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t = 0.81, p = 0.42)

However, with the emergence of a body of data documenting differences in autistic brains that were most likely of physiological originparticularly neuropathological identification of neural and glial inflammation associated with enlargement of the areas of the brain, including cerebrum, that continue to grow and mature postnatallythe assumption of congenital origin came under question, since the processes of generating such changes are often associated with environmental etiologies including oxidative stress and neuroinflammation generated by noxious environmental exposures, including activation of glial cells [46, 271, 315, 377, 411, 522, 548]

Retained mucus initiates inflammation even in the absence of infection, creating a microenvironment that sustains bacterial colonization, amplifies mucus production, and drives progressive structural lung damage, including bronchiectasis, ultimately underpinning chronic lung disease and respiratory failure in CF [34]

Recent studies demonstrated the role of epigenetics in EndMT in atherosclerotic mouse models