A possible role for nitric oxide in osteoclastogenesis associated with cholesteatoma.

Hypothesis: This study was designed to investigate the potential role of nitric oxide in cholesteatoma-induced bone resorption, in vitro and in vivo.

Background: Cholesteatoma is a disease of inflammatory bone resorption in the middle ear leading to hearing loss and vestibular dysfunction. Inappropriate activation of osteoclasts causes the morbidity associated with this disease.

Role for c-Jun N-terminal kinase in beta-cell recovery from nitric oxide-mediated damage.

Treatment of rat islets with the cytokine IL-1 results in the inhibition of mitochondrial function and insulin secretion, events that are mediated by beta-cell expression of iNOS [inducible nitric oxide (NO) synthase] and production of NO. beta-Cells recover from the inhibitory actions of NO, produced following 24 h incubation with IL-1, on islet oxidative metabolism and insulin secretion if iNOS enzymatic activity is inhibited and the islets are cultured (in the presence of IL-1 and iNOS inhibitors) for a brief period of 8 h. Islet recovery from cytokine- and NO-mediated damage is an active process that requires new gene expression, and NO itself is one activator of this recovery process.