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ethyl sulfide/œdème

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Inflammatory biomarkers of sulfur mustard analog 2-chloroethyl ethyl sulfide-induced skin injury in SKH-1 hairless mice.

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Sulfur mustard (HD) is an alkylating and cytotoxic chemical warfare agent, which inflicts severe skin toxicity and an inflammatory response. Effective medical countermeasures against HD-caused skin toxicity are lacking due to limited knowledge of related mechanisms, which is mainly attributed to the

A dorsal model for cutaneous vesicant injury by 2-chloroethyl ethyl sulfide using C57BL/6 mice.

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To evaluate stem cell-derived therapeutics for cutaneous vesicant injuries, we developed a dorsal exposure model using C57BL/6 black mice and half-mustard, 2-chloroethyl ethyl sulfide (CEES). The dorsal side of a mouse was exposed to 1-5 microl of CEES for 10 minutes and then decontaminated. The

Prophylactic protection by N-acetylcysteine against the pulmonary injury induced by 2-chloroethyl ethyl sulfide, a mustard analogue.

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Mustard gas exposure causes adult respiratory distress syndrome associated with lung injury. The purpose of this study was to investigate whether an antioxidant, such as N-acetylcysteine (NAC), has any protective effect. Guinea pigs were given single exposure (0.5-6 mg/kg body weight) of
Sulfur mustard is a potent vesicant that induces inflammation, edema and blistering following dermal exposure. To assess molecular mechanisms mediating these responses, we analyzed the effects of the model sulfur mustard vesicant, 2-chloroethyl ethyl sulfide, on EpiDerm-FT™, a commercially available

Mustard vesicating agent-induced toxicity in the skin tissue and silibinin as a potential countermeasure.

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Exposure to the vesicating agents sulfur mustard (SM) and nitrogen mustard (NM) causes severe skin injury with delayed blistering. Depending upon the dose and time of their exposure, edema and erythema develop into blisters, ulceration, necrosis, desquamation, and pigmentation changes, which persist

Protection from half-mustard-gas-induced acute lung injury in the rat.

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The chemical warfare agent analog, 2-chloroethyl ethyl sulfide, known as 'half-mustard gas' (HMG), is less toxic and less of an environmental hazard than the full molecule and has been shown to produce an acute lung injury in rats when instilled via intrapulmonary injection. This injury is

Doxycycline hydrogels as a potential therapy for ocular vesicant injury.

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OBJECTIVE The goals of this study were (1) to compare the injury at the basement membrane zone (BMZ) of rabbit corneal organ cultures exposed to half mustard (2 chloroethyl ethyl sulfide, CEES) and nitrogen mustard with that of in vivo rabbit eyes exposed to sulfur mustard (SM); (2) to test the

TRPA1 and CGRP antagonists counteract vesicant-induced skin injury and inflammation.

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The skin is highly sensitive to the chemical warfare agent in mustard gas, sulfur mustard (SM) that initiates a delayed injury response characterized by erythema, inflammation and severe vesication (blistering). Although SM poses a continuing threat, used as recently as in the Syrian conflict, no
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