Deafness, culture, and choice.

Assembly of the cochlear gap junction macromolecular complex requires connexin 26.

Hereditary deafness affects approximately 1 in 2,000 children. Mutations in the gene encoding the cochlear gap junction protein connexin 26 (CX26) cause prelingual, nonsyndromic deafness and are responsible for as many as 50% of hereditary deafness cases in certain populations. Connexin-associated deafness is thought to be the result of defective development of auditory sensory epithelium due t...

Children\'s Deafness

This is an article about children's deafness, it's ethiology, diagnosis, treatment, and educa­tional treatment. Here I have given a brief account about the deafness itself and it's in­dividual and social complications, also it's im­pression on the psychological well baing of the child. Then I have discussed, rather in detail, the ethiology of .children's deafness and I have given some statistic...

Deafness/Disability - problematising notions of identity, culture and structure

Failure of Fluid Absorption in the Endolymphatic Sac Initiates Cochlear Enlargement that Leads to Deafness in Mice Lacking Pendrin Expression

Mutations of SLC26A4 are among the most prevalent causes of hereditary deafness. Deafness in the corresponding mouse model, Slc26a4(-/-), results from an abnormally enlarged cochlear lumen. The goal of this study was to determine whether the cochlear enlargement originates with defective cochlear fluid transport or with a malfunction of fluid transport in the connected compartments, which are t...

Reconsidering cochlear implants: the lessons of Martha's Vineyard.

I distinguish and assess three separate arguments utilized by the opponents of cochlear implants: that treating deafness as a medical condition is inappropriate since it is not a disability; that so treating it sends a message to the Deaf that they are of lesser worth; and that the use of such implants would signal the end of Deaf culture. I give some qualified support to the first and second c...