Thematische Bibliographien / Neuromuscular transmission

Auswahl der wissenschaftlichen Literatur zum Thema „Neuromuscular transmission“

Autor: Grafiati

Veröffentlicht am 4. Juni 2021

Zuletzt aktualisiert am 2. März 2023

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Zeitschriftenartikel zum Thema "Neuromuscular transmission":

MacLean, Ian C. „Neuromuscular Transmission“. Physical Medicine and Rehabilitation Clinics of North America 1, Nr. 1 (November 1990): 43–52. http://dx.doi.org/10.1016/s1047-9651(18)30745-9.

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Parker, C. „Neuromuscular transmission“. Postgraduate Medical Journal 74, Nr. 870 (01.04.1998): 255. http://dx.doi.org/10.1136/pgmj.74.870.255-a.

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Torda, T. A. „Monitoring Neuromuscular Transmission“. Anaesthesia and Intensive Care 30, Nr. 2 (April 2002): 123–33. http://dx.doi.org/10.1177/0310057x0203000202.

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Persistent neuromuscular blockade is not uncommon in the recovery room and contributes to postoperative morbidity and possibly mortality. The use of neuromuscular monitoring and intermediate rather than long-acting neuromuscular blocking drugs have been shown to reduce its incidence. Clinically available methods of detecting and quantitating neuromuscular blockade are reviewed. The writer concludes that such monitoring should be routine when neuromuscular blocking drugs are used.

Beemer, G. H., und P. H. Goonetilleke. „Monitoring neuromuscular transmission“. Current Anaesthesia & Critical Care 7, Nr. 2 (April 1996): 101–6. http://dx.doi.org/10.1016/s0953-7112(96)80065-2.

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Pascuzzi, Robert. „Disorders of Neuromuscular Transmission“. Seminars in Neurology 24, Nr. 02 (15.07.2004): 137. http://dx.doi.org/10.1055/s-2004-830898.

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Weissman, J. D. „Electromyography: Neuromuscular Transmission Studies“. Neurology 39, Nr. 8 (01.08.1989): 1141. http://dx.doi.org/10.1212/wnl.39.8.1141-b.

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Meistelman, Claude. „Monitoring of neuromuscular transmission“. Current Opinion in Anaesthesiology 6, Nr. 4 (August 1993): 720–25. http://dx.doi.org/10.1097/00001503-199308000-00024.

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Wareham, Anthony C. „Neuromuscular function and transmission“. Anaesthesia & Intensive Care Medicine 6, Nr. 6 (Juni 2005): 203–5. http://dx.doi.org/10.1383/anes.6.6.203.65787.

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Krendel, David. „Hypermagnesemia and Neuromuscular Transmission“. Seminars in Neurology 10, Nr. 01 (März 1990): 42–45. http://dx.doi.org/10.1055/s-2008-1041252.

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WINDSOR, J. P. W., P. S. SEBEL und P. J. FLYNN. „The neuromuscular transmission monitor“. Anaesthesia 40, Nr. 2 (22.02.2007): 146–51. http://dx.doi.org/10.1111/j.1365-2044.1985.tb10705.x.

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Dissertationen zum Thema "Neuromuscular transmission":

Carvalho, Vanessa Henriques 1974. „Ação dos anestésicos locais na transmissão neuromuscular e influência no bloqueio produzido pelo pancurônio : eficácia da neostigmina e da 4-aminopiridina na reversão do bloqueio neuromuscular: estudo experimental“. [s.n.], 2013. http://repositorio.unicamp.br/jspui/handle/REPOSIP/312496.

