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While this model provided detailed imaging and immune cell incorporation, they lacked TER assessment as well, and biomechanical stretch, limiting their ability to fully replicate inhalation-induced alveolar dysfunction

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As such, one plausible mechanistic account is that repeated stimulation of high densities of nAChRs by nicotine may contribute to neurotoxicity within discrete regions and/or increase the vulnerability of those regions to other volatile compounds in tobacco smoke [19] which ultimately manifest as gray matter decreases