role of cerebro-cerebellar and striatal networks during the execution period of cognitive and motivational task. The data showed that the anterior part of the right lobule VI was activated by the motor task, while its posterior part was specifically activated by verbal encouragement. Measurements of psychophysiological interaction revealed a closed connectivity loop formed by the cerebral cortex, the cerebellum and the red nuclei. The third study (C) concerned the effect of instruction on neuromuscular parameters of FDS and EDC muscles during motor execution. The results showed that the Maximum Voluntary Force, the Maximum Rate of Force Development and the associated electromyographic signal are the highest (p < 0.05) with cognitive, motivational and verbal encouragement condition
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8

Dubreil, Véronique. "Contribution à l'étude électrophysiologique et pharmacologique des systèmes gabaergiques régulateurs de l'activité des neurones DUM du dernier ganglion abdominal de la blatte, periplaneta americana l." Angers, 1996. http://www.theses.fr/1996ANGE0006.

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L'utilisation de techniques essentiellement électrophysiologiques nous a permis de montrer de nouveaux aspects concernant la physiologie et la pharmacologie des systèmes gabaergiques régulateurs de l'activité électrique de cellules neurosécrétrices identifiées, appelées neurones DUM, dans le dernier ganglion abdominal de la blatte periplaneta americana. Tout d'abord, les récepteurs gabaergiques des neurones DUM sont de différents types. Leur sensibilité à la picrotoxine (PTX), antagoniste des récepteurs gabaergiques couples à un canal aux ions chlorure, permet d'en distinguer deux types : les uns sensibles, les autres résistants. Les deux types génèrent des réponses hyperpolarisantes sensibles aux variations de concentration extracellulaire en ions chlorure, mais de cinétiques différentes. D'autre part, la localisation des récepteurs gabaergiques sensibles à la PTX sur les neurones DUM les sépare en deux sous-types : les uns sont situés sur les neurites et reçoivent les afférences inhibitrices de ces neurones, ils sont donc synaptiques, alors que les autres situes sur le soma sont extra-synaptiques. L'efficacité des afférences inhibitrices des neurones DUM est assurée grâce à un mécanisme qui maintient la distribution transmembranaire des ions chlorure en faisant sortir ces derniers de la cellule contre leur gradient électrochimique. Ce mécanisme est un cotransport cl#-/k#+ qui utilise l’énergie du gradient électrochimique des ions potassium et fait ainsi sortir simultanément les ions potassium et chlorure. Les études pharmacologiques réalisées sur les récepteurs gabaergiques sensibles à la PTX situés sur le soma des neurones DUM montrent que ces récepteurs sont qualitativement identiques aux récepteurs gabaergiques sensibles à la PTX décrits dans les autres préparations nerveuses d'insecte. Les agonistes gabaergiques les plus efficaces sont le taca, l'isoguvacine et le muscimol et le seul antagoniste efficace parmi les antagonistes gabaergiques testes est la PTX.
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Miller, Christian. "Effets comparés de deux modalités d'entraînement sur le développement de la force musculaire : électrostimulation et contraction volontaire." Paris 11, 1989. http://www.theses.fr/1989PA112382.

