Academic literature on the topic 'Clomethiazole'

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Journal articles on the topic "Clomethiazole"

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Kong, Robert S., John Butterworth, Wynne Aveling, David A. Stump, Michael J. G. Harrison, John Hammon, Jan Stygall, Kashemi D. Rorie, and Stanton P. Newman. "Clinical Trial of the Neuroprotectant Clomethiazole in Coronary Artery Bypass Graft Surgery." Anesthesiology 97, no. 3 (September 1, 2002): 585–91. http://dx.doi.org/10.1097/00000542-200209000-00011.

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Background The neuroprotective property of clomethiazole has been demonstrated in several animal models of global and focal brain ischemia. In this study the authors investigated the effect of clomethiazole on cerebral outcome in patients undergoing coronary artery bypass surgery. Methods Two hundred forty-five patients scheduled for coronary artery bypass surgery were recruited at two centers and prospectively randomized to clomethiazole edisilate (0.8%), 225 ml (1.8 mg) loading dose followed by a maintenance dose of 100 ml/h (0.8 mg/h) during surgery, or 0.9% NaCl (placebo) in a double-blind trial. Coronary artery grafting was completed during moderate hypothermic (28-32 degrees C) cardiopulmonary bypass. Plasma clomethiazole was measured at several intervals during and up to 24 h after the end of infusion. A battery of eight neuropsychological tests was administered preoperatively and repeated 4-7 weeks after surgery. Analysis of the change in neuropsychological test scores from baseline was used to determine the effect of treatment. Results Neuropsychological assessments were completed in 219 patients (110 clomethiazole; 109 placebo). The mean plasma concentration of clomethiazole during surgery was 66.2 microm. There was no difference between the clomethiazole and placebo group in the postoperative change in neuropsychological test scores. Conclusion Clomethiazole did not improve cerebral outcome following coronary artery bypass surgery.
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&NA;. "Clomethiazole." Reactions Weekly &NA;, no. 1014 (August 2004): 8. http://dx.doi.org/10.2165/00128415-200410140-00020.

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&NA;. "Clomethiazole." Drugs in R & D 1, no. 1 (January 1999): 20–21. http://dx.doi.org/10.2165/00126839-199901010-00006.

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&NA;. "Clomethiazole." Reactions Weekly &NA;, no. 533 (January 1995): 7. http://dx.doi.org/10.2165/00128415-199505330-00019.

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Vaishnav, Anand, and Helmi L. Lutsep. "GABA Agonist: Clomethiazole." Current Medical Research and Opinion 18, sup2 (January 2002): s5—s8. http://dx.doi.org/10.1185/030079902125000651.

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Wahlgren, N. G., K. W. Ranasinha, T. Rosolacci, C. L. Franke, P. M. M. van Erven, T. Ashwood, and L. Claesson. "Clomethiazole Acute Stroke Study (CLASS)." Stroke 30, no. 1 (January 1999): 21–28. http://dx.doi.org/10.1161/01.str.30.1.21.

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Heinemann, F., and H. J. Assion. "Hepatotoxic Side-Effect of Clomethiazole." Pharmacopsychiatry 29, no. 05 (September 1996): 196–97. http://dx.doi.org/10.1055/s-2007-979571.

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Jostell, K. G., S. Agurell, L. G. Allgén, B. Kuylenstierna, J. E. Lindgren, G. Åberg, and G. Österlöf. "Pharmacokinetics of Clomethiazole in Healthy Adults." Acta Pharmacologica et Toxicologica 43, no. 3 (March 13, 2009): 180–89. http://dx.doi.org/10.1111/j.1600-0773.1978.tb02253.x.

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Petersson, Tomas, and Sven Engström. "Surface and interfacial properties of clomethiazole." International Journal of Pharmaceutics 132, no. 1-2 (April 1996): 231–42. http://dx.doi.org/10.1016/0378-5173(95)04375-6.

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Norene, M. F., P. A. Christensen, P. Thiessen, and P. Glenting. "Clomethiazole Treatment in a Child with Status Epilepticus." Acta Paediatrica 76, no. 5 (September 1987): 839–40. http://dx.doi.org/10.1111/j.1651-2227.1987.tb10575.x.

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Dissertations / Theses on the topic "Clomethiazole"

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Clarkson, Andrew N., and n/a. "Lasting neuroprotection with clomethiazole following hypoxia-ischaemia-induced neurodegeneration : a mechanistic study." University of Otago. Department of Pharmacology & Toxicology, 2005. http://adt.otago.ac.nz./public/adt-NZDU20070424.120005.