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Orientador: Angélica de Fátima de Assunção Braga
Tese (doutorado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas
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Resumo: Os anestésicos locais (AL) podem interagir com os bloqueadores neuromusculares (BNM) e modificar as suas propriedades farmacocinéticas e farmacodinâmicas, no entanto o mecanismo dessa interação é controverso. Este estudo experimental, realizado em preparações nervo frênico - hemidiafragma de rato e músculo biventer cervicis de pintainho, teve por objetivo avaliar o efeito de diferentes AL na transmissão neuromuscular e sua influência no bloqueio produzido pelo pancurônio. Foram avaliados os seguintes parâmetros: efeito na transmissão neuromuscular dos AL (ropivacaína, levobupivacaína, mistura em excesso enantiomérico de bupivacaína) e do pancurônio empregados isoladamente; o bloqueio produzido pelo pancurônio em preparações previamente expostas aos AL; a eficácia da neostigmina e da 4-aminopiridina na reversão do bloqueio neuromuscular produzido pelo pancurônio isoladamente e em preparações previamente expostas aos AL; a ação dos AL na resposta contraturante à acetilcolina; seus efeitos nos potenciais de membrana e nos potenciais de placa terminal em miniatura. Os resultados foram expressos em médias e desvios padrão e analisados através dos testes t de Student, Wilcoxon, Anova, Kruskall-Wallis e Mann-Whitney. Adotou-se um nível de significância de 5% (p<0,05). Na preparação nervo frênico - hemidiafragma de rato, os AL nas concentrações empregadas, não alteraram a amplitude das respostas musculares mas, potencializaram o efeito do pancurônio. O bloqueio neuromuscular foi parcial e totalmente revertido com a neostigmina e com a 4-aminopiridina, respectivamente. Não causaram alteração significativa nos potenciais de membrana e produziram diminuição progressiva na amplitude e na frequência dos potenciais de placa terminal em miniatura. Na preparação biventer cervicis de pintainho os AL, com exceção da ropivacaína, promoveram diminuição na resposta contraturante da acetilcolina. Os resultados obtidos neste estudo demonstram um sinergismo entre os fármacos estudados, resultante das ações pré e pós-juncionais dos anestésicos locais
Abstract: Local anaesthetics (LA) may interact with neuromuscular blockers and modify their pharmacokinetic and pharmacodynamic properties. However, the mechanism of this interaction is controversial. This experimental study, conducted in rat phrenic nerve diaphragm preparations and chick biventer cervicis, aimed to evaluate the effect of different LA in neuromuscular transmission and its influence on pancuronium induced blockade. The following parameters were evaluated: the effect on neuromuscular transmission of LA (ropivacaine , levobupivacaine mixture enantiomeric excess bupivacaine) and pancuronium used in isolation; the blockade produced by pancuronium in preparations previously exposed to LA; the effectiveness of neostigmine and 4 - aminopyridine in the reversal of neuromuscular blockade produced by pancuronium alone and in preparations previously exposed to AL; the action of LA in the contractile response to acetylcholine; its effects on membrane potentials and miniature endplate potentials. The results were expressed as means and standard deviations and analyzed using Student's t, Wilcoxon, ANOVA, Kruskal-Wallis and Mann-Whitney tests. A significance level of 5 % (p < 0,05) was adopted . In the rat phrenic nerve diaphragm preparation the LA, in the concentrations used, did not alter the amplitude of muscle response but potentiated the effect of pancuronium. Neuromuscular blockade was partially and fully reversed with neostigmine and 4- aminopyridine, respectively. There was no significant change in membrane potential and a progressive decrease in the amplitude and frequency of miniature endplate potentials was produced. In the chick biventer cervicis preparation the LA, with the exception of ropivacaine, led to a decrease in the contractile response to acetylcholine. The results of this study demonstrate a synergistic effect between the drugs studied, resulting from prejunctional and postjunctional actions of LAs
Doutorado
Farmacologia
Doutora em Farmacologia

England, Adrian James. „The effect of moderate hypothermia on neuromuscular transmission and neuromuscular blockade“. Thesis, Imperial College London, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.338687.

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Dusl, Marina. „Novel pathomechanisms implicated in defects of neuromuscular transmission“. Diss., Ludwig-Maximilians-Universität München, 2015. http://nbn-resolving.de/urn:nbn:de:bvb:19-180274.

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Budd, Timothy Charles. „An immunological investigation of neuromuscular transmission in insects“. Thesis, University of Nottingham, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.334782.

