The study included 12 eligible investigations covering 1388 patients, with the pooled risk ratio (RR) estimating the effectiveness of the postoperational prostheses between the titanium and non-titanium group, with a combined RR of 1.12 (95% confidence interval (CI): 0.98-1.27, p = 0.09), as well as their stability, with a combined RR of 1.47 (95% CI: 0.76-2.84, p = 0.26).

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3D reconstruction of CT images clearly displayed the detailed structures of the temporal bone. Quantitative data of the facial nerve and its adjacent structures are very useful for temporal bone surgery.

Our results indicate adequate and reliable anatomic information can be obtained using reconstructed CTA on an individualized basis.

Cochlear inner hair cell (IHC) ribbon synapses play an important role in sound encoding and neurotransmitter release. Previous reports show that both noise and aminoglycoside exposures lead to reduced numbers and morphologic changes of synaptic ribbons. In this work, we determined the distribution of N-methyl-D-aspartate receptors (NMDARs) and their role in the gentamicin-induced pathological changes of cochlear IHC ribbon synaptic elements. In normal mature mouse cochleae, the majority of NMDARs were distributed on the modiolar side of IHCs and close to the IHC nuclei region, while most of synaptic ribbons and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) were located on neural terminals closer to the IHC basal poles. After gentamicin exposure, the NMDARs increased and moved towards the IHC basal poles. At the same time, synaptic ribbons and AMPARs moved toward the IHC bundle poles on the afferent dendrites. The number of ribbon synapse decreased, and this was accompanied by increased auditory brainstem response thresholds and reduced wave I amplitudes. NMDAR antagonist MK801 treatment reduced the gentamicin-induced hearing loss and the pathological changes of IHC ribbon synapse, suggesting that NMDARs were involved in gentamicin-induced ototoxicity by regulating the number and distribution of IHC ribbon synapses.

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