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Biological Terrorist Agents
Published in Robert A. Burke, Counter-Terrorism for Emergency Responders, 2017
Bacterial toxins can be classified as membrane-damaging. This group includes Escherichia coli (hemolysins), Aeromonas, Pseudomonas, and Staphylococcus alpha (cytolysins and phospholipases). Toxins from bacterium are reasonably easy to produce but possess a varying degree of stability. Many of those toxins function by interfering with bodily functions and kill by creating pores in cell membranes. Their toxicity levels are much lower than the protein toxins and are less likely as terrorist threats. Marine toxins may be developed from marine organisms. Examples include saxitoxin, tetrodotoxin, palytoxin, brevetoxins, and microcystin. Saxitoxin is a sodium-channel blocker and is most toxic by inhalation compared to the other routes of exposure. Saxitoxin and tetrodotoxin are very similar in mechanical action, toxicity, and physical attributes. They can be lethal within a few minutes when inhaled. Saxitoxin could be used as a terrorist agent in localized scenarios. It has not yet been chemically synthesized efficiently, or easily created in large quantities from natural sources; therefore, it is not likely to be aerosolized and used over a large area. Palytoxin is produced from soft coral and is very toxic. It is, however, difficult to produce or harvest from nature and is an unlikely agent for large-scale terrorist use. The brevetoxins, hepatotoxins, and microcystin have limited toxicity and are unlikely agents for terrorist activities.
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Published in Michael Hehenberger, Zhi Xia, Huanming Yang, Our Animal Connection, 2020
Michael Hehenberger, Zhi Xia, Huanming Yang
The skin of some species contains the powerful poison tetrodotoxin, a neurotoxin similar to the pufferfish venom. These salamanders tend to be slow-moving and have bright warning coloration to advertise their toxicity. Tetrodotoxin is the most toxic nonprotein substance known. Ingestion of even a minute fragment of skin is deadly. Tetrodotoxin is a sodium channel blocker. It inhibits the firing of action potentials in neurons by binding to the voltage-gated sodium channels in nerve cell membranes and blocking the passage of sodium ions (responsible for the rising phase of an action potential) into the neuron. This prevents the nervous system from carrying messages and thus muscles from flexing in response to nervous stimulation.
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Published in Michael Hehenberger, Zhi Xia, Our Animal Connection, 2019
The skin of some species contains the powerful poison tetrodotoxin, a neurotoxin similar to the pufferfish venom. These salamanders tend to be slow-moving and have bright warning coloration to advertise their toxicity. Tetrodotoxin is the most toxic nonprotein substance known. Ingestion of even a minute fragment of skin is deadly. Tetrodotoxin is a sodium channel blocker. It inhibits the firing of action potentials in neurons by binding to the voltagegated sodium channels in nerve cell membranes and blocking the passage of sodium ions (responsible for the rising phase of an action potential) into the neuron. This prevents the nervous system from carrying messages and thus muscles from flexing in response to nervous stimulation.
A review of algal toxin exposures on reserved federal lands and among trust species in the United States
Published in Critical Reviews in Environmental Science and Technology, 2022
Zachary R. Laughrey, Victoria G. Christensen, Robert J. Dusek, Sarena Senegal, Julia S. Lankton, Tracy A. Ziegler, Lee C. Jones, Daniel K. Jones, Brianna M. Williams, Stephanie Gordon, Gerald A. Clyde, Erich B. Emery, Keith A. Loftin
Saxitoxins are neurotoxins produced by several species of freshwater cyanobacteria and marine algae (Supplemental Table 1). Saxitoxin acts as a sodium channel blocker that can affect gastrointestinal, neurological, and neuromuscular function that may lead to respiratory paralysis and death (Christensen & Khan, 2020; Cusick & Sayler, 2013). Saxitoxin producing organisms have been found along the Atlantic, Pacific, and Gulf coasts of the United States. Saxitoxin exposure has been documented in 22 Trust species including: 12 species of marine mammals, 8 species of birds, and 1 reptile and 1 fish species (Supplementary Tables 8 and 9) in 5 states (Supplementary Table 10 and Figure 2). Exposure to saxitoxins is primarily by consumption of contaminated prey species (Deeds et al., 2008).
