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Cell Reports ◽  
2021 ◽  
Vol 36 (5) ◽  
pp. 109483 ◽  
Author(s):  
Perry W.E. Spratt ◽  
Ryan P.D. Alexander ◽  
Roy Ben-Shalom ◽  
Atehsa Sahagun ◽  
Henry Kyoung ◽  
...  

Author(s):  
Thomas Chambon ◽  
Eric Heitz ◽  
Laurent Belcour
Keyword(s):  

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
R. I. Woodward ◽  
Y. S. Lo ◽  
M. Pittaluga ◽  
M. Minder ◽  
T. K. Paraïso ◽  
...  

AbstractMeasurement-device-independent quantum key distribution (MDI-QKD) is a technique for quantum-secured communication that eliminates all detector side-channels, although is currently limited by implementation complexity and low secure key rates. Here, we introduce a simple and compact MDI-QKD system design at gigahertz clock rates with enhanced resilience to laser fluctuations—thus enabling free-running semiconductor laser sources to be employed without spectral or phase feedback. This is achieved using direct laser modulation, carefully exploiting gain-switching and injection-locking laser dynamics to encode phase-modulated time-bin bits. Our design enables secure key rates that improve upon the state of the art by an order of magnitude, up to 8 bps at 54 dB channel loss and 2 kbps in the finite-size regime for 30 dB channel loss. This greatly simplified MDI-QKD system design and proof-of-principle demonstration shows that MDI-QKD is a practical, high-performance solution for future quantum communication networks.


2021 ◽  
Author(s):  
Perry W.E. Spratt ◽  
Roy Ben-Shalom ◽  
Atehsa Sahagun ◽  
Caroline M. Keeshen ◽  
Stephan J. Sanders ◽  
...  

Loss-of-function variants in the gene SCN2A, which encodes the sodium channel NaV1.2, are strongly associated with autism spectrum disorder and intellectual disability. An estimated 20-30% of children with these variants are co-morbid for epilepsy, with altered neuronal activity originating in neocortex, a region where NaV1.2 channels are expressed predominantly in excitatory pyramidal cells. This is paradoxical, as sodium channel loss in excitatory cells would be expected to dampen neocortical activity rather than promote seizure. Here, we examined pyramidal neurons lacking NaV1.2 channels and found that they were intrinsically hyperexcitable, firing high-frequency bursts of action potentials (APs) despite decrements in AP size and speed. Compartmental modeling and dynamic clamp recordings revealed that NaV1.2 loss prevented potassium channels from properly repolarizing neurons between APs, increasing overall excitability by allowing neurons to reach threshold for subsequent APs more rapidly. This cell-intrinsic mechanism may therefore account for why SCN2A loss-of-function can paradoxically promote seizure.


Author(s):  
Gunjan Mandal ◽  
Sunil Rajan ◽  
Sanjeeb Kumar Ghosh ◽  
Saikat Hazra ◽  
Raghavendra Molthati ◽  
...  
Keyword(s):  

2020 ◽  
Author(s):  
Arunashish Datta ◽  
Mayukh Nath ◽  
David Yang ◽  
Shreyas Sen

AbstractHuman Body Communication (HBC) has come up as a promising alternative to traditional radio frequency (RF) Wireless Body Area Network (WBAN) technologies. This is essentially due to HBC providing a broadband communication channel with enhanced signal security in the physical layer due to lower radiation from the human body as compared to its RF counterparts. An in-depth understanding of the mechanism for the channel loss variability and associated biophysical model needs to be developed before EQS-HBC can be used more frequently in WBAN consumer and medical applications. Biophysical models characterizing the human body as a communication channel didn’t exist in literature for a long time. Recent developments have shown models that capture the channel response for fixed transmitter and receiver positions on the human body. These biophysical models do not capture the variability in the HBC channel for varying positions of the devices with respect to the human body. In this study, we provide a detailed analysis of the change in path loss in a capacitive-HBC channel in the electroquasistatic (EQS) domain. Causes of channel loss variability namely: inter-device coupling and effects of fringe fields due to body’s shadowing effects are investigated. FEM based simulation results are used to analyze the channel response of human body for different positions and sizes of the device which are further verified using measurement results to validate the developed biophysical model. Using the bio-physical model, we develop a closed form equation for the path loss in a capacitive HBC channel which is then analyzed as a function of the geometric properties of the device and the position with respect to the human body which will help pave the path towards future EQS-HBC WBAN design.


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