Carbamate

Polyureas (PURs) are a competitive polymer to their analogs, polyurethanes (PUs). Whereas PUs’ main functional group is carbamate (urethane), PURs contain urea. In this revision, a comprehensive overview of PUR properties, from synthesis to technical applications, is displayed. Preparative routes that can be used to obtain PURs using diisocianates or harmless reagents such as CO2 and NH3 are explained, and aterials, urea monomers and PURs are discussed; PUR copolymers are included in this discussion as well. Bulk to soft components of PUR, as well as porous materials and meso, micro or nanomaterials are evaluated. Topics of this paper include the general properties of aliphatic and aromatic PUR, followed by practical synthetic pathways, catalyst uses, aggregation, sol–gel formation and mechanical aspects.

Organophosphate (OP) and carbamate acetylcholinesterase (AChE) inhibitors produce seizures and lethality in mammals. Anticonvulsant and neuroprotective properties of N-methyl-D-aspartate (NMDA) antagonists encourage the investigation of their effects in AChE inhibitor-induced poisonings. In the present study, the effects of dizocilpine (MK-801, 1 mg/kg) or 3-((RS)-2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid (CPP, 10 mg/kg), alone or combined with muscarinic antagonist atropine (1.8 mg/kg), on convulsant and lethal properties of an OP pesticide dichlorvos or a carbamate drug physostigmine, were studied in mice. Both dichlorvos and physostigmine induced dose-dependent seizure activity and lethality. Atropine did not prevent the occurrence of convulsions but decreased the lethal effects of both dichlorvos and physostigmine. MK-801 or CPP blocked or attenuated, respectively, dichlorvos-induced convulsions. Contrariwise, NMDA antagonists had no effect in physostigmine-induced seizures or lethality produced by dichlorvos or physostigmine. Concurrent pretreatment with atropine and either MK-801 or CPP blocked or alleviated seizures produced by dichlorvos, but not by physostigmine. Both MK-801 and CPP co-administered with atropine enhanced its antilethal effects in both dichlorvos and physostigmine poisoning. In both saline- and AChE inhibitor-treated mice, no interaction of the investigated antidotes with brain cholinesterase was found. The data indicate that both muscarinic ACh and NMDA receptor-mediated mechanisms contribute to the acute toxicity of AChE inhibitors, and NMDA receptors seem critical to OP-induced seizures.