Ablation for the treatment of Brugada syndrome: current status and future prospects
Published in Expert Review of Medical Devices, 2020
Alessandro Rizzo, Carlo de Asmundis, Pedro Brugada, Mark La Meir, Gian-Battista Chierchia
In 2018 Talib et al [34] described their retrospective, multicenter, observational study on the endocardial ablation approach of patients with symptomatic BrS. The investigators performed endocardial RF ablation in 21 patients with BrS and frequent drug resistant VF/electrical storms from an initial group of 123 patients. Their endocardial ablation strategy was a stepwise approach. First, they attempted to identify and ablate a VF trigger and then performed an endocardial mapping and ablation of VF substrates that exhibited abnormal fractionated low-voltage ventricular electrograms. VF-triggering PVCs were localized by mapping the earliest local electrogram relative to the onset of the QRS complex during a ventricular ectopy. To induce the triggering PVC, sodium channel blocker provocation with intravenous pilsicainide infusion was administered. Ablation was performed using RF energy, with a target temperature of 55°C and a maximum power of 50 W, or using an externally irrigated 3.5-mm-tip catheter (Thermocool, Biosense Webster, Diamond Bar, CA). Locations of abnormal electrograms, defined as fractionated electrograms (multicomponent with an amplitude of 50 ms), or isolated late potentials (inscribed entirely after the QRS complex), and low-voltage electrograms (<1 mv), were tagged during sinus rhythm mapping.
Fatigue: Is it all neurochemistry?
Published in European Journal of Sport Science, 2018
More recently, Hasegawa et al. (2008), Hasegawa, Ishiwata, et al. (2005) and Hasegawa, Meeusen, et al. (2005) performed a series of experiments on the effects of tetrodotoxin (TTX) and bupropion (a DA/NA reuptake inhibitor) on exercise behaviour and/or thermoregulation in freely moving or exercising rats. TTX, a poison of the Japanese puffer fish that acts as a sodium channel blocker, is widely used for blockage of neurotransmission in specific brain regions. When employed together with brain microdialysis, this method can be used to elucidate possible mechanisms of neurotransmitter action (Hasegawa, Ishiwata, et al., 2005). Hasegawa, Ishiwata, et al. (2005) concluded that perfusion of TTX into the PO/AH induced a significant increase in body temperature with a significant decrease in tail temperature and an elevation in heart rate. Interestingly, the TTX-induced hyperthermia was found without a change in exercise behaviour. Hasegawa, Meeusen, et al. (2005) and Hasegawa et al. (2008) looked at the effects of bupropion on thermoregulation and brain neurotransmitter levels in freely moving rats and on performance in exercising rats. In freely moving rats, the injection of the dual DA and NA reuptake inhibitor induced a significant increase in brain and core temperature with a decrease in heat loss responses (decreased tail temperature). These thermal responses were accompanied by an increase of the extracellular concentrations of NA and DA with no effect on serotonin release in the PO/AH (Hasegawa, Meeusen, et al., 2005). In a follow-up experiment the rats were forced to exercise at a speed of 26 m min−1 on a treadmill until exhaustion at 18°C (no drug), 30°C with saline or 30°C with bupropion (Hasegawa et al., 2008). Running time to exhaustion was significantly shorter at 30°C than at 18°C. At 30°C, running time to exhaustion was significantly increased by bupropion compared with the saline condition. Furthermore, significantly higher brain and core temperatures were observed in the bupropion trial. These changes in brain and core temperature were accompanied by an increase in the extracellular concentrations of DA and NA in the PO/AH.