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With the outbreak of World War II, conservation issues fell into the background of concerns, proving the difficulty of maintaining mindfulness of human–nature relationships when social crises erupt. The experience of the Dust Bowl focused the attention of conservationists and many natural scientists on the consequences of indiscriminate exploitation of sensitive lands, highlighting especially the systemic nature of the soil erosion problem. In practical terms, the New Deal programs in the USA vastly increased governmental support for conservation programs, though often with little consideration of ultimate conservation goals. The Depression forced conservationists and nonconservationists alike to consider the connections between human economic systems and the sources of wealth in nature. The social and environmental convulsions of the 1930s and 1940s fundamentally altered perspectives and priorities within the conservation movement. This chapter explores oxidative injury, different pathways to attenuate biomarkers of oxidative damage associated with anti-AChE exposure, and the extent to which such attenuation is accompanied by rescue from neurodegeneration.Ĭurt Meine, in Encyclopedia of Biodiversity (Second Edition), 2013 Conservation Amid Crisis: The 1930s and 1940s
STEREOGRAM OF CONVULSION FREE
Research also has revealed that seizure-induced early increases in biomarkers of global free radical damage (F2-IsoPs) and the selective peroxidation biomarkers of neuronal membranes (F4-NeuroPs) were accompanied by dendritic degeneration of pyramidal neurons in the CA1 hippocampal area, as evaluated by Golgi impregnation and Neurolucida-assisted morphometry. The resulting brain damage appears to be associated with oxidative stress and consequent degeneration of pyramidal neurons from the CA1 hippocampal region of the brain. The progression of events includes initial high cholinergic activity followed by activation of glutamatergic neurons, inflammation, and neuronal injury. Seizures, convulsions, and central nervous system (CNS) lesions are typical results of the systemic application of sublethal doses of anticholinesterase (anti-AChE) agents.
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Gupta, in Handbook of Toxicology of Chemical Warfare Agents (Third Edition), 2020 Abstract As a result of this process, glutamatergic receptor antagonists remain the only solution for the delayed treatment of such convulsions ( Lallement et al., 1999a,b Niquet et al., 2019). 65.2 Myhrer et al., 2004).Īs mentioned earlier, even the use of benzodiazepines has a narrow window of effectiveness following intoxication with nerve agents, since with the passage of time these convulsions became more dependent on the glutamatergic receptor activity and relatively independent on the activity of cholinergic receptors and even the GABA A/benzodiazepine-receptor complex. The same combination had to be used to stop the soman-induced convulsions even after 1 mg/kg of scopolamine, but administered 10, instead of 3 min after the onset of convulsion ( Fig. When the dose of scopolamine was lower (0.5 mg/kg) and the timing remained the same as in the previous experiment, the convulsion would be stopped only after administration of diazepam (10 mg/kg) and pentobarbital (30 mg/kg). and when it was injected 4–9 min after the occurrence of convulsions, they ceased after another 15 min. In the experiment presented here, 1.6 LD 50 of soman was used and scopolamine, a very liposoluble antimuscarinic drug, had to be used, but its effect depended on its dose and time of administration. A high dose of scopolamine given outside the cholinergic window requires additional treatment (C). A high dose of scopolamine is sufficient to terminate seizures (B). A low dose of scopolamine requires additional treatment (A). Experimental design for demonstration of how insufficient prophylactic treatment can be compensated for by adjunct postexposure treatment.