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Le but de ce travail est de préciser les possibilités d'adaptations physiologiques du muscle soumis à un entraînement visant à l'amélioration de la force maximale. Deux modalités d'entraînement isométrique mono­angulaire sont pratiquées : l'une sous électrostimulation (ES) l'autre en contraction volontaire (CV). Leurs effets respectifs sur les caractéristiques de la relation Couple-Angle de flexion du coude et de l'activité électromyographique des principaux agonistes et antagonistes sont comparés. Des augmentations significatives de la force sont observées après ES comme après CV. Les deux modes d'entraînement aboutissent à des résultats équivalents si les niveaux de couple externe exercés pendant l'entraînement sont identiques. En outre, l'amélioration de la force se révèle spécifique de l'angle entraîné. Elle est accompagnée d'une élévation du niveau d'activation maximale des muscles agonistes associée à une stabilité de l'activité myoélectrique des antagonistes, quel que soit le mode d'entraînement. L'existence d'une adaptation d'ordre neurophysiologique impliquant une meilleure activation du pool de motoneurones des fléchisseurs semble être à l'origine des gains de force observés. Ce mécanisme d'adaptation qui apparaît après ES et après CV semble régulé par l'intensité du couple externe exercé pendant l'entraînement. Le rôle déterminant que pourrait jouer une modification de l'efficacité des muscles posturaux dans le processus d'amélioration de la force maximale est ici suggéré
The purpose of this study was to examine some physiological muscle adaptations to strengthening. The effects of monoangular isometric strength training using Electrical Stimulation (ES) or Voluntary Contraction (CV) upon the Torque-Length relationship and the electromyographic activity of the agonist and antagonist muscles were compared. Maximum Voluntary Isometric Force was significantly increased beth by electrical stimulation and voluntary contraction. The two training modes yielded similar results when the electrically evoked torque and the isometric flexion torque exerced on the ergometric device, along the training sessions were equal. In this way, the increase of voluntary strength was specific to the training angle with beth training procedures. Moreover some electromyagraphic evidence was revealed with ES and CV training indicating a greater increase in the motor unit activation of the agonist at the training. So that, a neural adaptation to training seems to be unavoidable even with electrical stimulation training. This neural mechanism would be driven by the level of the isometric torque exerced on the ergometric device. We emphasize the rôle of the postural muscle in the process of strength development
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Tran-Drouin, Simon. "Sélectivité fonctionnelle de ligands orthostériques du récepteur FP de la PGF[indice inférieur 2alpha]." Mémoire, Université de Sherbrooke, 2010. http://savoirs.usherbrooke.ca/handle/11143/4054.

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Les ligands orthostériques transmettent un signal complexe aux cellules en se fixant à l'intérieur de la pochette de liaison de leur récepteur cible. Le changement conformationel qui en résulte modifie l'efficacité du récepteur à recruter et activer les seconds messagers en amont des voies de signalisation, soit les protéines G hétérotrimériques dans le cas des récepteurs couplés aux protéines G (GPCRs). Ces variations entraînent une vaste gamme de modifications dans le milieu intracellulaire. Par exemple, l'activation de la protéine G q provoque entre autres l'activation de la phospholipase C? (PLC? ), la production d'inositol 1,4,5-trisphosphate (1P3), puis l'activation des protéines kinases C (PKC). L'activation de la protéine G s , pour sa part, stimule l'activité de l'adénylate cyclase (AC), ce qui entraîne la production d'AMPc et l'activation de la protéine kinase A (PKA). Un ligand n'influence pas nécessairement deux voies de signalisation indépendantes de façon similaire, ce qui lui confère la propriété de sélectivité fonctionnelle. Dans ce travail, nous avons caractérisé le profil pharmacologique de ligands orthostériques du récepteur FP de la PGF2? à l'aide d'un clone HEK-293-SL exprimant le récepteur FP de façon stable. La mesure de la production d'IP3 a permis d'évaluer la voie de la PLC alors que la mesure de la production d'AMP c a permis d'évaluer la voie de l'AC. Pour chacune d'entre elles, le fluprostenol s'est comporté comme un agoniste complet moins puissant que l'agoniste naturel. Le composé synthétique Al-8810 s'est comporté comme un agoniste partiel de la voie de la PLC, alors qu'il s'est avéré être un antagoniste de la voie de l'AC. Ces résultats démontrent que l'activité d'un ligand vis-à-vis un récepteur dépend du groupe d'effecteurs observé, ce qui illustre le concept de sélectivité fonctionnelle des ligands. L'étude des composés allostériques THG113 et THG113.824 démontre que ces derniers n'influencent pas la signalisation déclenchée en aval du récepteur FP par son agoniste naturel. Ces résultats suggèrent qu'ils agiraient comme antagoniste des effets de la PGF 2? par un mécanisme indépendant du récepteur FP. [Symboles non conformes]
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Books on the topic "Agoniste - Antagoniste"

1

Freye, Enno. Opioid Agonists, Antagonists and Mixed Narcotic Analgesics. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-71854-0.

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Albrecht, Fleckenstein, ed. Cardiovascular effects of dihydropyridine-type calcium antagonists and agonists. Berlin: Springer-Verlag, 1985.

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Fleckenstein, Albrecht, Cornelius Van Breemen, Rainer Gross, and Friedrich Hoffmeister, eds. Cardiovascular Effects of Dihydropyridine-Type Calcium Antagonists and Agonists. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-70499-4.

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Small peptides: Chemistry, biology, and clinical studies. Amsterdam: Elsevier, 1993.

