Maturation of cochlear nonlinearity as measured by distortion product otoacoustic emission suppression growth in humans.

The growth of distortion product otoacoustic emission (DPOAE) suppression follows a systematic, frequency-dependent pattern. The pattern is consistent with direct measures of basilar-membrane response growth, psychoacoustic measures of masking growth, and measures of neural rate growth. This pattern has its basis in the recognized nonlinear properties of basilar-membrane motion and, as such, the DPOAE suppression growth paradigm can be applied to human neonates to study the maturation of cochlear nonlinearity.

Progressive hearing loss in mice lacking the cyclin-dependent kinase inhibitor Ink4d.

Maintenance of the post-mitotic state in the post-natal mammalian brain is an active process that requires the cyclin-dependent kinase inhibitors (CKIs) p19Ink4d (Ink4d) and p27Kip1 (Kip1). In animals with targeted deletions of both Ink4d and Kip1, terminally differentiated, post-mitotic neurons are observed to re-enter the cell cycle, divide and undergo apoptosis. However, when either Ink4d or Kip1 alone are deleted, the post-mitotic state is maintained, suggesting a redundant role for these genes in mature neurons.

Distortion Product Otoacoustic Emissions: A Tool for Hearing Assessment and Scientific Study.

Distortion product otoacoustic emissions (DPOAEs) reflect outer hnir cell integrity and cochlear function. When used appropriately in the audiology clinic, they are an effective diagnostic tool and can detect hearing loss with accuracy. DPOAEs are easily and rapidly recorded in newborns and children, and provide basic hearing screening information as well as detailed diagnostic information in cases of suspected hearing loss.