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Artykuły w czasopismach na temat "Lacosamide"
Saria, Marlon G., Courtney Corle, Jethro Hu, Jeremy D. Rudnick, Surasak Phuphanich, Maciej M. Mrugala, Laura K. Crew i in. "Retrospective analysis of the tolerability and activity of lacosamide in patients with brain tumors". Journal of Neurosurgery 118, nr 6 (czerwiec 2013): 1183–87. http://dx.doi.org/10.3171/2013.1.jns12397.
Pełny tekst źródła&NA;. "Lacosamide". Reactions Weekly &NA;, nr 1392 (marzec 2012): 32. http://dx.doi.org/10.2165/00128415-201213920-00107.
Pełny tekst źródła&NA;. "Lacosamide". Reactions Weekly &NA;, nr 1357 (czerwiec 2011): 21. http://dx.doi.org/10.2165/00128415-201113570-00070.
Pełny tekst źródła&NA;. "Lacosamide". Reactions Weekly &NA;, nr 1362 (lipiec 2011): 20. http://dx.doi.org/10.2165/00128415-201113620-00070.
Pełny tekst źródła&NA;. "Lacosamide". Reactions Weekly &NA;, nr 1371 (październik 2011): 22–23. http://dx.doi.org/10.2165/00128415-201113710-00079.
Pełny tekst źródła&NA;. "Lacosamide". Reactions Weekly &NA;, nr 1404 (czerwiec 2012): 25–26. http://dx.doi.org/10.2165/00128415-201214040-00079.
Pełny tekst źródła&NA;. "Lacosamide". Reactions Weekly &NA;, nr 1406 (czerwiec 2012): 27. http://dx.doi.org/10.2165/00128415-201214060-00093.
Pełny tekst źródła&NA;. "Lacosamide". Reactions Weekly &NA;, nr 1413 (sierpień 2012): 31. http://dx.doi.org/10.2165/00128415-201214130-00112.
Pełny tekst źródłaCross, Sarah A., i Monique P. Curran. "Lacosamide". Drugs 69, nr 4 (2009): 449–59. http://dx.doi.org/10.2165/00003495-200969040-00005.
Pełny tekst źródła&NA;. "Lacosamide". Reactions Weekly &NA;, nr 1316 (sierpień 2010): 28–29. http://dx.doi.org/10.2165/00128415-201013160-00093.
Pełny tekst źródłaRozprawy doktorskie na temat "Lacosamide"
Reamtong, Onrapak. "The identification and characterisation of the target proteins of the anti-epileptic drug R-lacosamide". Thesis, University of Manchester, 2010. https://www.research.manchester.ac.uk/portal/en/theses/the-identification-and-characterisation-of-the-target-proteins-of-the-antiepileptic-drug-rlacosamide(2e2e4b3b-4101-46e3-886f-ff56c62d2b59).html.
Pełny tekst źródłaErrington, Adam C., i n/a. "Electrophysiological studies on the mechanism of action of the novel antiepileptic drug lacosamide". University of Otago. Department of Pharmacology & Toxicology, 2007. http://adt.otago.ac.nz./public/adt-NZDU20080613.162038.
Pełny tekst źródłaBeyreuther, Bettina [Verfasser], Carsten [Akademischer Betreuer] Korth i Rüdiger [Akademischer Betreuer] Seitz. "Lacosamide has protective disease modifying properties in experimental vincristine neuropathy / Bettina Beyreuther. Gutachter: Carsten Korth ; Rüdiger Seitz". Düsseldorf : Universitäts- und Landesbibliothek der Heinrich-Heine-Universität Düsseldorf, 2014. http://d-nb.info/1047666243/34.
Pełny tekst źródłaMoutal, Aubin, Lindsey A. Chew, Xiaofang Yang, Yue Wang, Seul Ki Yeon, Edwin Telemi, Seeneen Meroueh i in. "(S)-lacosamide inhibition of CRMP2 phosphorylation reduces postoperative and neuropathic pain behaviors through distinct classes of sensory neurons identified by constellation pharmacology". LIPPINCOTT WILLIAMS & WILKINS, 2016. http://hdl.handle.net/10150/621224.
