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Unraveling the Noise: An Investigation Plan for Signal Interference in Hearing Aids

Bluetooth Low Energy (BLE) has revolutionized the performance of hearing aids with functionalities like seamless audio streaming and enhanced auditory functions. However, BLE operates within the highly congested 2.4 GHz frequency band, making it susceptible to signal interference that can degrade performance, reduce audio quality, and impact user experience. This paper documents interference patterns in BLE communication and introduces practical mitigation techniques aimed at improving the reliability of hearing aids. Attack vectors associated with Bluetooth enabled hearing aids include communication jamming, the interception of data between target devices, and GATT handle exploitation. Attackers could also use the vulnerabilities to block communications or intercept sensitive audio streams, posing significant security and privacy risks. These threats compromise two critical components of the CIA triad: (1) availability, by causing persistent connectivity issues, and (2) integrity, by enabling unauthorized data modifications. It is necessary to deal with these problems to ensure hearing aids work well and safely. This study investigates the impact of BLE signal interference on hearing aids, using tools such as HackRF [1], a Python tool to simulate interference scenarios, and Ubertooth [2] to sniff Bluetooth traffic between hearing aids and the device with the application. This paper investigates testing of BLE traffic in search of specific interference patterns that would impact the functionality of hearing aids, including jamming and flooding. This research focuses on developing robust mitigation techniques with the aim of securing BLE-enabled hearing aids against those vulnerabilities.

Baldwin, David [Savannah River National Laboratory↗

Kölliker's Organ Functions as a Developmental Hub in Mouse Cochlea Regulating Spiral Limbus and Tectorial Membrane Development

Kölliker's organ is a transient developmental structure in the mouse cochlea that undergoes significant remodeling postnatally. Utilizing an epithelial-specific conditional deletion mouse model of Prdm16 (marker and regulator of Kölliker's organ), we show that Prdm16 is required for interdental cell development, and thereby the development of the limbal domain of the tectorial membrane and its medial anchorage to the spiral limbus. Additionally, we show that Kölliker's organ is involved in normal tectorial membrane collagen fibril development and maturation. Interestingly, mesenchymal cells of the spiral limbus underneath Prdm16 -deficient Kölliker's organ failed to produce interstitial matrix proteins, resulting in a hypoplastic and truncated spiral limbus, indicating a non-cell autonomous role of Prdm16 in regulating spiral mesenchymal matrix development. Single-cell RNA sequencing identified differentially expressed genes in Prdm16 -deficient Kölliker's organ suggesting a role for connective tissue growth factor (CTGF) downstream Prdm16 in epithelial-mesenchymal signaling involved in spiral limbus matrix deposition. Prdm16 -deficient mice showed a hearing deficit, as indicated by elevated auditory brainstem response thresholds at most frequencies, consistent with the cochlear structural defects. Both sexes were studied. This work establishes Prdm16 as a deafness gene in mice through its role in regulating Kölliker's organ development. Such understanding recognizes Kölliker's organ as a developmental hub regulating multiple surrounding cochlear structures.

Zhang, Hongji↗