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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.
Since we showed that steroid interventions did not play a role in attenuating the inflammation observed in this model of cigarette smoke exposure and influenza infection, we examined whether another anti-inflammatory agent would attenuate the observed dysregulation in the inflammatory response.
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To find out if this protein is also involved in COPD pathogenesis, Harald von Melchner and colleagues knocked out Sesn2 in a mouse model of cigarette-smoke-induced pulmonary emphysema.
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.
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.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com