Littérature scientifique sur le sujet « Neuropathy target esterase »
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Articles de revues sur le sujet "Neuropathy target esterase"
GLYNN, Paul. « Neuropathy target esterase ». Biochemical Journal 344, no 3 (8 décembre 1999) : 625–31. http://dx.doi.org/10.1042/bj3440625.
Texte intégralGLYNN, Paul. « Neuropathy target esterase ». Biochemical Journal 344, no 3 (15 décembre 1999) : 625. http://dx.doi.org/10.1042/0264-6021:3440625.
Texte intégralHou, Wei-Yuan, Ding-Xin Long et Yi-Jun Wu. « Effect of Inhibition of Neuropathy Target Esterase in Mouse Nervous Tissues In Vitro on Phosphatidylcholine and Lysophosphatidylcholine Homeostasis ». International Journal of Toxicology 28, no 5 (20 juillet 2009) : 417–24. http://dx.doi.org/10.1177/1091581809340704.
Texte intégralGlynn, Paul. « Axonal Degeneration and Neuropathy Target Esterase ». Archives of Industrial Hygiene and Toxicology 58, no 3 (1 septembre 2007) : 355–58. http://dx.doi.org/10.2478/v10004-007-0029-z.
Texte intégralSeifert, Josef. « A Tentative Mechanism of Solubilization of Neuropathy Target Esterase from Chicken Embryo Brain by Phospholipase A2 ». Scientific World JOURNAL 8 (2008) : 346–49. http://dx.doi.org/10.1100/tsw.2008.51.
Texte intégralLush, Michael, David Read et Paul Glynn. « Molecular cloning of neuropathy target esterase ». Toxicology Letters 88 (octobre 1996) : 27. http://dx.doi.org/10.1016/s0378-4274(96)80098-1.
Texte intégralGlynn, Paul. « Neurodegeneration involving neuropathy target esterase (NTE) ». Toxicology Letters 164 (septembre 2006) : S9. http://dx.doi.org/10.1016/j.toxlet.2006.06.023.
Texte intégralGlynn, Paul. « Neuropathy target esterase and phospholipid deacylation ». Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids 1736, no 2 (septembre 2005) : 87–93. http://dx.doi.org/10.1016/j.bbalip.2005.08.002.
Texte intégralBertoncin, Daniela, Alessandra Russolo, Stefano Caroldi et Marcello Lotti. « Neuropathy Target Esterase in Human Lymphocytes ». Archives of Environmental Health : An International Journal 40, no 3 (mai 1985) : 139–44. http://dx.doi.org/10.1080/00039896.1985.10545905.
Texte intégralThomas, Thomas C., András Székács, Bruce D. Hammock, Barry W. Wilson et Mark G. McNamee. « Affinity chromatography of neuropathy target esterase ». Chemico-Biological Interactions 87, no 1-3 (juin 1993) : 347–60. http://dx.doi.org/10.1016/0009-2797(93)90063-5.
Texte intégralThèses sur le sujet "Neuropathy target esterase"
Lush, Michael John. « Molecular cloning of neuropathy target esterase ». Thesis, University of Leicester, 1998. http://hdl.handle.net/2381/29627.
Texte intégralRezaie-Moazen, Nima. « Characterisation of neuropathy target esterase in mammalian cells ». Thesis, University of Leicester, 2005. http://hdl.handle.net/2381/30775.
Texte intégralZaccheo, Oliver. « Analysis of the yeast homologue of neuropathy target esterase ». Thesis, University of Leicester, 2003. http://hdl.handle.net/2381/30772.
Texte intégralAtkins, Jane. « Biochemical characterisation of the catalytic domain of neuropathy target esterase ». Thesis, University of Leicester, 2000. http://hdl.handle.net/2381/29643.
Texte intégralMeredith, C. « Biochemical studies on neuropathy target esterase and its role in the initiation of delayed neuropathy by some organophosphorus esters ». Thesis, University of Cambridge, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.373779.
Texte intégralEmerick, Guilherme Luz [UNESP]. « Avaliação de neurotoxicidade de formas enantioméricas de praguicidas organifosforados : estudos in vitro, in vivo e de neuroproteção ». Universidade Estadual Paulista (UNESP), 2012. http://hdl.handle.net/11449/106391.
