In order to improve the surface forming quality and machining efficiency of composite materials and reduce tool wear, a two-dimensional rotary ultrasonic combined electro-machining (2DRUEM) technology with low electrical conductivity and low current density was proposed in this study. Additionally, a gap detection unit of the machining system was designed with the integration of grinding force and gap current, and the average errors and maximum errors of the model were 5.61% and 12.08%, respectively, which were better than single detection. Furthermore, the machining parameters were optimally selected via NSGA-II, and the maximum machining surface roughness error was 5.9%, the maximum material removal rate error was 5.5%, and the maximum edge accuracy error was 8.9%, as established through experiments.

Auditory processing disorder is the most common problem affecting veterans after blast exposure, but the distinct impacts of blast-related traumatic brain injury and blast-related hearing loss are unknown. Independently, both hearing loss and blast exposure affect the entire auditory processing pathway at the molecular and physiological levels. Here, we identified distinct changes to the primary auditory cortex (AI) and temporal processing in mice following blast exposure both with and without protected hearing. Our results show that blast-exposure alone activated microglia in AI, but hearing loss was required for reductions in the density of parvalbumin-expressing interneurons. Although blast exposure impaired the temporal following response, these impairments were more severe with concurrent unilateral hearing loss, further resulting in impairments in behavioral gap detection. Taken together, these results indicate that protecting hearing during blast exposure can prevent most impairments to auditory processing but does not fully protect temporal processing.

This study investigated the effect of sound therapy combined with drug therapy (SDT) on gap detection threshold and speech recognition scores in patients with sudden sensorineural hearing loss (SSNHL).
Patients with SSNHL were grouped randomly into SDT and drug therapy (DT) groups. All patients received standard drug treatment and patients in the SDT group additionally received sound stimulation for the affected ears for 6 days. Pure tone audiogram, speech recognition scores at normal and time-compressed rates under quiet and noisy conditions, and the gap detection threshold of the SDT and DT groups before treatment and on day 6 and 30 after treatment were compared.
There were 20 patients in the SDT group and 24 in the DT group. The pure tone thresholds of affected ears were significantly lower in the SDT group on day 6 after treatment than those in the DT group at 125 and 250 Hz. Significantly lower gap detection thresholds and higher speech recognition scores under noisy conditions were observed at the normal and time-compressed rates in the SDT group than those in the DT group on day 6 and 30 after treatment. Significant correlations were observed between the gap thresholds and speech recognition scores in a noisy environment at normal and time-compressed rates on day 6 and 30.
SDT may improve the recovery of hearing abilities, such as the gap in noise thresholds and speech recognition in noise, in the case of SSNHL.
ChiCTR-IOR-17012262.

Gap detection or gap pre-pulse inhibition of the acoustic startle (GPIAS) has been successfully used in rat and guinea pig models of tinnitus, yet this system has been proven to have low efficacy in CBA mice, with low basal GPIAS and subtle tinnitus-like effects. Here, we tested five mouse strains (CBA, BalbC, CD-1, C57BL/6 and 129sv) for pre-pulse inhibition (PPI) and gap detection with varying interstimulus intervals (ISI) and found that mice from a CBA genetic background had the poorest capacities of suppressing the startle response in the presence of a pre-pulse or a gap. CD-1 mice displayed variable responses throughout all ISI. Interestingly, C57BL/6, 129sv and BalbC showed efficient suppression with either pre-pulses or gaps with shorter ISI. The glutamate aspartate transporter (GLAST) is expressed in support cells from the cochlea and buffers the excess of glutamate. We hypothesized that loss of GLAST function could sensitize the ear to tinnitus-inducing agents, such as salicylate. Using shorter ISI to obtain a greater dynamic range to assess tinnitus-like effects, we found that disruption of gap detection by salicylate was exacerbated across various intensities of a 32-kHz narrow band noise gap carrier in GLAST knockout (KO) mice when compared to their wild-type (WT) littermates. Auditory brainstem responses (ABR) and distortion-product otoacoustic emission (DPOAE) were performed to evaluate the effects on hearing functions. Salicylate caused greater auditory threshold shifts (near 15 dB) in GLAST KO mice than in WT mice across all tested frequencies, despite similarly reduced DPOAE. Despite these changes, inhibition using broad-band gap carriers and 32 kHz pre-pulses were not affected. Our study suggests that GLAST deficiency could become a useful experimental model to decipher the mechanisms underlying drug-induced tinnitus. Future studies addressing the neurological correlates of tinnitus in this model could provide additional insights into the mechanisms of tinnitus.

CONCLUSIONS: Scopolamine, a tropane alkaloid drug that mainly acts as an antagonist of muscarinic acetylcholine receptors, was found to reduce the local field potentials (LFP) of auditory cortex (AC) evoked by tone and gap-offsets whose effects may compensate the cortical hyperexcitability related to tinnitus.
OBJECTIVE: To study the effects of scopolamine on the AC and the inferior colliculus (IC) of awake rats in order to understand scopolamine\'s effect on tinnitus and gap detection.
METHODS: Silent gaps (duration varied from 2-100 ms) embedded in otherwise continuous noise were used to elicit AC and IC response. Gap evoked AC and IC field potentials were recorded from awake rats before and after treatment of scopolamine (3 mg/kg, i.m.).
RESULTS: Acute injection of scopolamine (3 mg/kg, i.m.) induced a significant reduction of the AC response, but not the IC response, to the offset of the gaps embedded in white noise. The results suggest that scopolamine may reduce AC neural synchrony.