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Luheshi, G. N. „Diabetes in the rat and postganglionic neuromuscular transmission“. Thesis, University of Newcastle Upon Tyne, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.287330.

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Dissanayake, Kosala Nimanthi. „Evaluation of neuromuscular transmission in organophosphorus pesticide toxicity“. Thesis, University of Edinburgh, 2015. http://hdl.handle.net/1842/15837.

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Organophosphorus (OP) pesticide toxicity is a global health problem. Respiratory failure due to neuromuscular transmission dysfunction accounts for about 300,000 deaths annually in rural Asia. However, the clinical manifestation is complex, and described in terms of acute, intermediate, and chronic syndromes. The underlying mechanism of toxicity is still unclear. OP pesticides contain inhibitors of acetylcholinesterase (AChE), for example dimethoate, emulsified in an organic solvent, typically cyclohexanone. A hypothesized mechanism is initial excitotoxicity through inhibition of acetylcholinesterase followed by failure of neuromuscular synaptic transmission. I tested this electrophysiologically in vitro by measuring properties of spontaneous miniature endplate potentials (MEPPs) and evoked endplate potentials (EPPs) in isolated sciatic nerve/flexor digitorum brevis muscles from mice, bathed in HEPES-buffered mammalian physiological saline (MPS). Muscle action potentials were abolished with μ-conotoxin (2μM). First, we tested the effects of plasma taken from Göttingen minipigs instilled orally (isofluorane anaesthesia) with a formulated pesticide (2.5ml/kg) whose active ingredient is dimethoate dissolved in cyclohexanone. This plasma abolished evoked synaptic transmission and increased spontaneous MEPP frequency within 60-180 minutes of bath application. However plasma from minipigs instilled with dimethoate alone produced no failure of transmission. Plasma contained either pesticide or dimethoate significantly increased the half decay time of EPPs. However, pesticide-plasma also contained the metabolites omethoate (100μM) and cyclohexanol (5 mM). We found that bath application of omethoate alone caused a potent dose-dependent increase in EPP decay time. Cyclohexanol (5 mM) also increased EPP decay time but it also decreased both the excitability of axons and MEPP amplitude. In combination, omethoate and cyclohexanol produced greater disruption of neuromuscular transmission than either dimethoate or cyclohexanone, alone or in combination and this was particularly evident in isometric tension recordings, in which prolonged after-contraction and slow relaxation were observed during and immediately following tetanic stiumuation in the presence of omethoate and cyclohexanol. Voltage-clamp recordings of endplate currents (EPC) partially supported the EPP observations. Surprisingly, cyclohexanol-treated preparations showed no significant increase in EPC and MEPC decay time. However, there was some evidence of activity-dependent decline in MEPC amplitude in cyclohexanol while quantal content in these preparations showed evidence of an increase suggesting a homeostatic response in evoked transmitter release with cyclohexanol treatment. Analysis of presynaptic currents in cyclohexanol treated preparations also revealed preliminary evidence of sensitivity to cyclohexanol compared to control preparations. Finally, I tested the effects NMJ transmission of 24hr exposure to OP pesticide and its metabolites using a novel organ culture system, utilising a mouse mutant (WldS) with a slow nerve degeneration phenotype. After incubation of 24 hrs with MPS + pesticides and metabolites, these muscles showed significant reduction in function (response to nerve stimuli with EPP/action potential ± MEPPs) compared to control cultures. Together, the data indicate that failure of neuromuscular transmission by pesticide-plasma cannot be explained solely by dimethoate-mediated inhibition of acetylcholinesterase. Rather, a combination of metabolic breakdown products exerts potent, harmful presynaptic and postsynaptic effects. Either blocking the metabolic conversion of the constituents of OP pesticides, or transiently blocking their effects on receptors may therefore be an effective strategy for treatment of OP pesticide toxicity.

Kalliomäki, Jarkko. „Parallel processing of nociceptive information evidence for multiple reflex and ascending nociceptive pathways /“. Lund : Dept. of Physiology and Biophysics, University of Lund, 1992. http://books.google.com/books?id=PMlqAAAAMAAJ.

