2-chloroethyl ethyl sulfide

07/01/2009 - "The purpose of this study is to assess the ability to detect and monitor progression of half-mustard [2-chloroethylethylsulfide (CEES)] airway injuries with OCT techniques. "
12/15/2011 - "Together, our results show that CEES causes both direct and oxidative DNA damage, suggesting that to rescue SM-caused skin injuries, pleiotropic agents (or cocktails) are needed that could target multiple pathways of mustard skin toxicities."
07/01/2014 - "Results from this study demonstrate the potential therapeutic efficacy of AEOL 10150 against CEES-mediated cutaneous lesions, supporting AEOL 10150 as a medical countermeasure against SM-induced skin injuries. "
12/03/2007 - "Although R24Q Kunitz-domain 1 lacked trypsin and plasmin inhibitory activity, it promoted wound closure of untreated and 2-chloroethyl ethyl sulfide-treated cells but to a much lesser degree. "
07/10/2007 - "Although R24Q Kunitz-domain 1 lacked trypsin and plasmin inhibitory activity, it promoted wound closure of untreated and 2-chloroethyl ethyl sulfide-treated cells but to a much lesser degree. "

12/01/2019 - "On the other hand, CEES exposure disrupts the protein carbonylation (PC) and lipid peroxidation (LPO) in keratinocytes leading to inflammation, crash of the cell-cell communication, cell cycle deregulation, and apoptosis via Erk1/2-PI3K/Akt pathways. "
12/01/2019 - "Relevance of Erk1/2-PI3K/Akt signaling pathway in CEES-induced oxidative stress regulates inflammation and apoptosis in keratinocytes."
01/01/2017 - "However, the molecular mechanisms of macrophage activation and NO production leads to apoptosis and inflammation after 2-chloroethyl ethyl sulphide (CEES) exposure remains unclear. "
05/15/2012 - "These data demonstrate that RNS, generated via iNOS play a role in the pathogenic responses to CEES, augmenting oxidative stress and inflammation and suppressing tissue repair. "
08/01/2011 - "DAA-I attenuated the early processes of inflammation seen in the CEES-inoculated mice. "

01/01/2012 - "These findings indicate that TF pathway inhibition could be an effective strategy to prevent airway obstruction after SM or CEES inhalation."
02/01/2015 - "Intratracheal heparin 1 hr after CEES inhalation improved survival, oxygenation, airway obstruction, and clinical distress. "
10/01/2013 - "Airway obstruction in the form of fibrin-containing casts was evident in central conducting airways of rats receiving CEES. "
12/01/2010 - "To develop a rat inhalation model for airway obstruction with the SM analog 2-chloroethyl ethyl sulfide (CEES), and to investigate the pathogenesis of bronchial cast formation. "

09/26/2008 - "CEES exposure caused lung injury with evidence of fibrosis. "
05/01/2008 - "The data demonstrate that delivery of antioxidants via liposomes to CEES-injured lungs is, depending on liposomal content, protective against ALI, prevents the appearance of proinflammatory mediators in bronchoalveolar fluids, and suppresses progressive fibrosis. "
05/01/2008 - "When lung fibrosis 3 weeks after CEES was quantitated by using hydroxyproline content, liposomes containing NAC or NAC + glutathione had no effects, but liposomes containing alpha/gamma-tocopherol alone or with NAC significantly suppressed the increase in lung hydroxyproline. "

01/01/2009 - "Thus, our study indicates that CEES-induced lung injury is associated with desensitization of beta(2)-AR."
09/26/2008 - "The present study examines the relationship between CEES induced lung injury and MAPKs signaling pathway. "
05/01/2017 - "Lung injury was developed in guinea pigs by intratracheal exposure of CEES (0.5 mg/kg). "
05/01/2008 - "Accordingly, the liposomal strategy may be therapeutically useful in CEES-induced lung injury in humans."
01/01/2003 - "Signal transduction events in lung injury induced by 2-chloroethyl ethyl sulfide, a mustard analog."