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Subsequent to an hypoxic-ischaemic (HI)-insult a multi-faceted complex cascade of events occurs that ultimately results in cellular and neurological impairments within cortical and sub-cortical central nervous system (CNS) regions. In the present studies a modified �Levine� rat-pup model of HI (left carotid artery ligation + 1 hour global hypoxia on post-natal day (PND) 26) was employed to assess the neuroprotective properties of clomethiazole (CMZ; a γ-aminobutyric acid (GABA)A receptor agonist). In this study, histological and electrophysiological paradigms were used to assess the long-term neuroprotective properties of CMZ (414mg/kg/day via mini-pumps). Key enzymes involved in inflammation, namely nitric oxide synthase (NOS) and arginase, were also examined to assess other potential CMZ mechanisms. Assessments were carried out 3- and 90-days post-HI, with extensive ipsilateral CNS lesions evident at a gross histological level, at both the early and long-term stages, with CMZ significantly decreasing the lesion size at 3- and 90-days (P<0.01; P<0.05). Evoked field potential analyses were used to assess hippocampal CA1 neuronal activity ex vivo. Electrophysiological measurements contralateral to the occlusion revealed impaired neuronal function following HI relative to short- and long-term controls (P<0.001, 3- and 14-days; P<0.01, 90-days), with CMZ providing near complete protection (P<0.001 at 3- and 14-days; P<0.01 at 90-days). Both inducible NOS (iNOS) and arginase activities were significantly increased at 3-days (P<0.01), with arginase activity remaining elevated at 90-days post-HI (P<0.05) ipsilaterally. CMZ suppressed the HI-induced increase in iNOS and arginase activities (P<0.001; P<0.05). These data provide evidence of long-term functional neuroprotection afforded by CMZ in a model of HI-induced neurodegeneration. In addition, under conditions of HI, functional deficits were not restricted to the ipsilateral hemisphere and were due, at least in part, to changes in the activity of NOS and arginase. Underlying mitochondrial dysfunction is eminently present in many neuropathological conditions. The full extent of mitochondrial dysfunction in cortical, hippocampal and cerebellar tissues was assessed following HI. Assessment of mitochondrial FAD-linked respiration at both 1- and 3-days post-HI revealed a significant decrease in activity from ipsilateral cortical and hippocampal regions (P<0.001). In addition, significant changes in respiratory function were also evident in contralateral regions and cerebellum, 3-days post-HI (P<0.05). Assessment of the mitochondrial electron transport chain (complexes I-V) and mitochondrial markers of integrity (citrate synthase) and oxidative stress (aconitase) confirmed ipsilateral mitochondrial impairment following HI. Complexes I, II-III, V and citrate synthase were also impaired, in contralateral regions and cerebellum, 3-days post-HI. CMZ treatment provided significant protection to all mitochondrial aspects of neuronal tissue assessed. This study provides evidence of the full extent of mitochondrial damage following an HI-insult and may contribute, in part, to the impairment seen contralaterally. In addition, protection afforded by CMZ extends to preservation of mitochondrial function and integrity. Cerebral ischaemia-induced angiogenesis has been shown within and around infarcted regions and may contribute to a more favourable neurological outcome. The level of angiogenesis was examined using platelet endothelial cell adhesion molecule-1 (PECAM-1 / CD31). CD31 immunolabelling 7-days post-HI revealed a significant increase in angiogenesis compared with non-intervention controls (P<0.001). Treatment with CMZ decreased the level of angiogenesis compared to HI + saline (P<0.001) back to non-intervention control levels. Conversely, N[omega]-nitro-L-arginine methyl ester (L-NAME) treatment (5mg/kg/day) exacerbated the ischaemic lesion (P<0.001) and resulted in a marked decrease in angiogenesis compared to non-intervention controls (P<0.001). The extent of cerebral infarction in these studies is dependent on the level of NOS activity with CMZ increasing total NOS levels compared to HI + saline, while L-NAME halted the HI-induce increase in total NOS activity (P<0.001). These results show for the first time, that angiogenesis may be used as an assessment of neurodegeneration / neuroprotection in pathologies of cerebral ischaemia and are directly correlated with changes in NOS activity. These studies have therefore shown that following HI, damage also occurs contralateral to the occlusion, and is not restricted to the ipsilateral hemisphere. In addition, the neuroprotective effects of CMZ have been shown to extend out to 90-days post-HI, whereby significant protection to CA1 neuronal activity was seen. These studies also provide in vivo evidence that CMZ may also afford neuroprotection via anti-inflammatory pathways, as evidenced by a decrease in iNOS and arginase activities. Furthermore, these studies have also show evidence that angiogenesis (CD31) can be used as a diagnostic tool to assess neuroprotection / neurodegeneration.
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Gilby, Krista Lynn. "An investigation into the mechanism responsible for Clomethiazole-induced neuroprotection in a rat model of severe global ischemia." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape4/PQDD_0016/NQ57363.pdf.

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Hartig, Kerstin. "Auswirkungen von Clomethiazol auf den Schlaf gesunder Probanden." [S.l.] : [s.n.], 2004. http://deposit.ddb.de/cgi-bin/dokserv?idn=970388586.