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Morgan, Gareth P. „Neuromuscular transmission in murine muscular dystrophy (129 ReJ strain)“. Thesis, Aston University, 1985. http://publications.aston.ac.uk/12486/.

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Zhu, Chuan. „Src signaling in neuromuscular junction induction /“. View abstract or full-text, 2010. http://library.ust.hk/cgi/db/thesis.pl?BIOL%202010%20ZHU.

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Loyola, Yolanda Christina de Sousa. „Influencia dos anestesicos locais no bloqueio neuromuscular produzido por diferentes bloqueadores neuromusculares : estudo experimental“. [s.n.], 2006. http://repositorio.unicamp.br/jspui/handle/REPOSIP/310900.

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Orientador: Angelica de F. de Assunção Braga
Tese (doutorado) - Universidade Estadual de Campinas, Faculdade de Ciencias Medicas
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Resumo: Os anestésicos locais comumente empregados na prática clínica podem interagir com os bloqueadores neuromusculares e potencializar seus efeitos. Muitos autores estudaram esta interação mas o mecanismo envolvido na potencialização do bloqueio neuromuscular e a ação dos anestésicos locais nos sítios pré e pós juncionais não foram completamente elucidados. Neste trabalho através de experimentos específicos na junção neuromuscular foram estudados os seguintes parâmetros: o efeito dos anestésicos locais procaína e lidocaína na transmissão neuromuscular; a sua influência no bloqueio neuromuscular produzido pela d-tubocurarina e pelo rocurônio; a eficácia da neostigmina e da 4-aminopirídina na reversão do bloqueio produzido pela associação anestésicos locais - bloqueadores neuromusculares; os efeitos dos anestésicos locais nos potenciais de membrana e potenciais de placa terminal em miniatura. Avaliou-se também em preparações diafragma de rato cronicamente desnervado e biventer cervicis de pintainho os efeitos dos anestésicos locais na ação contraturante da acetilcolina. Os resultados foram expressos em médias e desvios padrão e analisados através dos testes de Wilcoxon e Mann-Witney, adotando-se um nível de significância de 5% (p < 0,05). Nas preparações nervo frênico - diafragma de rato, sob estimulação elétrica indireta, os anestésicos locais nas concentrações empregadas, não alteraram a amplitude das respostas musculares mas potencializaram os efeitos da d- tubocurarina e do rocurônio.. Este bloqueio foi parcialmente e totalmente revertido pela neostigmina e pela 4-aminopiridina, respectivamente. A procaína e a lidocaína não causaram alteração significativa nos potenciais de membrana, não demonstrando ação despolarizante na fibra muscular. A procaína causou diminuição na amplitude e na freqüência dos potenciais de placa terminal em miniatura (pptms) e a lidocaína, ao contrário, promoveu um aumento inicial na freqüência dos pptms seguida de bloqueio. Nas preparações biventer cervicis de pintainho e diafragma de rato cronicamente desnervado, a procaína e a lidocaína promoveram diminuição significativa na resposta contraturante da acetilcolina evidenciando um efeito pós-juncional. Os resultados obtidos demonstram um sinergismo entre as drogas devido principalmente a um efeito pós-juncional
Abstract: Local anesthetics commonly used in clinical practice can interact with neuromuscular blockers and potentiate their effects. Many authors studied this interaction, but the mechanism involved in the potentiation of neuromuscular blockers and the action of local anesthetics in the pre and postjunctional sites were not completely elucidated- In this study, in specific experiments in the neuromuscular junction the following parameters were studied: the effects of the local anesthetics procaine and lidocaine in the neuromuscular transmission; its influence on the neuromuscular blockade produced by d-tubocurarine and by rocuronium; the efficacy of neostigmine and of 4-aminopyhdine in the reversion of the blockade produced by the association of local anesthetics - neuromuscular blockers; the effects of local anesthetics on the membrane potentials and miniature end - plate potentials. It was also evaluated in chronically denervated rat diaphragm preparation and chick biventer cervicis preparation the effects of local anesthetics on acetylcholine contracture. The results were expressed in average and standard deviation and analyzed through the Wilcoxon and Mann-Witney tests, adopting a level of significance of 5% (p <0.05). In rat phrenic nerve diaphragm preparations under indirect electric stimulation, local anesthetics in the concentrations used did not change the amplitude of the muscle response but potentiated the effects of d-tubocurarine and of rocuronium. This blockade was partially and totally reverted by neostigmine and by 4-aminopyridine, respectively. Procaine and lidocaine caused no significant alteration in the membrane potentials, not demonstrating depolarizing action in the muscle fiber. Procaine caused a decrease in the amplitude and frequency of the miniature end - plate potentials {meps) and lidocaine, in contrast, promoted an initial increase in the frequency of meps followed by blockade. In chick biventer cervicis preparations and chronically denervated rat diaphragm, procaine and lidocaine promoted a significant decrease in the response to acetylcholine contracture evidencing a post-junctional effect. The results obtained demonstrate a synergism among the drugs mainly due to a postjunctional effect
Doutorado
Doutor em Farmacologia

