Using Coding to Improve Localization and Backscatter Communication Performance in Low-Power Sensor Networks

Backscatter communication is an emerging wireless technology that recently has gained an increase in attention from both academic and industry circles. The key innovation of the technology is the ability of ultra-low power devices to utilize nearby existing radio signals to communicate. As there is no need to generate their own energetic radio signal, the devices can benefit from a simple design, are very inexpensive and are extremely energy efficient compared with traditional wireless communication. These benefits have made backscatter communication a desirable candidate for distributed wireless sensor network applications with energy constraints.

The backscatter channel presents a unique set of challenges. Unlike a conventional one-way communication (in which the information source is also the energy source), the backscatter channel experiences strong self-interference and spread Doppler clutter that mask the information-bearing (modulated) signal scattered from the device. Both of these sources of interference arise from the scattering of the transmitted signal off of objects, both stationary and moving, in the environment. Additionally, the measurement of the location of the backscatter device is negatively affected by both the clutter and the modulation of the signal return.

This work proposes a channel coding framework for the backscatter channel consisting of a bi-static transmitter/receiver pair and a quasi-cooperative transponder. It proposes to use run-length limited coding to mitigate the background self-interference and spread-Doppler clutter with only a small decrease in communication rate. The proposed method applies to both binary phase-shift keying (BPSK) and quadrature-amplitude modulation (QAM) scheme and provides an increase in rate by up to a factor of two compared with previous methods.

Additionally, this work analyzes the use of frequency modulation and bi-phase waveform coding for the transmitted (interrogating) waveform for high precision range estimation of the transponder location. Compared to previous methods, optimal lower range sidelobes are achieved. Moreover, since both the transmitted (interrogating) waveform coding and transponder communication coding result in instantaneous phase modulation of the signal, cross-interference between localization and communication tasks exists. Phase discriminating algorithm is proposed to make it possible to separate the waveform coding from the communication coding, upon reception, and achieve localization with increased signal energy by up to 3 dB compared with previous reported results.

The joint communication-localization framework also enables a low-complexity receiver design because the same radio is used both for localization and communication.

Simulations comparing the performance of different codes corroborate the theoretical results and offer possible trade-off between information rate and clutter mitigation as well as a trade-off between choice of waveform-channel coding pairs. Experimental results from a brass-board microwave system in an indoor environment are also presented and discussed.

Temporomandibular joint pain: a critical role for Trpv4 in the trigeminal ganglion.

Temporomandibular joint disorder (TMJD) is known for its mastication-associated pain. TMJD is medically relevant because of its prevalence, severity, chronicity, the therapy-refractoriness of its pain, and its largely elusive pathogenesis. Against this background, we sought to investigate the pathogenetic contributions of the calcium-permeable TRPV4 ion channel, robustly expressed in the trigeminal ganglion sensory neurons, to TMJ inflammation and pain behavior. We demonstrate here that TRPV4 is critical for TMJ-inflammation-evoked pain behavior in mice and that trigeminal ganglion pronociceptive changes are TRPV4-dependent. As a quantitative metric, bite force was recorded as evidence of masticatory sensitization, in keeping with human translational studies. In Trpv4(-/-) mice with TMJ inflammation, attenuation of bite force was significantly less than in wildtype (WT) mice. Similar effects were seen with systemic application of a specific TRPV4 inhibitor. TMJ inflammation and mandibular bony changes were apparent after injections of complete Freund adjuvant but were remarkably independent of the Trpv4 genotype. It was intriguing that, as a result of TMJ inflammation, WT mice exhibited significant upregulation of TRPV4 and phosphorylated extracellular-signal-regulated kinase (ERK) in TMJ-innervating trigeminal sensory neurons, which were absent in Trpv4(-/-) mice. Mice with genetically-impaired MEK/ERK phosphorylation in neurons showed resistance to reduction of bite force similar to that of Trpv4(-/-) mice. Thus, TRPV4 is necessary for masticatory sensitization in TMJ inflammation and probably functions upstream of MEK/ERK phosphorylation in trigeminal ganglion sensory neurons in vivo. TRPV4 therefore represents a novel pronociceptive target in TMJ inflammation and should be considered a target of interest in human TMJD.