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Akhlaghi, Shirin. The metabolic effects of beta-agonists and antagonists: Focus on beta-1 selectivity. Birmingham: University of Birmingham, 1994.

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Freye, Enno. Opioid agonists, antagonists and mixed narcotics analgesics: Theoretical background and considerations for practical use. Berlin: Springer, 1987.

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Jain, K. K. Serotonin-modulating drugs: Therapeutic applications and commercial opportunities. [Waltham, MA]: Decision Resources, Inc., 1999.

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Neill, Joanna Caroline. The effects of 5-hydroxytryptamine receptor agonists and antagonists on food and fluid intake in the rat. Birmingham: University of Birmingham, 1989.

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Organon Round Table Conference (3rd 1992 Paris, France). GnRH, GnRH analogs, gonadotropins, and gonadal peptides: The proceedings of the third Organon Round Table Conference, Paris, 1992. London: Parthenon Pub. Group, 1993.

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Angerer, Erwin von. The estrogen receptor as a target for rational drug design. New York: Springer, 1995.

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Book chapters on the topic "Agoniste - Antagoniste"

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Nayler, Winifred G. "Synthetische Calcium-Agonisten." In Calcium-Antagonisten, 117–28. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-75233-9_9.

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Waldvogel, Herman Hans. "Agonist-Antagonisten." In Analgetika Antinozizeptiva Adjuvanzien, 348–60. Berlin, Heidelberg: Springer Berlin Heidelberg, 2001. http://dx.doi.org/10.1007/978-3-642-56710-0_40.

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Nayler, Winifred G. "Natürlich vorkommende Calcium-Antagonisten und -Agonisten." In Calcium-Antagonisten, 129–38. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-75233-9_10.

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Sarver, Cory. "Agonist/Antagonist Agents." In Pain, 307–9. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-99124-5_67.

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Bloch, Michael H., Michael H. Bloch, Mark A. Geyer, David C. S. Roberts, Eileen M. Joyce, Jonathan P. Roiser, John H. Halpern, et al. "Histaminic Agonists and Antagonists." In Encyclopedia of Psychopharmacology, 587–90. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_294.

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Andrews, Anne M., Greg A. Gerhardt, Lynette C. Daws, Mohammed Shoaib, Barbara J. Mason, Charles J. Heyser, Luis De Lecea, et al. "Nicotinic Agonists and Antagonists." In Encyclopedia of Psychopharmacology, 887–99. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_304.

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Hill, Stephen J. "Histaminic Agonists and Antagonists." In Encyclopedia of Psychopharmacology, 1–6. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-27772-6_294-2.

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Rollema, Hans, Daniel Bertrand, and Raymond S. Hurst. "Nicotinic Agonists and Antagonists." In Encyclopedia of Psychopharmacology, 1–21. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-27772-6_304-2.

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Daly, J. W. "Adenosine Agonists and Antagonists." In Purines in Cellular Signaling, 3–12. New York, NY: Springer New York, 1990. http://dx.doi.org/10.1007/978-1-4612-3400-5_1.

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Hill, Stephen J. "Histaminic Agonists and Antagonists." In Encyclopedia of Psychopharmacology, 743–48. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-36172-2_294.

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Conference papers on the topic "Agoniste - Antagoniste"

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Hernández Huerta, Daniel, and Jessenia Paola Morillo González. "Psicosis dual, ¿puede ser el agonismo parcial dopaminérgico D3 una diana terapéutica?" In 22° Congreso de la Sociedad Española de Patología Dual (SEPD) 2020. SEPD, 2020. http://dx.doi.org/10.17579/sepd2020p136.