Mehr Quellen

Bücher zum Thema "Neuromuscular transmission":

Oh, Shin J. Electromyography: Neuromuscular transmission studies. Baltimore: Williams & Wilkins, 1988.

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Angela, Vincent, und W. Wray Dennis, Hrsg. Neuromuscular transmission: Basic and applied aspects. Manchester, UK: Manchester University Press, 1990.

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David, Evered, und Whelan Julie, Hrsg. Placticity of the neuromuscular system. Chichester, N.Y: Wiley, 1988.

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Bowman, W. C. Pharmacology of neuromuscular function. 2. Aufl. London: Wright, 1990.

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Akoev, G. N. Funkt͡s︡ionalʹnai͡a︡ organizat͡s︡ii͡a︡ mekhanoret͡s︡eptorov. Leningrad: Izd-vo "Nauka", Leningradskoe otd-nie, 1985.

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Morgan, Gareth Philip. Neuromuscular transmission in murine muscular dystrophy (129 ReJ strain). Birmingham: University of Aston. Department of Pharmaceutical Sciences, 1985.

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Clifford, Rose F., Jones Rosemary Ph D und Vrbová Gerta, Hrsg. Neuromuscular stimulation: Basic concepts and clinical implications. New York, N.Y: Demos, 1989.

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David, Evered, und Whelan Julie, Hrsg. Plasticity of the neuromuscular system. Chichester: Wiley, 1988.

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V, Evarts Edward, Wise Steven P und Bousfield David, Hrsg. The motor system in neurobiology. Amsterdam: Elsevier Biomedical Press, 1985.

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Keynes, R. D. Nerve and muscle. 4. Aufl. Cambridge: Cambridge University Press, 2011.

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Buchteile zum Thema "Neuromuscular transmission":

Allen, Molly, und Rebecca A. Johnson. „Neuromuscular Transmission Monitoring“. In Veterinary Anesthetic and Monitoring Equipment, 271–84. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2018. http://dx.doi.org/10.1002/9781119277187.ch21.

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Salih, Mustafa A. M. „Neuromuscular Transmission Disorders“. In Textbook of Clinical Pediatrics, 3493–502. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-02202-9_373.

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Rana, Abdul Qayyum, Ali T. Ghouse und Raghav Govindarajan. „Neuromuscular Transmission Disorders“. In Neurophysiology in Clinical Practice, 153–63. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-39342-1_19.

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Salih, Mustafa A. M., und Peter B. Kang. „Neuromuscular Transmission Disorders“. In Clinical Child Neurology, 1257–79. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-319-43153-6_42.

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Skeie, G. O., S. Apostolski, A. Evoli, N. E. Gilhus, I. Illa, L. Harms, D. Hilton-Jones, A. Melms, J. Verschuuren und H. Westgaard Horge. „Autoimmune Neuromuscular Transmission Disorders“. In European Handbook of Neurological Management, 321–31. Oxford, UK: Wiley-Blackwell, 2010. http://dx.doi.org/10.1002/9781444328394.ch19.

