Rita Sahar

TL;DR: It is suggested that the chronic inflammation and prolonged impairment of corneal innervation are playing a role in the pathogenesis of the delayed LSCD following SM exposure by creating a pathological microenvironment to limbal epithelial stem cells, thus, leading to their slow death and to a second cascade of pathological events eventually resulting in severe long-term injuries.

TL;DR: Sarin has a potent acute and long-term central neurotoxicity, which must be considered in the design of therapeutic regimes, and frontal cortex damage was specific to soman poisoning.

TL;DR: The experimental model for sulfur mustard-induced acute and delayed ocular lesions in rabbits is useful for studying the pathological mechanisms of HD-ocular lesions, and may serve for testing potential therapies.

TL;DR: It is shown that topically applied steroid treatment, administered after HD exposure, attenuated the extent of neovascularization, one of the characteristics of delayed ocular pathology in rabbits.

TL;DR: It is suggested that brain lesions are not common for all ChE inhibitors and that convulsions per se are not the only factor leading to brain damage following the administration of soman, and that degenerative process might be due to a secondary effect, unrelated to soman's clinical toxicity, but leading to long-term brain injuries.