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Objetivos: Revisión sobre el efecto del agonismo parcial del receptor dopaminérgico D3 en las psicosis duales Material y métodos Búsqueda bibliográfica en MEDLINE introduciendo los términos "schizophrenia", "dopamine D3 receptor partial agonist" y "substance use disorder". Resultados y conclusiones Existe creciente evidencia sobre la eficacia del agonismo parcial dopaminérgico en los trastornos por uso de sustancias (TUS), más allá de su eficacia contrastada en el tratamiento de la esquizofrenia. Aportan como principales ventajas una baja probabilidad de abuso (respecto a los agonistas completos) así como una mejor tolerabilidad (comparados con los antagonistas). En los últimos años, el receptor dopaminérgico D3, debido a su alta distribución en el sistema límbico (donde se encuentra el núcleo accumbens, implicado en los sistemas de motivación y recompensa) se ha postulado como una diana terapéutica prometedora para trastornos relacionados con la dopamina, como son la esquizofrenia y los TUS. En dicha línea, cariprazina (antipsicótico con mayor afinidad por el receptor D3, donde presenta un mecanismo de agonismo parcial, y con eficacia demostrada en los síntomas positivos y negativos de la esquizofrenia) mostraba en una investigación básica ser igual de eficaz que aripiprazol y bifeprunox en reducir el efecto reforzante de la cocaína, así como en la prevención de recaídas. En conclusión, el agonismo parcial del receptor dopaminérgico D3 se posiciona como una alternativa farmacológica a considerar en el tratamiento de las psicosis duales. Una mayor investigación al respecto y la evidencia empírica de la práctica clínica precisarán su verdadero rol.
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Vocke, Robert D., Curt S. Kothera, and Norman M. Wereley. "Mechanism and Bias Considerations for Design of a Bi-Directional Artificial Muscle Actuator." In ASME 2012 Conference on Smart Materials, Adaptive Structures and Intelligent Systems. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/smasis2012-8114.

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Pneumatic artificial muscles (PAMs), or McKibben actuators, have received considerable attention for robotic manipulators and in aerospace applications due to their similarity to natural muscles. Like natural muscles, PAMs are a purely contractile actuator, so that, in order to produce bidirectional or rotational motion, they must be arranged in an agonist/antagonist pair, which inherently limits the deflection of the system due to the high parasitic stiffness of the antagonistic PAM. This study presents two methods for increasing the performance of an antagonistic PAM system by decreasing the passive parasitic moment, rather than increasing the active moment. The first involves selection of the kinematic mechanism geometry, and the second involves the introduction of bias into the system, both in terms of PAM contraction, and passive (antagonistic) PAM pressure. It was found with the proper selection of design parameters, including mechanism geometry, PAM geometry, and bias conditions, that an ideal actuator configuration can be found that maximizes deflection for a given arbitrary loading. When comparing a baseline design to an improved design for a simplified case, a nearly 50% increase in maximum deflection was predicted simply by optimizing mechanism geometry and bias contraction.
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Moffat, Katrina J., and D. Euan MacIntyre. "REGULATION OF RECEPTOR-OPERATED Ca2− CHANNEL OPENING IN HUMAN PLATELETS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644677.

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Agonist-induced elevation of the platelet intracellular free Ca2+ concentration ([Ca2−]i), as monitored using quin2, is not electrically mediated and is attenuated by removal of extracellular Ca2− and by lanthanides (e.g Gd3−).Collectively these data suggest that elevation of [Ca2−]i in platelets derives in part via influx of external Ca2−presumably through a receptor-operated Ca2− channel (ROC). Hal lam & Rink (FEBS Lett. 186: 175: 1985) showed that Mn2−also enters platelets via these ROC. To investigate the possible regulatory mechanisms that govern ROC status, we utilized quin2-labelled human platelets suspended in a Ca2+-free Hepes buffered Tyrodes solution, and monitored agonist-induced Mn2+-mediated quenching of quin2 fluorescence as an index of ROC opening.Thrombin (Th, 0.01-1 U/ml), Vasopressin (VP, 10-1000 nM) and the TxA2-mitnetic, EP171 (1-100 nM) all induced ROC opening which occurred rapidly (<30s), was maximal within 30-60s and thereafter declined. Gd3+ (≤2 mM) markedly impaired this Mn2ࢤ-mediated quenching of quin2 fluorescence induced by all 3 agonists. The adenylate cyclase stimulant PGD2 (3-3000 nM) and the guanylate cyclase stimulant sodium nitroprusside (0.01-10 μM) impaired ROC opening induced by Th (0.5 U/ml), VP (100 nM) and EP171 (25 nM) whether added to platelets ≤120sbefore or 30s after the agonists. In contrast, agents that selectively antagonize, at the receptor level, the effects of VP (e.g. d(CH2)5Tyr Me AVP, 10 ¼H) or EP171 (e.g.EP092, 250nM), or that inhibit the action of Th(e.g. Hirudin 1 U/ml)only impaired ROC opening when added to platelets simultaneously with or before the agonist.These results indicate that, although initiated by agonist-receptor interaction, maintenance of the open state of ROC in human platelets does not require continued receptor occupancy or activation by agonist. Moreover, besides acting to impair the transduction processes initiated following occupancy by agonist of platelet Vi, TP and Thrombin receptors, cAMP-and cGMP-dependent reactions also can terminate or otherwise limit opening of ROC.
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Schultz, Joshua A., and Jun Ueda. "Analysis of Antagonist Stiffness for Nested Compliant Mechanisms in Agonist-Antagonist Arrangements." In ASME 2011 Dynamic Systems and Control Conference and Bath/ASME Symposium on Fluid Power and Motion Control. ASMEDC, 2011. http://dx.doi.org/10.1115/dscc2011-5953.

