Il progetto Lab2Go per la diffusione della pratica laboratoriale nell’insegnamento delle discipline STEM nelle scuole secondarie di II grado

Per avvicinare gli studenti alle scienze sperimentali, Sapienza Università di Roma e l’INFN hanno ideato il progetto Lab2go. Nato a Roma nell’ambito della fisica, si è diffuso in gran parte d’Italia e ha coinvolto altre discipline. Durante la pandemia COVID-19, sono state introdotte numerose attività on-line, compatibili con la didattica digitale a distanza; per la Fisica la proposta di Lab2Go si è espressa attraverso seminari on-line (Lab2go@home) mostrando esperienze effettuabili con l’utilizzo di materiale povero, app per smartphone e dispositivi digitali quali, ad esempio, Arduino

Hydrogen sulfide causes vanilloid receptor 1-mediated neurogenic inflammation in the airways

1. Hydrogen sulfide (H(2)S) is described as a mediator of diverse biological effects, and is known to produce irritation and injury in the lung following inhalation. Recently, H(2)S has been found to cause contraction in the rat urinary bladder via a neurogenic mechanism. Here, we studied whether sodium hydrogen sulfide (NaHS), used as donor of H(2)S, produces responses mediated by sensory nerve activation in the guinea-pig airways. 2. NaHS evoked an increase in neuropeptide release in the airways that was significantly attenuated by capsaicin desensitization and by the transient receptor potential vanilloid 1 (TRPV1) antagonist capsazepine. In addition, NaHS caused an atropine-resistant contraction of isolated airways, which was completely prevented by capsaicin desensitization. Furthermore, NaHS-induced contraction was reduced by TRPV1 antagonism (ruthenium red, capsazepine and SB366791), and was abolished by pretreatment with the combination of tachykinin NK(1) (SR140333) and NK(2) (SR48968) receptor antagonists. 3. In anesthetized guinea-pigs, intratracheal instillation of NaHS increased the total lung resistance and airway plasma protein extravasation. These two effects were reduced by TRPV1 antagonism (capsazepine) and tachykinin receptors (SR140333 and SR48968) blockade. 4. Our results provide the first pharmacological evidence that H(2)S provokes tachykinin-mediated neurogenic inflammatory responses in guinea-pig airways, and that this effect is mediated by stimulation of TRPV1 receptors on sensory nerves endings. This novel mechanism may contribute to the irritative action of H(2)S in the respiratory system