Faculty Bibliography

Propagation measurements at 28 GHz were conducted in outdoor urban environments in New York City using four different transmitter locations and 83 receiver locations with distances of up to 500 m. A 400 mega-chip per second channel sounder with steerable 24.5 dBi horn antennas at the transmitter and receiver was used to measure the angular distributions of received multipath power over a wide range of propagation distances and urban settings. Measurements were also made to study the small-scale fading of closely-spaced power delay profiles recorded at half-wavelength (5.35 mm) increments along a small-scale linear track (10 wavelengths, or 107 mm) at two different receiver locations. Our measurements indicate that power levels for small-scale fading do not significantly fluctuate from the mean power level at a fixed angle of arrival. We propose here a new lobe modeling technique that can be used to create a statistical channel model for lobe path loss and shadow fading, and we provide many model statistics as a function of transmitter-receiver separation distance. Our work shows that New York City is a multipath-rich environment when using highly directional steerable horn antennas, and that an average of 2.5 signal lobes exists at any receiver location, where each lobe has an average total angle spread of 40.3 degrees and an RMS angle spread of 7.8 degrees. This work aims to create a 28 GHz statistical spatial channel model for future 5G cellular networks.

Inhibitory synapse dysfunction may contribute to many developmental brain disorders, including the secondary consequences of sensory deprivation. In fact, developmental hearing loss leads to a profound reduction in the strength of inhibitory postsynaptic currents (IPSCs) in the auditory cortex, and this deficit persists into adulthood. This finding is consistent with the general theory that the emergence of mature synaptic properties requires activity during development. Therefore, we tested the prediction that inhibitory strength can be restored following developmental hearing loss by boosting GABAergic transmission in vivo. Conductive or sensorineural hearing loss was induced surgically in gerbils prior to hearing onset and GABA agonists were then administered for one week. IPSCs were subsequently recorded from pyramidal neurons in a thalamocortical brain slice preparation. Administration of either a GABA(A) receptor a1 subunit specific agonist (zolpidem), or a selective GABA reuptake inhibitor (SGRI), rescued IPSC amplitude in hearing loss animals. Furthermore, this restoration persisted in adults, long after drug treatment ended. In contrast, a GABA(B) receptor agonist baclofen did not restore inhibitory strength. IPSCs could also be restored when SGRI administration began 3 weeks after sensory deprivation. Together, these results demonstrate long-lasting restoration of cortical inhibitory strength in the absence of normal experience. This suggests that in vivo GABA(A) receptor activation is sufficient to promote maturation, and this principle may extend to other developmental disorders associated with diminished inhibitory function.

While the plasticity of excitatory synaptic connections in the brain has been widely studied, the plasticity of inhibitory connections is much less understood. Here, we present recent experimental and theoretical findings concerning the rules of spike timing-dependent inhibitory plasticity and their putative network function. This is a summary of a workshop at the COSYNE conference 2012.

Allergic fungal sinusitis (AFS), also referred to as allergic fungal rhinosinusitis (AFRS), is a noninvasive, eosinophilic form of recurrent chronic allergic hypertrophic rhinosinusitis. AFS has distinct clinical, histopathological, and prognostic findings that differentiate it from other forms of sinusitis. The core pathogenesis and optimum treatment strategies remain debated. Concerns surround the use of immunotherapy for AFS because allergen-specific immunoglobulin G (IgG) induced by immunotherapy could theoretically incite a Gell and Coombs type III (complex mediated) reaction. Type I hypersensitivity is established by high serum levels of allergen-specific IgE to various fungal antigens and positive Bipolaris skin test results. Type III hypersensitivity is established by an IgG-mediated process defined by the presence of allergen-specific IgG that forms complexes with fungal antigen inducing an immunologic inflammatory response. These reveal the multiple immunologic pathways through which AFS can impact host responses. Recent literature establishing benefits of fungal immunotherapy and no evidence of type III-mediated reactions, severe local reactions, or delayed reactions, indicate that application of AFS desensitization is a reasonable therapeutic strategy for this difficult to manage entity. Our review should encourage further clinical acceptance of AFS desensitization because the existing literature on this subject shows benefits of fungal immunotherapy and no evidence of type III-mediated reactions, severe local reactions, or delayed reactions.

BACKGROUND: Previous studies suggest that semicircular canal dehiscences (SCDs) have a developmental origin. OBJECTIVE: We hypothesized that if SCDs originate during development, incidence of radiographic SCDs in young children will be higher than in adults. MATERIALS AND METHODS: Thirty-four temporal bone HRCTs of children younger than 2 years and 40 temporal bone HRCTs of patients older than 18 years were reformatted and re-evaluated for presence of SCD or canal thinning. Results were compared with indications for HRCT and clinical information. RESULTS: SCDs were detected in 27.3% of children younger than 2 years of age (superior, 13.8%; posterior, 20%) and in 3% of adults (P < 0.004). Of children with one radiographic dehiscence, 55.6% had multiple and 44% had bilateral SCDs on HRCT. No lateral canal SCDs were present. Thinning of bone overlying the semicircular canals was found in 44% of children younger than 2 years and 2.5% of adults (P < 0.0001). CONCLUSION: SCDs are more common on HRCTs of very young children. This supports the hypothesis that SCDs originate from discontinuation of bone deposition/maturation. However, SCDs on imaging do not necessarily correlate with canal dehiscence syndrome and should therefore be interpreted carefully.