Adina Amir

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: 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: The ability to ameliorate sulfur mustard‐induced oedema by treatment with anti‐inflammatory drugs was reported previously after screening four steroids and four non‐steroidal anti-inflammatory drugs (NSAIDs) using the mouse ear vesicant model.

TL;DR: This in vivo study showed the involvement of M MP-9 and MMP-2 during different phases of the SM-induced ocular injury, and the potential of doxycycline treatment as a post exposure measure for reducing the acute injury and as a preventive therapy for ameliorating the delayed pathology.