The purpose of this study was to find an antidote against death adder envenomation that can be used in cases of emergency, when antivenoms are not readily available (Papua New Guinea and the Australian outback). Such an antidote should allow bite victims to survive until established treatment is possible. Death adder venom is thought to act postsynaptically at the neuromuscular junction to reduce responses to acetylcholine. This causes severe flaccid paralysis and finally death, which is usually a consequence of respiratory failure. Albino Wistar rats were injected with a lethal dose of crude death adder venom. At the onset of severe envenomation symptoms, anticholinesterases (neostigmine and edrophonium) in conjunction with atropine sulfate were administered. At the minimum lethal dose (0.15 mg/kg) all animals survived as a result of the anticholinesterase treatment. The expected survival time of animals subjected to higher venom doses was significantly extended. These results indicate that death adder bite victims may gain valuable time, if anticholinesterases can be administered during the initial critical stage of envenomation.
"The present study tested the hypothesis that neostigmine, given IN, would be an effective initial treatment of Naja naja envenomed mice. The early use of AChEIs leads to a considerable increase in the LD50 in mice and rats having undergone experimental envenomation [15, 16]. Our study is distinguished from those by the replacement of parenteral neostigmine with topically applied IN neostigmine. "
[Show abstract][Hide abstract] ABSTRACT: Objective. Most snakebite deaths occur prior to hospital arrival; yet inexpensive, effective, and easy to administer out-of-hospital treatments do not exist. Acetylcholinesterase inhibitors can be therapeutic in neurotoxic envenomations when administered intravenously, but nasally delivered drugs could facilitate prehospital therapy for these patients. We tested the feasibility of this idea in experimentally envenomed mice. Methods. Mice received intraperitoneal injections of Naja naja venom 2.5 to 10 times the estimated LD50 and then received 5 μ L neostigmine (0.5 mg/mL) or 5 μ L normal saline by nasal administration. Animals were observed up to 12 hours and survivors were euthanized. Results. 100% of control mice died. Untreated mice injected with 2.5× LD50 Naja naja died at average 193 minutes after injection, while 10 of 15 (67%) of treated mice survived and were behaviorally normal by 6 hours (P < 0.02). In the 5× LD50 group, survival was prolonged from 45 minutes to 196 minutes (P = 0.01) and for 10× LD50 mice, survival increased from 30 to 175 minutes (P < 0.02). Conclusion. This pilot suggests that intranasal drugs can improve survival and is the first direct demonstration that such an approach is plausible, suggesting means by which treatment could be initiated before reaching the hospital. Further investigation of this approach to neurotoxic and other types of envenomation is warranted.
Journal of Tropical Medicine 05/2014; 2014:131835. DOI:10.1155/2014/131835
[Show abstract][Hide abstract] ABSTRACT: This paper treats directional couplers consisting of a rectangular cavity with four waveguide ports. Since the present couplers possess a very simple structure, they are useful for applications at higher microwave and millimeter-wave frequencies, and in a high-power microwave system. Directional couplers with various power-split ratios at X-band are investigated theoretically and experimentally. Furthermore, improvement of their bandwidth is presented
[Show abstract][Hide abstract] ABSTRACT: This is the first report of a phospholipase A2 (PLA2) from the venom of the common death adder, Acanthophis antarcticus. Acanthoxin is a basic, monomeric PLA2 of mol. wt 13,000, consistent with the weight of neurotoxic PLA2s from other Australian elapids. However, preliminary ultracentrifugation experimentation has shown that it is able to undergo concentration-dependent aggregation to form dimers. It has a relatively high degree of enzymatic activity (23.93 +/- 1.18 mumoles of phospholipid hydrolysed/min/mg protein), but a low level of toxicity (3.2 mg/kg, s.c.). Acanthoxin is known to exist as two isoforms (A1 and A2), both of which show a high degree of homology with numerous elapid PLA2 neurotoxins, in particular pseudexin A from the red-bellied black snake (Pseudechis porphyriacus).
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