L-N-Acetylcysteine treatment is associated with improved hearing outcome in sudden idiopathic sensorineural hearing loss.

Conclusion: Combination therapy corticosteroids plus an oral antioxidant L-N-acetylcysteine (LNAC) was associated with improved hearing over corticosteroids alone, particularly at the 6-month follow-up and at high frequencies (i.e. 4000 Hz).

The injured cochlea as a target for inflammatory processes, initiation of cell death pathways and application of related otoprotectives strategies.

One of the causes of sensorineural hearing loss is the loss of auditory hair cells following exposure to environmental stresses. Auditory hair cell death in response to cochlear trauma occurs via both necrosis and apoptosis. Apoptosis of hair cells involves the caspase and MAPK/JNK pathways which are activated by oxidative stress and secretion of inflammatory cytokines in response to trauma.

Single-stage total endoscopic resection of a plexiform neurofibroma of the maxillary sinus in a child with type 1 neurofibromatosis.

Plexiform neurofibromas are peripheral nerve sheath tumors associated with neurofibromatosis type 1. The maxillary sinus is an extremely rare location of the plexiform neurofibroma and only two adult cases have been previously reported. We report the first case of plexiform neurofibroma of the maxillary sinus occurring in a child with neurofibromatosis type 1.

Conservation of hearing and protection of auditory hair cells against trauma-induced losses by local dexamethasone therapy: molecular and genetic mechanisms.

Hypothesis: Dexamethasone (DXM) protects hearing against trauma-induced loss.

Materials: in vivo: A guinea pig model of electrode induced trauma (EIT)-induced hearing loss was used to locally deliver dexamethasone. In vitro: TNF-α-challenged organ of Corti explants treated with DXM or polymer-eluted DXM +/- PI3K/Akt/PkB/NFkB inhibitors were used for hair cells count and gene expression studies.