Sentence examples for models of cigarette from inspiring English sources

PPAR-activators are putative drug targets in COPD [35], [36], [37], yet no models of cigarette smoke exposure and viral or bacterial infection have examined their potential.

Although it is understood that treating the cytokine storm observed during an influenza infection with steroids is in-effective [22], [34], no studies to our knowledge involving models of cigarette smoke and virus have addressed if a steroid intervention would control the exacerbated responses observed in smokers.

Olodaterol was tested in murine and guinea pig models of cigarette smoke- and LPS-induced lung inflammation.

The potential therapeutic utility of inhibiting kinases [e.g. p38 MAPK (mitogen-activated protein kinase) and PI3K (phosphoinositide 3-kinase)] in COPD has been supported by data generated in animal models of cigarette smoke-induced lung inflammation.

This study evaluated the relationship between p38 MAPK activation and susceptibility to cigarette smoke (CS -induced emphysema, and whether its inhibition ameliorated the lung inflammation and injury in murine models of CS -inducedmokemphysemae.

Given that oxidative stress is elevated in COPD and that it is a major mechanism that leads to corticosteroid resistance in COPD through reduced activity and expression of HDAC2, animal models of cigarette smoke-induced COPD have explored the therapeutic utility of antioxidant compounds.

This paper applies a behavioral economics model of cigarette addiction to the issue of fossil fuel usage and climate change.

We investigated the effects of cigarette smoke on nasal mucosa in vitro and via a model of cigarette smoke exposure by using animals deficient in complement components.

This animal model of cigarette smoke and H1N1 influenza infection demonstrates that smoke-exposed animals are differentially primed to respond to viral insult.

To this end, we delivered a dose of corticosteroids, which we had previously shown in a model of cigarette smoke and non-typeable Haemophilus influenzae infection to attenuate exaggerated inflammatory responses [21].

Along similar lines, the viral titres observed at both days five and seven post-infection did not reach statistical significance; in contrast, in our model of cigarette smoke exposure and Haemophilus influenzae infection, systemic corticosteroid treatment significantly impaired bacterial clearance from the lungs of infected mice.