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Investigation of the permeability of human stratum corneum to sarinMatheson, Lloyd Edward. January 1970 (has links)
Thesis (Ph. D.)--University of Wisconsin--Madison, 1970. / Typescript. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 143-151).
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Studies concerning chemical warfare agents Part A. The thermodynamic activity of sarin in solution. Part B. Exploratory investigation of the effects of solvents on skin lipids and skin penetration /Kinkel, Arlyn W. January 1958 (has links)
Thesis (Ph. D.)--University of Wisconsin--Madison, 1958. / Typescript. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 81-84).
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Mediation of complex formation in the hydrolysis of sarinSchwartz, Michael A., January 1959 (has links)
Thesis (Ph. D.)--University of Wisconsin--Madison, 1959. / Typescript. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 68-71).
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Kinetic Analysis of Rat Blood and Tissue and Human Blood Acetylcholinesterase and Butyrylcholinesterase after Inhibition with Novel Nerve Agent Surrogates and Reactivation with Novel OximesDezell, Steven Archie 06 May 2017 (has links)
Organophosphates (OPs) are used in agriculture via pesticides, and warfare and terrorism via nerve agents. OPs can inhibit acetylcholinesterase (AChE) activity in the nervous system, leading to the buildup of acetylcholine (ACh), and overstimulation of the nervous system and eventual asphyxiation and death. The development of novel blood-brain barrier () penetrating pyridinium oxime reactivators have previously demonstrated efficacy towards treatment of OP poisoning after exposure of rats to a sarin or a VX surrogate, nitrophenyl isopropyl methylphosphonate (NIMP) and nitrophenyl ethyl methylphosphonate (NEMP), respectively. An effective oxime antidote capable of penetrating the and restoring nervous system activity after exposure to a cyclosarin surrogate, nitrophenyl cyclohexyl methylphosphonate (NCMP), has yet to be determined. In Chapter 2, in vitro testing of the efficacy of 17 total novel oxime candidates to utilize against NCMP was conducted with a modified Ellman’s AChE assay. Pools of naïve adult male rat brains were utilized as the AChE source. The first variable investigated was the measurement of AChE activity after inhibition with NCMP and subsequent reactivation with one of the oximes. The second variable investigated restoration of AChE activity after simultaneous oxime and NCMP incubation. The final variable investigated the restoration of AChE activity after simultaneous 2-PAM, oxime and NCMP incubation. A thorough kinetic analysis of our best oximes has yet to be accomplished. In Chapter 3, the best oxime antidotes for NEMP and NIMP were used for kinetic analysis with a modified 96-well plate Ellman’s AChE assay. Protein concentrations were analyzed with a modified Lowry protein tube assay to ensure consistent analytical concentrations. The sources of AChE included pooled rat brain and skeletal muscle, and rat and human erythrocytes and plasma. Butyrylcholinesterase (BChE) activity was also measured in the rat and human plasma samples. The results of these studies strengthen the argument that our oxime antidotes can be used as potential therapeutic drugs for OP poisoning. The kinetic data provided critical information to help propose, for Chapter 4, a dynamic pharmacokinetic based model to predict human AChE or BChE activity after exposure to nerve agent surrogates (NEMP and NIMP) and the oximes (44.08 and 44.25).
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Neurodegeneration and Neuroinflammation in a Mouse Model of Sarin ExposureDavidson, Molly Elizabeth 27 September 2007 (has links)
No description available.
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Identifying additional neuroprotective mechanisms of novel phenoxyalkyl pyridinium oximes against organophosphorus compound toxicityPrice, Chiquita Yvette 08 August 2023 (has links) (PDF)
Our laboratory has invented a series of oxime acetylcholinesterase (AChE) reactivators (US Patent 9,227,937) that enter the brain, reduce time to cessation of seizure-like activities, and prevent organophosphorus compound (OP) neuropathology, not seen with the current U.S. approved AChE reactivator, pralidoxime (2-PAM). Thus, 2-PAM fails to protect the brain against damage and long-term cognitive and behavioral deficits seen in humans after OP exposure. However, the mechanisms by which these novel oximes provide central neuroprotection through preservation of neuronal cell structures from damage in a rat model are not fully understood by AChE reactivation alone. This dissertation investigated neurotoxic mechanisms of NIMP as potential targets for additional direct and indirect neuroprotection by our lead in vivo AChE reactivator, Oxime 20.
Male Sprague Dawley rats exposed to NIMP experienced neurotoxic effects in areas critical to OP-induced seizure generation (e.g., hippocampus and piriform cortex) such as the inhibition of multiple serine hydrolases (i.e., fatty acid amide hydrolase (FAAH), monoacylglycerol lipase (MAGL)), necrotic cell death evident by increased necrotic receptor-interacting serine/threonine-protein kinase 1 (RIPK1) levels and no apoptotic caspase-3 activity, and increased levels of neuroinflammation via elevated levels of pro-inflammatory oxylipins 4 days post lethal exposure. However, due to the lack of statistical significance, NIMP exposure did not definitively affect the subcellular location of either phosphorylated excitatory N-methyl-D-aspartate (NMDA) receptor or inhibitory γ-aminobutyric acid (GABA) receptor subunits.
Results suggested that Oxime 20 therapy provided neuroprotection after NIMP exposure, such as limited reactivation of other serine hydrolase targets, significantly decreased RIPK1 levels (i.e., necrotic environment) in the hippocampus, and significantly decreased inflammatory oxylipins 4 days post-NIMP exposure. Thus, reducing OP-induced neuroinflammation might be the main contributor to the neuroprotection (i.e., neuronal cell structure preservation) previously observed in our laboratory.
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Evaluation of CM-2,525 as a neuroprotectant against sarin: A comparison with 8-OH-DPATFurman, Amanda R. 14 June 2012 (has links)
No description available.
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Q-VE-OPh, a control caspase inhibitor for analyzing neuronal deathBricker, Rebecca L. 28 June 2012 (has links)
No description available.
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Resurrection of Aged AcetylcholinesteraseScarpitti, Brian T. January 2018 (has links)
No description available.
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Effect of low-dose sarin exposure on the neurochemistry of different brain structures in miceOswal, Dhawal Pravin 30 September 2009 (has links)
No description available.
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