Texte intégralFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
Universidade Estadual Paulista (UNESP)
Clinicamente, os sintomas da intoxicação por organofosforados (OPs) são divididos em quatro categorias: síndrome colinérgica, síndrome intermediária, transtornos neuropsiquiátricos crônicos induzidos por OPs e neuropatia retardada induzida por OPs (NRIOP). Há estudos que comprovam a ocorrência de casos de NRIOP em seres humanos após intoxicação por metamidofós, porém existe grande dificuldade de estudar esta neuropatia no modelo experimental (galinha), devido à forte crise colinérgica que ocorre após a inibição da acetilcolinesterase (AChE). Uma possível explicação para tal diferença de efeito entre a espécie humana e a galinha é o fato de que os OPs possuem centros assimétricos e, assim sendo, se apresentam sob formas enantioméricas que podem apresentar diferenças de inibição da AChE e da esterase susceptível à neuropatia (ESNp). Assim, o objetivo deste trabalho foi avaliar, em sangue de galinhas e de seres humanos, em cérebro de galinhas (in vitro e in vivo) e em células da linhagem SH-SY5Y de neuroblastoma humano, a neurotoxicidade de formas enantioméricas de compostos organofosforados utilizados como praguicidas, tendo o metamidofós como protótipo e utilizando a AChE, butirilcolinesterase (BChE), ESNp e a calpaína como biomarcadores. Inicialmente, foi feita a separação dos enantiômeros do metamidofós utilizando a técnica de cromatografia líquida de alta eficiência (CLAE) com emprego de fases estacionárias quirais de polissacarídeos, onde se obteve resolução de até 1,56 para os enantiômeros avaliados. A forma (+)-metamidofós apresentou maior toxicidade in vitro para a BChE em galinhas e para ESNp...
Clinically, the symptoms of organophosphorus (OP) poisoning are divided into four categories: acute cholinergic syndrome, intermediate syndrome, chronic organophosphorus-induced neuropsychiatric disorders (COPIND) and organophosphorus-induced delayed neuropathy (OPIDN). There are studies that prove the occurrence of OPIDN in humans after methamidophos poisoning, but there is great difficulty in studying this neuropathy in the experimental model (hen), due to strong cholinergic crisis that occurs after inhibition of acetylcholinesterase (AChE). One possible explanation for this difference in effect between humans and hens is the fact that the OPs have asymmetric centers and therefore, are presented as enantiomeric forms that may exhibit differences in inhibition of AChE and neuropathy target esterase (NTE). Thus, the objective of this study was to evaluate, in the blood of hens and humans, in the brains of chickens (in vitro and in vivo) and in the SH-SY5Y human neuroblastoma cells, the neurotoxicity of enantiomeric forms of OPs used as pesticides, having methamidophos as the prototype and using AChE, butyrylcholinesterase (BChE), NTE and calpain as biomarkers. Initially, the complete separation of the methamidophos enantiomers was obtained applying the technique of high performance liquid chromatography (HPLC) and using polysaccharide chiral stationary phases. A maximum resolution of 1.56 was gotten for the enantiomers evaluated. The form (+)-methamidophos presented higher in vitro toxicity than that of the (-)-methamidophos for BChE of hens and NTE of hens and humans... (Complete abstract click electronic access below)
Emerick, Guilherme Luz. « Avaliação de neurotoxicidade de formas enantioméricas de praguicidas organifosforados : estudos in vitro, in vivo e de neuroproteção / ». Araraquara : [s.n.], 2012. http://hdl.handle.net/11449/106391.
