Vestibular evaluation following cochlear implantation in patients with inner-ear anomalies.

OBJECTIVE: This cross-sectional study investigated vestibular function outcomes after cochlear implantation in patients with inner-ear anomalies. METHODS: Twenty-two patients with bilateral symmetric inner-ear anomalies and 28 patients with normal inner ears were included. All were congenitally or progressively deaf persons implanted unilaterally during the previous 15 years. Vestibular system function was assessed by vestibular-evoked myogenic potential and bithermal caloric tests. RESULTS: The vestibular-evoked myogenic potential abnormality rate in implanted ears with an inner-ear anomaly was 81.8 per cent, compared with 39.3 per cent in implanted ears with normal anatomy. In the non-implanted sides, the rate was 45.5 per cent (10 out of 22 cases) in the inner-ear anomaly patients compared with 17.9 per cent in patients with normal inner-ear structure. The respective abnormal caloric test rates in inner-ear anomaly versus normal anatomy patients were 81.8 per cent and 17.9 per cent (implanted ears), 77.3 per cent and 14.3 per cent (non-implanted sides). CONCLUSION: Inner-ear anomaly and implantation were both associated with more vestibular-evoked myogenic potential abnormalities; when occurring together, these factors showed a synergistic effect. Caloric test abnormality is mainly dependent on the presence of an inner-ear anomaly, but implantation is not associated with caloric abnormality.

Deferoxamine promotes mesenchymal stem cell homing in noise-induced injured cochlea through PI3K/AKT pathway.

OBJECTIVE: Over 5% of the world's population suffers from disabling hearing loss. Stem cell homing in target tissue is an important aspect of cell-based therapy, which its augmentation increases cell therapy efficiency. Deferoxamine (DFO) can induce the Akt activation, and phosphorylation status of AKT (p-AKT) upregulates CXC chemokine receptor-4 (CXCR4) expression. We examined whether DFO can enhance mesenchymal stem cells (MSCs) homing in noise-induced damaged cochlea by PI3K/AKT dependent mechanism. MATERIALS AND METHODS: Mesenchymal stem cells were treated with DFO. AKT, p-AKT protein and hypoxia inducible factor 1- α (HIF-1α) and CXCR4 gene and protein expression was evaluated by RT- PCR and Western blot analysis. For in vivo assay, rats were assigned to control, sham, noise exposure groups without any treatment or receiving normal, DFO-treated and DFO +LY294002 (The PI3K inhibitor)-treated MSCs. Following chronic exposure to 115 dB white noise, MSCs were injected into the rat cochlea through the round window. Number of Hoechst- labelled cells was determined in the endolymph after 24 hours. RESULTS: Deferoxamine increased P-AKT, HIF-1α and CXCR4 expression in MSCs compared to non-treated cells. DFO pre-conditioning significantly increased the homing ability of MSCs into injured ear compared to normal MSCs. These effects of DFO were blocked by LY294002. CONCLUSIONS: Pre-conditioning of MSCs by DFO before transplantation can improve stem cell homing in the damaged cochlea through PI3K/AKT pathway activation.