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Droste, Philipp [Verfasser], Georg [Gutachter] Juckel, and Gerhard [Gutachter] Reymann. "Clomethiazol versus Oxazepam im Alkoholentzug / Philipp Droste ; Gutachter: Georg Juckel, Gerhard Reymann ; Medizinische Fakultät." Bochum : Ruhr-Universität Bochum, 2021. http://d-nb.info/1228627150/34.

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Zinzgraf, Daniela. "Die Auswirkung von Clomethiazol auf das Schlaf-EEG alkoholabhängiger Patienten im akuten Entzug und im Verlauf der Abstinenz." [S.l.] : [s.n.], 2005. http://deposit.ddb.de/cgi-bin/dokserv?idn=975570234.

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Mayer, Carolin Verfasser], and Johannes [Akademischer Betreuer] [Kornhuber. "Der Einfluss von Clomethiazol, Clozapin und Valproinsäure auf die Expression von NPY und seinem Rezeptorsystem. / Carolin Mayer. Betreuer: Johannes Kornhuber." Erlangen : Universitätsbibliothek der Universität Erlangen-Nürnberg, 2012. http://d-nb.info/102895882X/34.

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Mayer, Carolin [Verfasser], and Johannes [Akademischer Betreuer] Kornhuber. "Der Einfluss von Clomethiazol, Clozapin und Valproinsäure auf die Expression von NPY und seinem Rezeptorsystem. / Carolin Mayer. Betreuer: Johannes Kornhuber." Erlangen : Universitätsbibliothek der Universität Erlangen-Nürnberg, 2012. http://d-nb.info/102895882X/34.

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Hartig, Kerstin [Verfasser]. "Auswirkungen von Clomethiazol auf den Schlaf gesunder Probanden / vorgelegt von Kerstin Hartig." 2004. http://d-nb.info/970388586/34.

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Ganzer, Florian [Verfasser]. "Vergleich zwischen Oxazepam und Clomethiazol in der medikamentösen Behandlung des Alkoholentzugs / vorgelegt von Florian Ganzer." 2008. http://d-nb.info/995284814/34.

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Zinzgraf, Daniela [Verfasser]. "Die Auswirkung von Clomethiazol auf das Schlaf-EEG alkoholabhängiger Patienten im akuten Entzug und im Verlauf der Abstinenz / vorgelegt von Daniela Zinzgraf." 2005. http://d-nb.info/975570234/34.

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Book chapters on the topic "Clomethiazole"

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Hoyer, Daniel, Eric P. Zorrilla, Pietro Cottone, Sarah Parylak, Micaela Morelli, Nicola Simola, Nicola Simola, et al. "Clomethiazole." In Encyclopedia of Psychopharmacology, 304. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_1815.

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Benkert, Otto, Ion Anghelescu, Christoph Fehr, Gerhard Gründer, Philip Heiser, Christoph Hiemke, Christian Lange-Asschenfeldt, et al. "Clomethiazol." In Pocket Guide Psychopharmaka von A bis Z, 50–52. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-01910-4_24.

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Tretter, F. "Clomethiazol." In Therapie von Entzugssyndromen, 171–78. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-78778-2_13.

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Beyer, Karl-Heinz. "Clomethiazol." In Biotransformation der Arzneimittel, 163–64. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-74386-3_84.

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Peter, Helga, and Thomas Penzel. "Clomethiazol." In Springer Reference Medizin, 1. Berlin, Heidelberg: Springer Berlin Heidelberg, 2020. http://dx.doi.org/10.1007/978-3-642-54672-3_399-1.

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Schuchardt, V., and W. Schwarzerz. "Das lebensbedrohliche Alkoholdelir — Kombinationstherapie mit Clomethiazol." In Delir und Delirprophylaxe in der Intensivmedizin, 23–31. Heidelberg: Steinkopff, 1991. http://dx.doi.org/10.1007/978-3-642-85416-3_3.

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Schuchardt, V. "Die Behandlung des schweren Alkoholdelirs — Kombinationstherapie mit Clomethiazol." In Therapie von Entzugssyndromen, 135–44. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-78778-2_10.

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Erhorn, Stephen. "Clomethiazole." In xPharm: The Comprehensive Pharmacology Reference, 1–6. Elsevier, 2007. http://dx.doi.org/10.1016/b978-008055232-3.61491-6.

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"Clomethiazole." In Encyclopedia of Psychopharmacology, 379. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-36172-2_200920.

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"Clomethiazole." In Meyler's Side Effects of Drugs: The International Encyclopedia of Adverse Drug Reactions and Interactions, 810–12. Elsevier, 2006. http://dx.doi.org/10.1016/b0-44-451005-2/00101-7.

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Conference papers on the topic "Clomethiazole"

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Hohmann, N., WE Haefeli, S. Mueller, H. Seitz, F. Schröder, H. Teng, B. Moreira, and T. Bruckner. "Clomethiazole improves alcoholic fatty liver in patients admitted to the hospital for alcohol detoxification therapy." In 36. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0039-3402136.

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