Texte intégralCoorientador: Regina Vincenzi Oliveira
Banca: Maria Palmira Daflon Gremião
Banca: Antonio Cardozo dos Santos
Banca: Rosângela Gonçalves Peccinini
Banca: Silvana Aparecida Calafatti
Resumo: Clinicamente, os sintomas da intoxicação por organofosforados (OPs) são divididos em quatro categorias: síndrome colinérgica, síndrome intermediária, transtornos neuropsiquiátricos crônicos induzidos por OPs e neuropatia retardada induzida por OPs (NRIOP). Há estudos que comprovam a ocorrência de casos de NRIOP em seres humanos após intoxicação por metamidofós, porém existe grande dificuldade de estudar esta neuropatia no modelo experimental (galinha), devido à forte crise colinérgica que ocorre após a inibição da acetilcolinesterase (AChE). Uma possível explicação para tal diferença de efeito entre a espécie humana e a galinha é o fato de que os OPs possuem centros assimétricos e, assim sendo, se apresentam sob formas enantioméricas que podem apresentar diferenças de inibição da AChE e da esterase susceptível à neuropatia (ESNp). Assim, o objetivo deste trabalho foi avaliar, em sangue de galinhas e de seres humanos, em cérebro de galinhas (in vitro e in vivo) e em células da linhagem SH-SY5Y de neuroblastoma humano, a neurotoxicidade de formas enantioméricas de compostos organofosforados utilizados como praguicidas, tendo o metamidofós como protótipo e utilizando a AChE, butirilcolinesterase (BChE), ESNp e a calpaína como biomarcadores. Inicialmente, foi feita a separação dos enantiômeros do metamidofós utilizando a técnica de cromatografia líquida de alta eficiência (CLAE) com emprego de fases estacionárias quirais de polissacarídeos, onde se obteve resolução de até 1,56 para os enantiômeros avaliados. A forma (+)-metamidofós apresentou maior toxicidade in vitro para a BChE em galinhas e para ESNp... (Resumo completo, clicar acesso eletrônico abaixo)
Abstract: Clinically, the symptoms of organophosphorus (OP) poisoning are divided into four categories: acute cholinergic syndrome, intermediate syndrome, chronic organophosphorus-induced neuropsychiatric disorders (COPIND) and organophosphorus-induced delayed neuropathy (OPIDN). There are studies that prove the occurrence of OPIDN in humans after methamidophos poisoning, but there is great difficulty in studying this neuropathy in the experimental model (hen), due to strong cholinergic crisis that occurs after inhibition of acetylcholinesterase (AChE). One possible explanation for this difference in effect between humans and hens is the fact that the OPs have asymmetric centers and therefore, are presented as enantiomeric forms that may exhibit differences in inhibition of AChE and neuropathy target esterase (NTE). Thus, the objective of this study was to evaluate, in the blood of hens and humans, in the brains of chickens (in vitro and in vivo) and in the SH-SY5Y human neuroblastoma cells, the neurotoxicity of enantiomeric forms of OPs used as pesticides, having methamidophos as the prototype and using AChE, butyrylcholinesterase (BChE), NTE and calpain as biomarkers. Initially, the complete separation of the methamidophos enantiomers was obtained applying the technique of high performance liquid chromatography (HPLC) and using polysaccharide chiral stationary phases. A maximum resolution of 1.56 was gotten for the enantiomers evaluated. The form (+)-methamidophos presented higher in vitro toxicity than that of the (-)-methamidophos for BChE of hens and NTE of hens and humans... (Complete abstract click electronic access below)
Doutor
Mercé, Théo. « High-throughput zebrafish larval locomotion assays of neuronal and muscular functions : Application to organophosphorus toxicity and antid ». Electronic Thesis or Diss., Bordeaux, 2024. http://www.theses.fr/2024BORD0011.
