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Lung inflammation in COPD is perpetuated by a number of factors that may include latent adenoviral infections, which increase the expression of mediators and adhesion molecules, 4 as well as recurrent bacterial and viral infections, which cause a chronic inflammatory state
Morgan et al ., 1996)
Cao, G., Li, H.-B., Yin, Z
A similar pattern emerged in vivo: in tobacco nuclei, the phaseseparation propensity of PIF4 mTAD , expressed as an mGFPmut2 fusion, was diminished (Fig