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Members of the animal kingdom produce motion by muscle contraction. Biological muscle can be viewed as a unidirectional actuator. To achieve bidirectional motion, each muscle has a corresponding antagonist muscle whose contraction produces motion in the opposite direction. This gives biological systems the unique ability to modulate the stiffness of a joint, which is important when interacting with the environment. Certain bio-inspired robotic systems incorporate antagonistic pairs in an attempt to produce similar desirable properties. The cellular actuator employs nested compliant mechanisms to produce human-scale motion from piezoelectric stack actuators, which on their own have a small displacement. The expression for the stiffness of the actuator composed of these mechanisms takes the form of a continued fraction, which results from the nested structure. In this way, the stiffness can be easily approximated to a desired degree of accuracy by considering only the outermost mechanisms.
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Rios Landeo, Ana Karina, Rafael Rodríguez García, Mireia Borràs Torralbo, Nuria Planet Nielsen, Isabel Alonso Fernandez, Anna Horta Llobet, Maria Martinez Ramirez, Claudia Bosch Ruiz, Meritxell Anton Soler, and Josep Cañete Crespillo. "Cariprazina y craving por cocaína." In 22° Congreso de la Sociedad Española de Patología Dual (SEPD) 2020. SEPD, 2020. http://dx.doi.org/10.17579/sepd2020p070.

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La adicción a la cocaína comparte, probablemente, los mismos circuitos subyacentes de la impulsividad. El transportador de dopamina (DAT) se ha identificado como el mecanismo de acción principal para el refuerzo de la adicción en el consumo de cocaína. Se ha demostrado que a largo plazo la anticipación de la recompensa y la búsqueda de sensaciones son más relevantes que la recompensa en sí misma. Además, la cocaína inhibe el transportador de norepinefrina (NET) y el transportador de serotonina (SERT). Los agonistas y antagonistas parciales de los receptores D2 y D₃ de dopamina podrían tener un importante papel en la prevención de recaídas en la adicción a la cocaína. Cariprazina se une preferentemente a receptores D3 de forma fásica, por lo que de esta manera podría ser útil para tratar el trastorno por dependencia de sustancias estimulantes, además de mejorar síntomas negativos, motivación y la cognición. Además, de ser agonista parcial del receptor 5HT1A y antagonista del receptor 5HT2B por lo que actuaría hipotéticamente como modulador y neutralizador de los efectos estimulantes de la cocaína y reduciendo el deseo por consumo. Métodos: Se realiza estudio observacional prospectivo, en pacientes en tratamiento con cariprazina (dosis entre 3 y 6mg/d) y trastorno por uso de cocaína con síntomas psicóticos , evaluando la respuesta al tratamiento mediante la anamnesis y tres cuestionarios: Escala de valoración de la gravedad selectiva para cocaína (CSSA) y Cuestionario de craving de cocaína (CCQ-GB) al inicio del tratamiento. Al mes de tratamiento, se revaloran escalas y se añade Inventario de actitudes al medicamento, (DAI) que valora la respuesta subjetiva a la medicación antipsicótica Resultados: pendientes.
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Martinez- Villalpando, Ernesto C., Jeff Weber, Grant Elliott, and Hugh Herr. "Design of an agonist-antagonist active knee prosthesis." In EMBS International Conference on Biomedical Robotics and Biomechatronics (BioRob 2008). IEEE, 2008. http://dx.doi.org/10.1109/biorob.2008.4762919.

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FIORIO, LUCA, FRANCESCO ROMANO, ALBERTO PARMIGGIANI, GIULIO SANDINI, and Francesco Nori. "Stiction Compensation in Agonist-Antagonist Variable Stiffness Actuators." In Robotics: Science and Systems 2014. Robotics: Science and Systems Foundation, 2014. http://dx.doi.org/10.15607/rss.2014.x.032.