Texte intégralThe growing prevalence of chemical contaminants poses major public health concerns, necessitating efficient methodologies for toxicological risk assessment. An initial work was carried out to optimize a new approach methodology (NAM) using zebrafish pre-feeding larvae, called the electric field pulse (EFP) motor response test (EFPMRT). The method aims to perform a high-throughput screening of chemicals inducing motor capabilities and postural control defects. The robustness, reproducibility, productivity, and transferability of EFPMRT were enhanced by developing a novel software tool, DanioTracker, performing the automated analysis of endpoints linked to EFP-induced locomotor behavior. Then, using a battery of tests, the neurotoxicity induced by organophosphorus (OPs) compounds and their metabolites was assessed. Behavioral disruptions were evaluated using EFPMRT and a complementary sensory-dependent neurobehavioral test, the visual motor response test (VMRT). Contributions of acetylcholinesterase (AChE) and neuropathy target esterase (NTE) inhibition to behavioral disruptions were tested. Chlorpyrifos, parathion and tri-ortho-cresyl-phosphate disturbed integrative swimming control functions in quantitatively distinct manners and decreased the neuromuscular capacities of pre-feeding larvae. Their respective metabolites chlorpyrifos-oxon, paraoxon and cresyl-saligenin-phosphate fully inhibited AChE, thus inducing a cholinergic syndrome. Comparative study of the antidotal efficacy of an AChE reactivator, pralidoxime, in mitigating some toxic effects was performed. The antidote induced a recovery of the cholinergic syndromes associated with metabolites exposure. Strikingly, pralidoxime (2-PAM) also partially restored hyperactivities induced by parent compounds apparently independently of the activities of AChE and NTE. However, it did not restore neuromuscular dysfunctions induced by parathion or tri-ortho-cresyl phosphate. This suggests the existence of one or more unknown OP-specific multiple modes of action (MOAs) associated with parent compound but not corresponding metabolites, of which some are restorable by 2-PAM. Overall, this work offers a robust, transferable NAM that contributes to a comprehensive chemical risk assessment strategy. It also uncovers potential alternative MOA for selected OPs, suggesting the need for further research on metabolites within regulatory frameworks, and contributes to understanding and preventing neurobehavioral disorders induced by environmental exposures alone or in mixtures
Livres sur le sujet "Neuropathy target esterase"
Ehrich, Marion. Relationship of neuropathy target esterase inhibition to neuropathology and ataxia in hens given organophosphorus esters. [Washington, D.C. ? : Environmental Protection Agency], 1993.
Trouver le texte intégralChapitres de livres sur le sujet "Neuropathy target esterase"
Wu, Yi-Jun, et Ping-An Chang. « Molecular Toxicology of Neuropathy Target Esterase ». Dans Anticholinesterase Pesticides, 109–20. Hoboken, NJ, USA : John Wiley & Sons, Inc., 2011. http://dx.doi.org/10.1002/9780470640500.ch9.
Texte intégralLush, Michael, David Read et Paul Glynn. « Molecular Cloning of Neuropathy Target Esterase ». Dans Archives of Toxicology, 413. Berlin, Heidelberg : Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-642-60682-3_39.
Texte intégralLotti, Marcello. « Neuropathy Target Esterase in Blood Lymphocytes ». Dans Biological Monitoring for Pesticide Exposure, 117–23. Washington, DC : American Chemical Society, 1988. http://dx.doi.org/10.1021/bk-1988-0382.ch009.
Texte intégralGlynn, Paul. « Neuropathy Target Esterase (NTE) : Molecular Characterisation and Cellular Localisation ». Dans Archives of Toxicology, 325–29. Berlin, Heidelberg : Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-642-60682-3_30.
Texte intégralMackay, C. E., B. D. Hammock et B. W. Wilson. « Identification of a 155 kDa Fraction that Possesses Neuropathy Target Esterase Activity ». Dans Enzymes of the Cholinesterase Family, 387–88. Boston, MA : Springer US, 1995. http://dx.doi.org/10.1007/978-1-4899-1051-6_74.
Texte intégralJohnson, Martin K., et Paul Glynn. « Neuropathy Target Esterase ». Dans Handbook of Pesticide Toxicology, 953–65. Elsevier, 2001. http://dx.doi.org/10.1016/b978-012426260-7.50050-1.
Texte intégralWijeyesakere, Sanjeeva J., et Rudy J. Richardson. « Neuropathy Target Esterase ». Dans Hayes' Handbook of Pesticide Toxicology, 1435–55. Elsevier, 2010. http://dx.doi.org/10.1016/b978-0-12-374367-1.00067-7.
Texte intégral« NTE (neuropathy target esterase) ». Dans Encyclopedia of Genetics, Genomics, Proteomics and Informatics, 1364. Dordrecht : Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6754-9_11590.
Texte intégralSrivastava, Devesh, Neeraj Kohli, Rudy J., Robert M. et Ilsoon Lee. « Neuropathy Target Esterase Biosensor ». Dans Intelligent and Biosensors. InTech, 2010. http://dx.doi.org/10.5772/7156.
Texte intégralJohnson, Martin K. « Molecular events in delayed neuropathy : experimental aspects of neuropathy target esterase ». Dans Clinical and Experimental Toxicology of Organophosphates and Carbamates, 90–113. Elsevier, 1992. http://dx.doi.org/10.1016/b978-0-7506-0271-6.50016-4.
Texte intégral