Vsky AA. Skin temperature: its role in thermoregulation. Acta Physiol. 2014;210:49807. 23. Cliff MA, Green BG. Sensitization and desensitization to capsaicin and menthol in the oral cavity: interactions and individual variations. Physiol Behav. 1996;59:4874. 24. Cliff MA, Green BG. Sensory irritation and coolness developed by menthol: proof for selective desensitization of irritation. Physiol Behav. 1994;56: 1021. 25. Kozyreva Tv, Tkachenko EY. Impact of menthol on human temperature sensitivity. Hum Physiol. 2008;34:221. ten.1134 S0362119708020138. 26. Green BG. Menthol modulates oral sensations of warmth and cold. Physiol Behav. 1985;35:4274. 27. Gillis DJ, House JR, Tipton MJ. The influence of menthol on thermoregulation and perception during exercise in warm, humid conditions. Eur J Appl Physiol. 2010;110:6098. 10.1007 s00421-010-1533-4.Li and Pauluhn Clin Trans Med (2017) six:19 DOI ten.1186s40169-017-0149-REVIEWOpen AccessPhosgene-induced acute lung injury (ALI): differences from chlorine-induced ALI and attempts to translate toxicology to clinical medicineWenli Li1 and Juergen Pauluhn1,2Abstract Background: Phosgene (carbonyl dichloride) gas is definitely an indispensable chemical inter-mediate used in several industrial processes. There is absolutely no clear consensus as to its time- and inhaled-dose-dependent etiopathologies and associated preventive or therapeutic treatment methods. Solutions: Cardiopulmonary function was examined in rats exposed by inhalation to the Retinol Epigenetic Reader Domain alveolar irritant phosgene or for the airway irritant chlorine for the duration of and following exposure. Terminal measurements focused on hematology, protein extravasation in bronchoalveolar lavage (BAL), and increased lung weight. Noninvasive diagnostic and prognostic endpoints in exhaled breath (carbon dioxide and nitric oxide) had been utilised to detect the clinically occult stage of pulmonary edema. Results: The very first event observed in rats following higher but sublethal acute exposure to phosgene was the stimulation of alveolar nociceptive vagal receptors. This afferent stimulation resulted in dramatic alterations in cardiopulmonary functions, ventilation: perfusion imbalances, and progressive pulmonary edema and phospholipoproteinosis. Hematology revealed hemoconcentration to be an early marker of pulmonary edema and fibrin as a discriminating endpoint that was constructive for the airway irritant chlorine and negative for the alveolar irritant phosgene. Conclusions: The application of each gas created typical ALIARDS (acute lung injuryacute respiratory distress syndrome) traits. Phosgene-induced ALI showed evidence of persistent apnea periods, bradycardia, and shifts of vascular fluid from the peripheral towards the pulmonary circulation. Carbon dioxide in expired gas was suggestive of elevated ventilation dead space and appeared to become a harbinger of progressively establishing lung edema. Treatment using the iNOS inhibitor aminoguanidine aerosol by inhalation decreased the severity of phosgene-induced ALI when applied at low dose-rates. Symptomatic therapy regimens were thought of inferior to causal modes of therapy. Keywords and phrases: Acute lung injury, Nociceptive sensory reflexes, Cardiopulmonary function, Biomarkers in expired gas Background Phosgene (carbonyl dichloride) gas is an indispensable chemical intermediate employed in a lot of industrial processes at a worldwide annual production scale ofCorrespondence: [email protected] two Covestro Deutschland AG, Global Phosgene Steering Group, K9, 565, 51365.