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Oliver-Butler, Kaitlin, Zane H. Epps, and Daniel Caleb Rucker. "Concentric agonist-antagonist robots for minimally invasive surgeries." In SPIE Medical Imaging, edited by Robert J. Webster and Baowei Fei. SPIE, 2017. http://dx.doi.org/10.1117/12.2255549.

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Hadvary, P., and H. R. Baumgartner. "SELECTIVE ANTAGONISTS OF PAF: INTERFERENCE WITH PLATELET FUNCTION AND EFFECT ON THROMBOGENESIS INDUCED BY SUBENDOTHELIUM." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643488.

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Platelet activating factor (PAF) is a very potent excitatory agonist of blood platelets but the physiological importance of this mediator in platelet thrombus formation is not known. We investigated the effect of two chemically unrelated selective inhibitors of PAF-induced platelet aggregation on thrombogenesis induced by rabbit aorta subendothelium (SE) using an ex vivo perfusion system.Ro 19-3704 is a highly potent inhibitor structurally related to PAF. This compound inhibits PAF-induced aggregation of rabbit platelets in platelet rich plasma in vitro competitively. Against 4 nM PAF, a concentration resulting in submaximal platelet aggre-gregation velocity, the IC50 was 70 nM. Inhibition was highly selective for PAF-induced aggregation, since aggregation induced by collagen (HORM, 5 yg/ml), ADP (1 yM) or thrombin (0.4 U/ml) was not inhibited even at a concentration as high as 10 yM. Bro-tizolam, a triazolobenzodiazepine reported to be a selective inhibitor of PAF-induced platelet activation, had in our system an IC50 of 200 nM. The selective benzodiazepine antagonist Ro 151788 was without effect on inhibition of PAF-induced platelet activation by brotizolam.Ro 19-3704 was given intravenously to rabbits as a bolus of 0.2 mg/kg followed by constant infusion of 0.02 mg/kg/min. This dosage provoked ex vivo a constant right shift ratio of the dose response curve for PAF-induced aggregation (RSR[PAF]) by a factor of 25 to 35. Brotizolam was given orally at a dose of 100 mg/ kg together with 300 mg/kg of Ro 15-1788 (to antagonize the central effects) 90 minutes before starting the perfusion experiment, resulting in a RSR[PAF] of 35 to 135. ADP induced platelet aggregation was not impaired by either compound. SE was exposed to the non-anticoagulated blood withdrawn from the carotid artery for 3 min at 2600 s-1 and for 20 min at 200 s-1 shear rate. Quantitative morphometric evaluation showed that SE coverage by platelets and by fibrin, thrombus area and thrombus height were all unchanged by the PAF antagonists at low and at high shear rates despite a very substantial inhibition of PAF-induced platelet aggregation. Therefore a major role of PAF in SE-induced thrombogenesis seems unlikely.
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Johnson, G. J., P. C. Dunlop, M. J. Rabiet, L. A. Leis, and AH L. From. "THE DIHYDROPYRIDINE CALCIUM CHANNEL AGONIST, BAY K 8644, AND THE ANTAGONIST, NIFEDIPINE, INHIBIT U46619-INDUCED HUMAN PLATELET ACTIVATION BY COMPETITIVE BINDING TO THE THROMBOXANE A22/PGH2 RECEPTOR." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643756.