Pełny tekst źródłaSchäfer, Carina [Verfasser], Stephanie [Akademischer Betreuer] Läer i Jörg [Akademischer Betreuer] Breitkreutz. "Development of a Combined Pharmacokinetic Model for Lacosamide and its Metabolite for Integrated Pharmacokinetic Modeling in Humans / Carina Schäfer. Gutachter: Stephanie Läer ; Jörg Breitkreutz". Düsseldorf : Universitäts- und Landesbibliothek der Heinrich-Heine-Universität Düsseldorf, 2016. http://d-nb.info/1081487828/34.
Pełny tekst źródłaPeckolt, Hannes [Verfasser]. "Untersuchungen zur Pharmakodynamik von Lacosamid mittels transkranieller Magnetstimulation / Hannes Peckolt". Kiel : Universitätsbibliothek Kiel, 2014. http://d-nb.info/104992908X/34.
Pełny tekst źródłaFlores, Teloxa Saúl. "Reacciones directas de la N-azidoacetil-1,3-tiazolidin-2-tiona catalizadas por complejos quirales de níquel(II) para la construcción enantioselectiva de enlaces carbono-carbono. Síntesis de la lacosamida y derivados de la β-hidroxifenilalanina". Doctoral thesis, Universitat de Barcelona, 2020. http://hdl.handle.net/10803/670070.
Pełny tekst źródłaIn this Doctoral dissertation new enantioselective and direct methodologies for the construction of carbon-carbon bonds through catalyzed reactions by chiral nickel(ll) complexes have been explored and optimized. In Chapter I, a direct, enantioselective and catalytic alkylation reaction of N-azidoacetyl-1,3- thiazolidine-2-thione with trimethyl orthoformate has been developed. According to the carried out optimization, we used 1,3-thiazolidine-2-thione as an achiral scaffold and [(R)-ToiBINAP]NiCI2 as a chiral catalyst in order to afford the best yield (82%) and enantiomeric excess (96%). Furthermore, as the scaffold has also the ability to act as an active ester, in Chapter II has been described the preparation of different amides in one pot processes with excellent yields (60-94%). These amides were easily transformed into potential biologically active compounds such as (R)-Iacosamide and analogues.In Chapter Ill, a one pot process to generate two stereogenic center have been described. In this methodology, the reaction of the nickel(ll) enolate derived from N-azidoacetyl-1,3-thiazolidin- 2-thione with p-anisaldehyde dimethylacetal has been optimized in a direct, catalytic and enantioselective reaction too. This protocol gave access in good yield (68%), highly diastereoselectivity (dr. 81:19), and excellent enantiomeric excess (99%) to anti α-azido- methoxycarboxylic adduct type. In Chapter IV, a new aldol and Michael type reactions methodologies have been developed from the reaction between N-azidoacetyl-1,3-thiazolidin-2-thione with aromatic aldehydes or α, β unsaturated aldehydes through direct, enantioselective and catalytic processes. Finally, in Chapter IV, a set of transformations has been detailed in which the scaffold act as an active ester giving access to a different β -hydroxyphenylalanine derivatives. The strategy involves the treatment with α-aminoesteres, primary and secondary amines, with enolates and reducing agents of some sililated aldols previously obtained in Chapter IV. In all the cases, the products were obtained in good to excellent yields.
Peng, Yi-Shuan, i 彭奕璇. "The mechanisms underlying the inhibitory effect of lacosamide on the voltage-gated sodium channels". Thesis, 2019. http://ndltd.ncl.edu.tw/handle/538v35.
