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Objective: The auditory steady-state response (ASSR) amplitudes fall in the presence of contralateral noise. However, whether and to what extent medial olivocochlear (MOC) activity involves in contralateral suppression of ASSR remain unclear. Therefore, we assess the role of MOC activity in contralateral suppression of ASSR., Methods: Mice were treated with strychnine to completely eliminate MOC activity and then measured ASSR amplitudes in the presence of contralateral noise., Results: The contralateral noise reduces ASSR amplitudes at some stimulus intensity. After treating with the strychnine to eliminate MOC activity, ASSR amplitudes recovered again., Conclusions: MOC activity participated in contralateral suppression of ASSR., Competing Interests: Declaration of Competing Interest None., (Copyright © 2022. Published by Elsevier B.V.)

The tympanic membrane plays an important role in the human hearing system, which is easily perforated under unfavorable conditions, leading to loss of hearing and otitis media. Many autologous materials and artificial materials have been used to repair a perforated tympanic membrane, but these materials sometimes can cause severe hearing loss because of their adhesion to the ossicle during the healing process and the postoperative process. Herein, we report Janus membranes with asymmetric cellular adhesion behaviors for regenerating the eardrum. These Janus membranes are constructed by co-depositing a tannic acid (TA)/3-aminopropyltriethoxysilane (APTES) coating on one surface of the polypropylene microfiltration membrane. Cellular experiments indicate that the Janus membranes have good biocompatibility and asymmetric cellular adhesion properties. The repair of the tympanic membrane perforation experiment and laser Doppler vibrometer (LDV) measurements prove that the hydrophilic surface of Janus membranes repairs perforated eardrums, and meanwhile the hydrophobic surface can avoid adhering to the inner ear tissue for reducing hearing loss. The Janus membranes have good prospects in the treatment of tympanic membrane perforation.

Purpose: To explore the feasibility of automatic detection based on air flow and blood oxygen in patients with sleep disordered breathing., Methods: This study proposes a new automated detection method for sleep disordered breathing based on overnight airflow and blood oxygen saturation (SaO 2 ). In this regard, local range (LR) of the airflow was adopted to detect apnea events and the SaO 2 sudden drops were used to help determine hypopnea events. Pearson correlation index was used to evaluate the relationship between the two automated methods (this study vs. Remlogic software) and the manual reports. Error and mean absolute error (MAE) were used to assess the two automated methods., Results: For all patients, the apnea-hypopnea index (AHI), apnea index (AI) and hypopnea index (HI) for our automated scoring and manual reports were highly correlated (the Pearson correlation index were 0.996, 0.995 and 0.928, respectively, P < 0.001). However, HI for Remlogic automated scoring and clinical manual reports was poorly correlated (r = 0.316, P < 0.001). Compared with the manual reports, mean absolute error of AHI, AI and HI between the two automated methods (this study vs. Remlogic software) were statistically significant (P < 0.0001). Furthermore, among the three subgroups (group 1, AHI < 15/h, group 2, 15/h ≤ AHI < 30/h and group 3, AHI ≥ 30/h), the mean error and MAE of AHI between the two automated methods were also statistically significant (P < 0.01)., Conclusions: Generally, good agreements were shown between our automated detection and clinical reports. This procedure is robust and effective, which would significantly shorten the analysis time.

Objective: To investigate the effects of long-term moderate noise on hearing functions, MOCR, and MEMR., Methods: Mice were exposed to the moderate noise (11.2 - 22.4 kHz, 80 dB SPL, 6 h/day, 4 weeks). Subsequently, the hearing functions, including threshold and input-output roles of ABR (auditory brainstem response) and cubic (2f 1 -f 2 ) DPOAEs (distortion product otoacoustic emissions) were evaluated. Also, MEMR and MOCR were assessed shortly after or at four weeks following the termination of exposure to the noise., Results: The mice's acoustic suppression reflex was strengthened, hearing functions and MEMR were unaffected four weeks after the moderate noise. For primary tones of 16, 20 and 24 kHz, the strengths of contralateral and ipsilateral suppression in the noise group were about double those recorded in the control group. In order to further determine whether the functional changes of the afferent or efferent nerves increased the strengths of acoustic suppression, the mouse's left ear was inserted the earplug, and then exposed the moderate noise for four weeks. The strengths of contralateral suppression at 16, 20 and 24 kHz were increased for the noise + earplug than for the control group and were indistinguishable between the noise + earplug and the noise group. While no significant changes were found in the strengths of ipsilateral suppression at all frequencies for the noise + earplug group compared with the control group. Under ketamine/xylazine anesthesia, the broadband suppressor noise did not stimulate the MEMR by 20 min post-induction at all frequencies in three groups., Conclusion: Our data demonstrated that the long-term moderate noise-exposure strengthened mice's MOCR by changing its afferent nerves, and unaffected cochlear hair cells and type I spiral ganglion neurons., Competing Interests: Declaration of Competing Interest The authors declare that they have no conflicts of interest., (Copyright © 2020. Published by Elsevier B.V.)

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.