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The dihydropyridine (DP) Ca2+ channel antagonist, nifedipine (NF), inhibits platelet aggregation .in vitro and ex vivo by an undefined mechanism. Inhibition of Ca2+ influx via Ca2+ channels is a postulated mechanism, but voltage-dependent Ca2+ channels have not been demonstrated in platelets. We previously observed that NF blocked thromboxane A2 (TXA2)-induced platelet aggregation and secretion. In order to further evaluate the mechanism of DP inhibition of platelet activation, we studied the effects of NF and BAY K 8644, (BAY), a DP with opposite (agonist) effects on muscle cells, on human platelet aggregation and secretion induced by the TXA2 mimic, U46619. We also observed the effects of DP on biochemical consequences of platelet activation: cytoplasmic ionized Ca2+ ([Ca2+]i) by fura-2 fluorescence; phosphorylation of 40,000 Dalton protein (40KP) substrate of protein kinase C by SDS-PAGE and [32p] counting; TXA2 formation by RIA of TXB2. 1μM BAY and 10μM NF inhibited the 2nd wave of platelet aggregation and secretion induced by ADP or epinephrine and blocked aggregation and secretion induced by U46619. A Schild plot gave a slope of -1 indicating competitive inhibition of U46619 by BAY (K1[=0.7μM).BAY and NF also blocked U46619-induced phosphorylation of 40KP, rise in [Ca2+]i and TXB2 formation. The (+)-(R) enantiomer of BAY (BAY+) was responsible for BAY inhibition. BAY, BAY(+), and the R enantiomer of another DP, 202-791, all functioned as competitive antagonists of [3H]-U4661 9 binding (K1[ for BAY=2.8 μM-comparable to known receptor antagonists, 13-azaprostanoic acid and BM 13.177; K1 for BAY(+)=0.69μM). Neither BAY nor NF inhibited[3H]-yohimbine binding to α adrenergic receptors.NF, BAY, BAY(+) and BAY(-) in nM concentrations slightly stimulated platelet aggregation,secretion and biochemical events induced by U46619 similar to their effects on muscle. Therefore, DP's do not inhibit platelet activation by blocking voltage-dependent Ca2+ channels. The mechanism of DP inhibition of TXA2-induced platelet activation is stereoselective, competitive binding to the TXA2/PGH2 receptor. DP's may exert similar effects on TXA2-induced vascular smooth muscle contraction.
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Reports on the topic "Agoniste - Antagoniste"

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Idakwo, Gabriel, Sundar Thangapandian, Joseph Luttrell, Zhaoxian Zhou, Chaoyang Zhang, and Ping Gong. Deep learning-based structure-activity relationship modeling for multi-category toxicity classification : a case study of 10K Tox21 chemicals with high-throughput cell-based androgen receptor bioassay data. Engineer Research and Development Center (U.S.), July 2021. http://dx.doi.org/10.21079/11681/41302.

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Deep learning (DL) has attracted the attention of computational toxicologists as it offers a potentially greater power for in silico predictive toxicology than existing shallow learning algorithms. However, contradicting reports have been documented. To further explore the advantages of DL over shallow learning, we conducted this case study using two cell-based androgen receptor (AR) activity datasets with 10K chemicals generated from the Tox21 program. A nested double-loop cross-validation approach was adopted along with a stratified sampling strategy for partitioning chemicals of multiple AR activity classes (i.e., agonist, antagonist, inactive, and inconclusive) at the same distribution rates amongst the training, validation and test subsets. Deep neural networks (DNN) and random forest (RF), representing deep and shallow learning algorithms, respectively, were chosen to carry out structure-activity relationship-based chemical toxicity prediction. Results suggest that DNN significantly outperformed RF (p < 0.001, ANOVA) by 22–27% for four metrics (precision, recall, F-measure, and AUPRC) and by 11% for another (AUROC). Further in-depth analyses of chemical scaffolding shed insights on structural alerts for AR agonists/antagonists and inactive/inconclusive compounds, which may aid in future drug discovery and improvement of toxicity prediction modeling.
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Zhang, Yixian. Regulation of Agonist--and Antagonist--Mediated Activation of Human Progesterone Receptors by Phosphorylation. Fort Belvoir, VA: Defense Technical Information Center, July 1996. http://dx.doi.org/10.21236/ada315692.

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Zhang, Yixian. Regulation of Agonist- and Antagonist-Mediated Activation of Human Progesterone Receptors by Phosphorylation. Fort Belvoir, VA: Defense Technical Information Center, July 1995. http://dx.doi.org/10.21236/ada303820.

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Keightley, Maria C. The Mechanism by Which Agonist and Antagonist Occupied Progesterone Receptors Regulate Target Genes. Fort Belvoir, VA: Defense Technical Information Center, June 1998. http://dx.doi.org/10.21236/ada350945.

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Slamon, Dennis J. Biologic Effects of HER-2/Neu Gene Overexpression and Agonists and Antagonists to the Receptor in Human Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, August 1998. http://dx.doi.org/10.21236/ada372028.

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Budil, David E. Characterizing the Dynamic Response of the Estrogen Receptor to Agonists and Antagonists by Multifrequency Electron Spin Resonance Spin-Labeling. Fort Belvoir, VA: Defense Technical Information Center, May 2009. http://dx.doi.org/10.21236/ada523891.

