Claire Delacour

TL;DR: A quick neuro-inflammatory gene response that does not subside over 7 days is indicated suggesting a potential role in the neurological consequences of soman-induced status epilepticus.

TL;DR: The ADC decrease observed in the present study suggests that brain edema in soman poisoning is mainly intracellular and cytotoxic, while anesthesia was shown to interrupt soman-induced seizures and to attenuate edema and cell change in certain sensitive brain areas.

TL;DR: Results suggest that the rebound of plasma ChE activity following inhibition provoked by the intravenous injection of 6 and 12 microg kg(-1) of VX was likely due to the release of butyrylcholinesterase into the blood stream from ChE producing organs.

TL;DR: The present review will address four points: the medical issues raised by the central effects of soman poisoning; the mechanism of Soman-induced brain damage; the use of antagonists of ionotropic glutamate receptors as anticonvulsants and neuroprotectants; and the search for new non-invasive methods to assess the progression of somAn-inducedbrain damage.

TL;DR: In this article, distortion product otoacoustic emissions (DPOAEs) were used to monitor cochlear functionality in rats administered with a moderate dose of organophosphorus nerve agent (45 μg/kg).