Pełny tekst źródła國立臺灣大學
生理學研究所
107
It has been shown that the genesis of nerve excitation and action potential conduction is mainly controlled by voltage-gated sodium channels. Abnormal neuronal excitation may lead to neurological disorders like epilepsy. The sodium channel inhibitors such as carbamazepine, phenytoin, lamotrigine, have been the mainstay of medical treatment of epilepsy. These prototypical anticonvulsants have been shown to bind to the fast-inactivated state rather than resting state of the sodium ion channel. Lacosamide (LCM) is a new generation anticonvulsant, which also inhibits sodium channel but is different from the prototypical ones. The molecular actions of LCM on sodium channels are not clear, although selective binding to the slow-inactivated state of the sodium channel was proposed. We found that LCM dose-dependently inhibits sodium currents at more depolarized holding potentials, and the inhibitory effect could be described by different one-to-one binding curves at different holding potentials, giving an apparent dissociation constant (KI) of ~ 150 μM at -70mV for LCM binding to the inactivated sodium ion channels. The apparent dissociation constant derived from the ratio between the binding rate constant of LCM and the unbinding rate from the sodium channel is ~155 μM (at -70mV). In addition, a KI of ~156 μM is derived from the LCM concentration-dependent shift of the inactivation curve. The apparent dissociation constant of LCM for the sodium channel of the inactive state is therefore about 150-156 μM, which is much smaller than that for the resting sodium channels (>10mM). On the other hand, different inactivation curves are constructed with 100 milliseconds or 18 seconds inactivating pulses at various voltages (fast inactivation curves, slow inactivation curves and “combined’’ inactivation curves) to show that the very slow kinetics of LCM action on the inactivated sodium channels. Furthermore, LCM slows recovery from the inactivated to the resting state. The slowing effect is much more manifest with inactivating pulse at -10 than -80 mv, indicating that the effect of LCM on the slow-inactivated sodium channels is greater than on the fast-inactivated state. Last but not the least, we also explored the effect of concomitant LCM and phenytoin & LCM and lidocaine on sodium currents, and found that the LCM and phenytoin have a different action on the fast inactivation and slow inactivation of sodium channels; however, LCM and lidocaine have a synergistic inhibitory action on fast inactivation of the sodium channels.
Doccini, Viola. "Efficacy, Long-term Efficacy and Tolerability of Lacosamide, Stiripentol, Fenfluramine Hydrochloride and Levetiracetam in children, adolescents and young adults with different types of epilepsy". Doctoral thesis, 2022. https://hdl.handle.net/2158/1293559.
Pełny tekst źródłaWilson, Sarah Marie. "Involvement of Collapsin Response Mediator Protein 2 in Posttraumatic Sprouting in Acquired Epilepsy". Thesis, 2014. http://hdl.handle.net/1805/5604.
Pełny tekst źródłaPosttraumatic epilepsy, the development of temporal lobe epilepsy (TLE) following traumatic brain injury, accounts for 20% of symptomatic epilepsy. Reorganization of mossy fibers within the hippocampus is a common pathological finding of TLE. Normal mossy fibers project into the CA3 region of the hippocampus where they form synapses with pyramidal cells. During TLE, mossy fibers are observed to innervate the inner molecular layer where they synapse onto the dendrites of other dentate granule cells, leading to the formation of recurrent excitatory circuits. To date, the molecular mechanisms contributing to mossy fiber sprouting are relatively unknown. Recent focus has centered on the involvement of tropomycin-related kinase receptor B (TrkB), which culminates in glycogen synthase kinase 3β (GSK3β) inactivation. As the neurite outgrowth promoting collapsin response mediator protein 2 (CRMP2) is rendered inactive by GSK3β phosphorylation, events leading to inactivation of GSK3β should therefore increase CRMP2 activity. To determine the involvement of CRMP2 in mossy fiber sprouting, I developed a novel tool ((S)-LCM) for selectively targeting the ability of CRMP2 to enhance tubulin polymerization. Using (S)-LCM, it was demonstrated that increased neurite outgrowth following GSK3β inactivation is CRMP2 dependent. Importantly, TBI led to a decrease in GSK3β-phosphorylated CRMP2 within 24 hours which was secondary to the inactivation of GSK3β. The loss of GSK3β-phosphorylated CRMP2 was maintained even at 4 weeks post-injury, despite the transience of GSK3β-inactivation. Based on previous work, it was hypothesized that activity-dependent mechanisms may be responsible for the sustained loss of CRMP2 phosphorylation. Activity-dependent regulation of GSK3β-phosphorylated CRMP2 levels was observed that was attributed to a loss of priming by cyclin dependent kinase 5 (CDK5), which is required for subsequent phosphorylation by GSK3β. It was confirmed that the loss of GSK3β-phosphorylated CRMP2 at 4 weeks post-injury was likely due to decreased phosphorylation by CDK5. As TBI resulted in a sustained increase in CRMP2 activity, I attempted to prevent mossy fiber sprouting by targeting CRMP2 in vivo following TBI. While (S)-LCM treatment dramatically reduced mossy fiber sprouting following TBI, it did not differ significantly from vehicle-treated animals. Therefore, the necessity of CRMP2 in mossy fiber sprouting following TBI remains unknown.