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Löscher, Wolfgang N. „Neuromuscular Transmission: Endplate Disorders“. In Atlas of Neuromuscular Diseases, 235–46. Vienna: Springer Vienna, 2014. http://dx.doi.org/10.1007/978-3-7091-1605-0_10.

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Howard, James F. „Toxic Neuromuscular Transmission Disorders“. In Myasthenia Gravis and Related Disorders, 255–77. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-156-7_16.

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Nyberg-Hansen, Rolf, und Leif Gjerstad. „Disorders of Neuromuscular Transmission“. In Immunopharmacology in Autoimmune Diseases and Transplantation, 325–33. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4899-1167-4_25.

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Howard, James F. „Toxic Neuromuscular Transmission Disorders“. In Myasthenia Gravis and Related Disorders, 327–54. Totowa, NJ: Humana Press, 2003. http://dx.doi.org/10.1007/978-1-59259-341-5_15.

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Howard, James F. „Toxic Neuromuscular Transmission Disorders“. In Neuromuscular Disorders in Clinical Practice, 1129–45. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-6567-6_52.

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Konferenzberichte zum Thema "Neuromuscular transmission":

Lochmüller, H. „Update on inherited neuromuscular transmission disorders (congenital myasthenic syndromes)“. In 24. Kongress des Medizinisch-Wissenschaftlichen Beirates der Deutschen Gesellschaft für Muskelkranke (DGM) e.V. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1684994.

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Mahmud, M., M. M. Rahman und S. Vassanelli. „Na+ channels at postsynaptic muscle membrane affects synaptic transmission at Neuromuscular Junction: A simulation study“. In 2012 34th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2012. http://dx.doi.org/10.1109/embc.2012.6346749.

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Kadenov, A. N., und O. V. Yakovleva. „Effect of hydrogen sulfide on the characteristics of the neuromuscular synapse terminals of the rat diaphragm“. In VIII Vserossijskaja konferencija s mezhdunarodnym uchastiem «Mediko-fiziologicheskie problemy jekologii cheloveka». Publishing center of Ulyanovsk State University, 2021. http://dx.doi.org/10.34014/mpphe.2021-102-104.

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Hydrogen sulfide is one of the gas-transmitters that also performs other biological functions. The antioxidant property of this substance is one of the important ones. The research was conducted on rats of both sexes between 6 and 18 days of age. We have shown that the offspring of females injected subcutaneously with hydrogen sulfide increased the area and luminescence of nerve terminals during postnatal ontogenesis, which can be further used to level the effects of hyperhomocysteinemia on synaptic transmission. Key words: neuromuscular synapse, fluorescent microscopy, hydrogen sulfide.

Zakyrjanova, Guzalja, und Alexey Petrov. „THE EFFECT OF 25-HYDROXYCHOLESTEROL ON NEUROMUSCULAR TRANSMISSION: THE ROLE OF PROTEIN KINASE C AND NMDA RECEPTORS“. In XV International interdisciplinary congress "Neuroscience for Medicine and Psychology". LLC MAKS Press, 2019. http://dx.doi.org/10.29003/m395.sudak.ns2019-15/183-184.

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Chen, Kai, Richard A. Foulds, Katharine Swift und Sergei Adamovich. „Experimental Study and Modeling of Equilibrium Point Trajectory Control in Single and Double-Joint Arm Movements“. In ASME 2009 International Mechanical Engineering Congress and Exposition. ASMEDC, 2009. http://dx.doi.org/10.1115/imece2009-10251.

