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Title: CSIscan: Learning CSI for Efficient Access Point Discovery in Dense WiFi Networks
Network densification through the deployment of WiFi access points (APs) is a promising solution towards achieving high connectivity rates required for emerging applications. A critical first step is to discover an AP before an active association between the client and the AP can be established. Legacy AP discovery procedures initiated by the client result in high latency in the order of a few 100 ms and waste spectrum, especially when clients need to frequently switch between multiple APs. We propose CSIscan that exploits the broadcast nature of WiFi channels by embedding discovery related information within an AP’s ongoing regular transmissions. The AP does this by intelligently distorting the transmitted OFDM frame by inducing perturbations in the preamble, and these injected ‘bits’ of information are detected via changes in the perceived channel state information (CSI). A deep learning framework allocates the optimal level of distortion on a per-subcarrier basis that keeps the resulting packet error rate to less than 1%. Existing clients perceive no changes in their ongoing communication, while potential new clients quickly obtain discovery information at the same time. We experimentally demonstrate that CSIscan reduces the overall WiFi latency from 150 ms to 10 ms and improves spectrum utilization with ∼ 72% reduction in the probe traffic. We show that CSIscan delivers up to 40 discovery information bits in the outgoing WiFi packet in an indoor environment.  more » « less
Award ID(s):
1923789
NSF-PAR ID:
10193347
Author(s) / Creator(s):
; ;
Date Published:
Journal Name:
IEEE International Conference on Network Protocols
Format(s):
Medium: X
Sponsoring Org:
National Science Foundation
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    Cardiac electrophysiology and Ca2+handling change rapidly during the fight‐or‐flight response to meet physiological demands.

    Despite dramatic differences in cardiac electrophysiology, the cardiac fight‐or‐flight response is highly conserved across species.

    In this study, we performed physiological sympathetic nerve stimulation (SNS) while optically mapping cardiac action potentials and intracellular Ca2+transients in innervated mouse and rabbit hearts.

    Despite similar heart rate and Ca2+handling responses between mouse and rabbit hearts, we found notable species differences in spatio‐temporal repolarization dynamics during SNS.

    Species‐specific computational models revealed that these electrophysiological differences allowed for enhanced Ca2+handling (i.e. enhanced inotropy) in each species, suggesting that electrophysiological responses are fine‐tuned across species to produce optimal cardiac fight‐or‐flight responses.

    Abstract

    Sympathetic activation of the heart results in positive chronotropy and inotropy, which together rapidly increase cardiac output. The precise mechanisms that produce the electrophysiological and Ca2+handling changes underlying chronotropic and inotropic responses have been studied in detail in isolated cardiac myocytes. However, few studies have examined the dynamic effects of physiological sympathetic nerve activation on cardiac action potentials (APs) and intracellular Ca2+transients (CaTs) in the intact heart. Here, we performed bilateral sympathetic nerve stimulation (SNS) in fully innervated, Langendorff‐perfused rabbit and mouse hearts. Dual optical mapping with voltage‐ and Ca2+‐sensitive dyes allowed for analysis of spatio‐temporal AP and CaT dynamics. The rabbit heart responded to SNS with a monotonic increase in heart rate (HR), monotonic decreases in AP and CaT duration (APD, CaTD), and a monotonic increase in CaT amplitude. The mouse heart had similar HR and CaT responses; however, a pronounced biphasic APD response occurred, with initial prolongation (50.9 ± 5.1 ms att = 0 svs. 60.6 ± 4.1 ms att = 15 s,P < 0.05) followed by shortening (46.5 ± 9.1 ms att = 60 s,P = NSvs. t = 0). We determined the biphasic APD response in mouse was partly due to dynamic changes in HR during SNS and was exacerbated by β‐adrenergic activation. Simulations with species‐specific cardiac models revealed that transient APD prolongation in mouse allowed for greater and more rapid CaT responses, suggesting more rapid increases in contractility; conversely, the rabbit heart requires APD shortening to produce optimal inotropic responses. Thus, while the cardiac fight‐or‐flight response is highly conserved between species, the underlying mechanisms orchestrating these effects differ significantly.

     
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