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The menopause
Published in Michael J. O’Dowd, The History of Medications for Women, 2020
Calabar bean the dried ripe seed of the Physostigma venosum Balfour, was the source of physostigmine, an anticholinesterase, which can cause cholinergic stimulation. In toxic doses it is used as an insecticide and a chemical warfare nerve gas. It was recommended for relief of the flatulence of the climacteric period.
Cholinergic Agonists
Published in Sahab Uddin, Rashid Mamunur, Advances in Neuropharmacology, 2020
Rupali Patil, Aman Upaganlawar
They are known as “nerve gases” and are the most powerful synthetic toxins known. In a preclinical study at nanogram doses, they show toxic effects. Dangerous used of these compounds occurred in warfare and terrorist attacks (Nozaki and Aikawa, 1995).
Chemical and Biological Threats to Public Safety
Published in Frank A. Barile, Barile’s Clinical Toxicology, 2019
The nerve gases were developed during World War II for possible use as chemical warfare agents; the first compound to be developed was tetraethyl pyrophosphate (TEPP). The biological action of the nerve gases, such as sarin (GB),* tabun (GA), and soman (GD), is similar to, but more toxic than, the organophosphate (OP) insecticides (see Chapter 28). The clear, colorless, tasteless liquids inhibit the action of acetylcholine esterase (ACh-∑) by forming an irreversible OP–ACh-∑ complex, rendering it incapable of hydrolyzing acetylcholine (ACh). Inhibition of the enzyme results in accumulation and over-stimulation of ACh at autonomic and somatic receptors. Excessive stimulation of nicotinic receptors is followed by skeletal muscle paralysis. These circumstances account for the toxic manifestations of OP insecticides as well as the nerve gases.
Neuroscience research in the Max Planck Society and a broken relationship to the past: Some legacies of the Kaiser Wilhelm Society after 1948
Published in Journal of the History of the Neurosciences, 2023
This section takes on a particular research tradition in the brain sciences that can be described as the highly regarded morphologico-pathological research paradigm. Since its heyday at the end of the nineteenth century, it encompassed investigations of brain tumor genesis, focal epilepsy work, stroke research, and the investigation of inherited and acquired neurodegenerative diseases (Strösser 1993, 12–13). Yet it is also of note that in the neuromorphological paradigm’s penumbra, neurochemical and neurophysiological research resumed based on previously gained structural insights, such as we saw in West German research initiatives on neuroleptic drugs since the 1950s, often conducted with the support of the pharmaceutical industry and having arisen in the context of basic research on nerve gases during the 1940s (Quadbeck 1959).
Human Rights Against Polluters: More Than Protecting “Susceptible” Populations
Published in The American Journal of Bioethics, 2018
Kristin Shrader-Frechette, Annrose Jerry
While the AFR improvements of Resnik et al. (2018) are praiseworthy and necessary, are they enough to balance the disproportionate power dynamics in most EJ decisionmaking? Probably not. Consider a typical case, that of child EJ victims of organophosphate pesticides like chlorpyrifos. Dow Chemical introduced chlorpyrifos in 1965. It quickly became one of the most-used US pesticides, with US sales of 8–21 million pounds each year (Grube et al 2011), and a major contributor to Dow's annual revenues of $48 billion. Because organophosphates like chlorpyrifos are neurotoxins derived from nerve gases developed by Nazi Germany for use in its death camps, chlorpyrifos is extremely toxic, causing more than 10,000 accidental-poisoning deaths every year (Rathood & Garg 2017). Chlorpyrifos also is a key reason that 500,000 of the 4 million US children born annually faces neurodevelopmental disorders such as autism, IQ losses, tremors, and attention-deficit-hyperactivity disorder (eg, Grandjean & Landrigan 2014, Shelton et al 2014).
A national toxicology program systematic review of the evidence for long-term effects after acute exposure to sarin nerve agent
Published in Critical Reviews in Toxicology, 2020
David A. Jett, Christopher A. Sibrizzi, Robyn B. Blain, Pamela A. Hartman, Pamela J. Lein, Kyla W. Taylor, Andrew A. Rooney
Sarin (CAS #: 107-44-8; GB; Isopropylmethylphosphonofluoridate) is a nerve agent developed for chemical warfare during World War II. This highly toxic chemical agent can cause death, seizures, and immediate symptoms caused by acetylcholinesterase (AChE; EC 3.1.1.7) inhibition, an increase in acetylcholine levels, and overstimulation of cholinergic receptors (Hulse et al. 2019). Sarin is sometimes referred to as “sarin nerve gas” even though it is a liquid at ambient temperatures. It is also known as GB, which is a two-character identifier assigned by the North Atlantic Treaty Organization (NATO). Sarin belongs to a chemically diverse group of organophosphorus chemicals that have at least one carbon atom bound to a phosphorous atom. The group includes other chemical weapons and agricultural pesticides such as ethyl parathion (CAS #: 56-38-2; parathion, phosphorothioic acid, O,O-diethyl O-(4-nitrophenyl) ester). This group will collectively be referred to as organophosphorus agents (OPs) in this article. Chemical weapons such as sarin are of immediate concern because of their current use in conflicts in the Middle East, and because of recent assassinations such as the Novichok incident in the UK, and the poisoning of Kim Jong-nam in Kuala Lumpur. Although prohibited by international treaties, it is likely that sarin continues to be used in conflicts around the world, as reported by the United Nations in Syria in 2013 (Sellström and Barbeschi 2013). Large-scale use of sarin in acts of terrorism are also of major concern, such as the Tokyo subway incident in 1995 when members of the terrorist group Aum Shinrikyo released sarin into rail cars resulting in several fatalities and over a thousand victims needing immediate medical attention (Yanagisawa et al. 2006).