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This paper discusses a new model of neuromuscular control of elbow and shoulder joints based on the Equilibrium Point Hypothesis (EPH). The earlier model [1] suggests that the incorporation of relative damping within reflex loops can maintain the dynamic simplicity of the EPH, while being robust over the range of human joint velocities. The model presented here, extends previous work with the use of experimental Electromyography data of 2 muscles to determine the timing parameters of the virtual trajectories and the inclusion of physiological time delays to account for neural transmission and muscle stimulation/activation delays. This model uses delays presented in the literature by other researchers, with a goal of contributing to a resolution of arguments regarding the controversial arguments in the planning sequences. Therefore, this study attempts to demonstrate the possibility for using descending CNS signals to represent relatively simple, monotonic virtual trajectories of the time varying Equilibrium Point for the control of human arm movement. In addition, the study demonstrates that these virtual trajectories were robust enough to control and coordinated movement of elbow and shoulder joints discussed.

Gomes, Maria Clara Cavalcante, Nathaly Bruna de Oliveira Silva, João Lucas Pessoa de Vasconcelos, Saulo Brivaldo Mendonça da Silva, Mariana Souza Bezerra Cavalcanti und Ana Bárbara Xavier da Silva. „USO DA TOXINA BOTULÍNICA COMO TERAPIA COADJUVANTE EM PACIENTES COM DOENÇA DE PARKINSON, DISFUNÇÕES TEMPOROMANDIBULARES E BRUXISMO“. In XXVII Semana de Biomedicina Inovação e Ciência. Editora IME, 2021. http://dx.doi.org/10.51161/9786588884119/46.

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Introdução: A toxina botulínica é uma neurotoxina produzida pelo Clostridium botulinum, causador do botulismo, doença neuroparalítica grave(1,3). Esta, é uma proteinase de zinco que realiza a clivagem de proteínas associadas a vesículas neuronais, responsáveis pela liberação de acetilcolina na junção neuromuscular(1). A doença de Parkinson (DP), afeta significativamente a vida dos pacientes, alguns não respondem às opções terapêuticas aplicadas costumeiramente, prejudicando ainda mais essa situação(2). Ademais, disfunções temporomandibulares (DTMs) e bruxismo do sono (BS), são condições que prejudicam significativamente os pacientes, causando dores e movimentos mandibulares restritos(4). A utilização da toxina botulínica, é vista ligada principalmente a fins estéticos, contudo sua utilidade vai muito além disso. Objetivos: Este resumo possui como objetivo avaliar e correlacionar o uso da toxina botulínica à doença de Parkinson, DTMs e Bruxismo como uma possível alternativa terapêutica. Métodos: Foi realizada uma pesquisa de artigos científicos nas plataformas Pubmed e Sciencedirect, buscando por meio dos descritores “botulinum toxin AND parkinsonism, botulinum toxin AND bruxism”, onde foi encontrado os artigos utilizados. Resultados: O uso de toxina botulínica mostrou diversos benefícios quando avaliado em pacientes com DP, DTMs e BS. Isso foi evidente ao avaliar a sialorréia, que acomete 86% dos pacientes com DP, caracterizando a incapacidade de controlar as secreções orais, que após a aplicação da toxina botulínica nas glândulas salivares houve a inibição da transmissão colinérgica parassimpática e simpática pósganglionar, promovendo a diminuição da secreção salivar(2). Além disso, a disfunção urinária ligada a DP também mostrou bons prognósticos quando submetidos à aplicação da toxina, agindo no músculo detrusor podendo trazer benefício por até 6 meses(2).Em pacientes com DTMs e BS, submetidos a uma sessão de injeção da toxina nos músculos temporal e masseter, foi possível observar uma melhora considerável nos níveis de dor, como também nos movimentos mandibulares, avaliados no pós-operatório, em um, três e seis meses após o tratamento(4). Conclusões: Dessa forma, é possível concluir que o uso da terapia com toxina botulínica nos distúrbios de parkinsonismo, disfunções temporomandibulares e bruxismo tem uma grande importância terapêutica coadjuvante auxiliando de forma significativa no tratamento dos sintomas dessas síndromes. Porém, mais estudos são necessários para melhor compreender os mecanismos dessa toxina em cada síndrome, bem como buscar a padronização de doses nas mesmas, além de sua utilização em outras enfermidades.