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Salamon, Dennis J. Biologic Effects of HER-2/Neu Gene Overexpression and Agonists and Antagonists to the Receptor in Human Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, August 1997. http://dx.doi.org/10.21236/ada354413.

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Budil, David E., and Robert N. Hanson. Characterizing the Dynamic Response of the Estrogen Receptor to Agonists and Antagonists by Multi-frequency Electron Spin Resonance Spin-Labeling. Fort Belvoir, VA: Defense Technical Information Center, May 2007. http://dx.doi.org/10.21236/ada472067.

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Halker Singh, Rashmi B., Juliana H. VanderPluym, Allison S. Morrow, Meritxell Urtecho, Tarek Nayfeh, Victor D. Torres Roldan, Magdoleen H. Farah, et al. Acute Treatments for Episodic Migraine. Agency for Healthcare Research and Quality (AHRQ), December 2020. http://dx.doi.org/10.23970/ahrqepccer239.

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Objectives. To evaluate the effectiveness and comparative effectiveness of pharmacologic and nonpharmacologic therapies for the acute treatment of episodic migraine in adults. Data sources. MEDLINE®, Embase®, Cochrane Central Registrar of Controlled Trials, Cochrane Database of Systematic Reviews, PsycINFO®, Scopus, and various grey literature sources from database inception to July 24, 2020. Comparative effectiveness evidence about triptans and nonsteroidal anti-inflammatory drugs (NSAIDs) was extracted from existing systematic reviews. Review methods. We included randomized controlled trials (RCTs) and comparative observational studies that enrolled adults who received an intervention to acutely treat episodic migraine. Pairs of independent reviewers selected and appraised studies. Results. Data on triptans were derived from 186 RCTs summarized in nine systematic reviews (101,276 patients; most studied was sumatriptan, followed by zolmitriptan, eletriptan, naratriptan, almotriptan, rizatriptan, and frovatriptan). Compared with placebo, triptans resolved pain at 2 hours and 1 day, and increased the risk of mild and transient adverse events (high strength of the body of evidence [SOE]). Data on NSAIDs were derived from five systematic reviews (13,214 patients; most studied was ibuprofen, followed by diclofenac and ketorolac). Compared with placebo, NSAIDs probably resolved pain at 2 hours and 1 day, and increased the risk of mild and transient adverse events (moderate SOE). For other interventions, we included 135 RCTs and 6 comparative observational studies (37,653 patients). Compared with placebo, antiemetics (low SOE), dihydroergotamine (moderate to high SOE), ergotamine plus caffeine (moderate SOE), and acetaminophen (moderate SOE) reduced acute pain. Opioids were evaluated in 15 studies (2,208 patients).Butorphanol, meperidine, morphine, hydromorphone, and tramadol in combination with acetaminophen may reduce pain at 2 hours and 1 day, compared with placebo (low SOE). Some opioids may be less effective than some antiemetics or dexamethasone (low SOE). No studies evaluated instruments for predicting risk of opioid misuse, opioid use disorder, or overdose, or evaluated risk mitigation strategies to be used when prescribing opioids for the acute treatment of episodic migraine. Calcitonin gene-related peptide (CGRP) receptor antagonists improved headache relief at 2 hours and increased the likelihood of being headache-free at 2 hours, at 1 day, and at 1 week (low to high SOE). Lasmiditan (the first approved 5-HT1F receptor agonist) restored function at 2 hours and resolved pain at 2 hours, 1 day, and 1 week (moderate to high SOE). Sparse and low SOE suggested possible effectiveness of dexamethasone, dipyrone, magnesium sulfate, and octreotide. Compared with placebo, several nonpharmacologic treatments may improve various measures of pain, including remote electrical neuromodulation (moderate SOE), magnetic stimulation (low SOE), acupuncture (low SOE), chamomile oil (low SOE), external trigeminal nerve stimulation (low SOE), and eye movement desensitization re-processing (low SOE). However, these interventions, including the noninvasive neuromodulation devices, have been evaluated only by single or very few trials. Conclusions. A number of acute treatments for episodic migraine exist with varying degrees of evidence for effectiveness and harms. Use of triptans, NSAIDs, antiemetics, dihydroergotamine, CGRP antagonists, and lasmiditan is associated with improved pain and function. The evidence base for many other interventions for acute treatment, including opioids, remains limited.
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