Książki na temat "Lacosamide"
Cavanna, Andrea E. Other antiepileptic drugs: rufinamide, lacosamide, perampanel. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198791577.003.0017.
Pełny tekst źródłaPollandt, Sebastian, i Lori Shutter. Antiseizure agents in critical illness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0045.
Pełny tekst źródłaCzęści książek na temat "Lacosamide"
Patsalos, P. N. "Lacosamide". W Antiepileptic Drug Interactions, 227. London: Springer London, 2012. http://dx.doi.org/10.1007/978-1-4471-2434-4_36.
Pełny tekst źródłaPatsalos, P. N. "Lacosamide". W Antiepileptic Drug Interactions, 59–64. London: Springer London, 2012. http://dx.doi.org/10.1007/978-1-4471-2434-4_9.
Pełny tekst źródłaPatsalos, Philip N. "Lacosamide". W Antiepileptic Drug Interactions, 51–54. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-32909-3_10.
Pełny tekst źródłaPatsalos, Philip N. "Lacosamide". W Antiepileptic Drug Interactions, 179. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-32909-3_39.
Pełny tekst źródłaBiton, Victor. "Lacosamide". W Atlas of Epilepsies, 1761–65. London: Springer London, 2010. http://dx.doi.org/10.1007/978-1-84882-128-6_269.
Pełny tekst źródłaSachdeo, Rajesh, i Roopal Karia. "Lacosamide". W The Treatment of Epilepsy, 489–97. Oxford, UK: John Wiley & Sons, Ltd, 2015. http://dx.doi.org/10.1002/9781118936979.ch37.
Pełny tekst źródłaPatsalos, Philip N. "Lacosamide". W Antiseizure Medication Interactions, 89–92. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-82790-8_15.
Pełny tekst źródłaPatsalos, Philip N. "Lacosamide". W Antiseizure Medication Interactions, 215. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-82790-8_47.
Pełny tekst źródłaTilz, Christian. "Anticonvulsant Agents: Lacosamide and Perampanel". W NeuroPsychopharmacotherapy, 1–20. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-319-56015-1_449-1.
Pełny tekst źródłaTilz, Christian. "Anti-convulsant Agents: Lacosamide and Perampanel". W NeuroPsychopharmacotherapy, 3761–80. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-62059-2_449.
Pełny tekst źródłaStreszczenia konferencji na temat "Lacosamide"
Hsu, L., K. Dekitani i J. Betancourt. "Lacosamide and Metoprolol: An Uncommon Yet Potentially Deadly Combination". W American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a1695.
Pełny tekst źródłaLi, S., i B. Lindgren. "Suppressing All the Electricity: A Case of Lacosamide Induced Atrioventricular Block". W American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a3481.
Pełny tekst źródłaBezerra, Rebeka Ellen de Alencar, Agda Yasmim Ferreira Correia, Héryka Wanessa do Nascimento Rolim, Júlia Ondrusch de Moraes Costa, Maressa Ferreira de Alencar Rocha, Palloma Abreu Tavares i Alinne Beserra de Lucena Marcolino. "Importance of individualized diagnosis and treatment in refractory epilepsy associated with intellectual disability". W XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.050.
Pełny tekst źródłaBorras, A., V. Delgadillo, N. Julia, V. Gonzalez, J. Armstrong, D. Yubero i C. Fons. "Pharmacological Combination of Sodium Channel Blockers (Oxcarbazepine and Lacosamide) to Control Seizures in Two Patients with Neonatal-Onset Epilepsy due to De Novo SCNA2 Heterozygous Mutation". W Abstracts of the 48th Annual Meeting of the SENP (Société Européenne De Neurologie Pédiatrique). Georg Thieme Verlag KG, 2022. http://dx.doi.org/10.1055/s-0042-1746213.
Pełny tekst źródłaPaulus, W. "Risiken einer antikonvulsiven Therapie mit Lacosamid in der Schwangerschaft". W 29. Deutscher Kongress für Perinatale Medizin. Deutsche Gesellschaft für Perinatale Medizin (DGPM) – „Hinterm Horizont geht's weiter, zusammen sind wir stark“. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-3401247.
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