Computational Modeling of the Mammalian Cochlea and Cochlea-Inspired Acoustic Devices

The cochlea is the primary organ in the inner ear associated with hearing, and is responsible for transducing pressure waves in air into neural potentials that can be processed by the central nervous system. The electro-mechanical properties of the cochlea are graded along the cochlear coil to act as a spectrum analyzer with low frequency sounds eliciting a larger vibrational motion at the apex of the coil and higher frequencies at the base. Further, the cochlea is not only a passive sensor, but also amplifies low amplitude sound and compresses high amplitude sound through a non-linear voltage regulated expansion and contraction of the motor protein prestin} in the lateral membrane of the outer hair cells (OHC). These mechanisms provide mammals with exceptional hearing abilities over a large dynamic range of acoustic intensity. However, this system is often partially or completely damaged, either due to genetic alterations leading to anatomical abnormalities, or due to exposure to acoustic or mechanical trauma. The overarching goal of the first part of this thesis is to develop a detailed fluid-structural-electrical model of the cochlea that describes the in vivo response of the cochlea to external stimuli as well as noise present in the system, to understand the mechanism of cochlear transduction and its associated pathologies. This will augment experimental studies by circumventing technological limitations of direct measurement in living cochleae through computer modeling, and assist in formulating new hypotheses that can be tested experimentally. Through our computational framework, we have developed estimates for the system noise incurred during mechanotransduction and show that taller stereocilia are more efficient at detecting vibrations in spite of experiencing more viscous noise. We have shown that the long-standing challenge of reconciling experimental observations in the base and the apex of the cochlea can be resolved by incorporating the correct cochlear geometry as well as consistently including the effects of the boundary layer in the lymphatic fluids. Further, we have explored the effect of longitudinal spread of current in the lymphatic fluids and analyzed their relevance for the generation and propagation of electrically evoked otoacoustic emissions. The second part of the thesis develops the theoretical foundations of a new class of non-reciprocal active linear acoustic media that allows vibrations to propagate primarily in one direction. The underlying control architecture is inspired from the phalangeal processes in the inner ear that have been hypothesized to support unidirectional wave propagation from the base to the apex of the cochlear spiral. These acoustic media can have widespread applications in noise and vibration control, as well as signal filtering and duplexing in the communications industry. We show that a cascaded series of non-collocated sensor-actuator pairs can break both spatial and temporal symmetries resulting in a dispersion relation that admits nonreciprocal wave transmission, and develop a generalized theory to derive the system characteristics of this class of active media. Further, we discuss a specific realization of this system using an air-borne acoustic medium and electrodynamic speaker-microphone pairs, and show that it achieves acoustic isolation of over 20 dB across a broad range of frequencies.PHDMechanical EngineeringUniversity of Michigan, Horace H. Rackham School of Graduate Studieshttps://deepblue.lib.umich.edu/bitstream/2027.42/155096/1/asasmal_1.pd

Analysis of Conduction and Radiation Heat Transfer in a Differentially Heated 2‐D Square Enclosure

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/137244/1/htj21221.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/137244/2/htj21221_am.pd

Android Based Bluetooth Appliance Control Mechanism 1

Abstract The proposed algorithm basically is an android application which possesses the capability to control any sort of electrical appliances remotely over the Bluetooth. The control mechanism mainly refers to the switching (on / off) of the appliances. It emphasizes on creating a virtual switch board, giving the user an exact experience of what he does regularly when switching off his bedroom lamp or his air -conditioner and for a lot of other household appliances

Contrasting mechanisms for hidden hearing loss: Synaptopathy vs myelin defects.

Hidden hearing loss (HHL) is an auditory neuropathy characterized by normal hearing thresholds but reduced amplitudes of the sound-evoked auditory nerve compound action potential (CAP). In animal models, HHL can be caused by moderate noise exposure or aging, which induces loss of inner hair cell (IHC) synapses. In contrast, recent evidence has shown that transient loss of cochlear Schwann cells also causes permanent auditory deficits in mice with similarities to HHL. Histological analysis of the cochlea after auditory nerve remyelination showed a permanent disruption of the myelination patterns at the heminode of type I spiral ganglion neuron (SGN) peripheral terminals, suggesting that this defect could be contributing to HHL. To shed light on the mechanisms of different HHL scenarios observed in animals and to test their impact on type I SGN activity, we constructed a reduced biophysical model for a population of SGN peripheral axons whose activity is driven by a well-accepted model of cochlear sound processing. We found that the amplitudes of simulated sound-evoked SGN CAPs are lower and have greater latencies when heminodes are disorganized, i.e. they occur at different distances from the hair cell rather than at the same distance as in the normal cochlea. These results confirm that disruption of heminode positions causes desynchronization of SGN spikes leading to a loss of temporal resolution and reduction of the sound-evoked SGN CAP. Another mechanism resulting in HHL is loss of IHC synapses, i.e., synaptopathy. For comparison, we simulated synaptopathy by removing high threshold IHC-SGN synapses and found that the amplitude of simulated sound-evoked SGN CAPs decreases while latencies remain unchanged, as has been observed in noise exposed animals. Thus, model results illuminate diverse disruptions caused by synaptopathy and demyelination on neural activity in auditory processing that contribute to HHL as observed in animal models and that can contribute to perceptual deficits induced by nerve damage in humans

Correction: Contrasting mechanisms for hidden hearing loss: Synaptopathy vs myelin defects.

[This corrects the article DOI: 10.1371/journal.pcbi.1008499.]