MIMO In Vivo

We present the performance of MIMO for in vivo environments, using ANSYS HFSS and their complete human body model, to determine the maximum data rates that can be achieved using an IEEE 802.11n system. Due to the lossy nature of the in vivo medium, achieving high data rates with reliable performance will be a challenge, especially since the in vivo antenna performance is strongly affected by near field coupling to the lossy medium and the signals levels will be limited by specified specific absorption rate (SAR) levels. We analyzed the bit error rate (BER) of a MIMO system with one pair of antennas placed in vivo and the second pair placed inside and outside the body at various distances from the in vivo antennas. The results were compared to SISO simulations and showed that by using MIMO in vivo, significant performance gain can be achieved, and at least two times the data rate can be supported with SAR limited transmit power levels, making it possible to achieve target data rates in the 100 Mbps.Comment: WAMICON 201

Microvillar and ciliary defects in zebrafish lacking an actin-binding bioactive peptide amidating enzyme

© The Author(s), 2018. This article is distributed under the terms of the Creative Commons Attribution License. The definitive version was published in Scientific Reports 8 (2018): 4547, doi:10.1038/s41598-018-22732-9.The assembly of membranous extensions such as microvilli and cilia in polarized cells is a tightly regulated, yet poorly understood, process. Peptidylglycine α-amidating monooxygenase (PAM), a membrane enzyme essential for the synthesis of amidated bioactive peptides, was recently identified in motile and non-motile (primary) cilia and has an essential role in ciliogenesis in Chlamydomonas, Schmidtea and mouse. In mammalian cells, changes in PAM levels alter secretion and organization of the actin cytoskeleton. Here we show that lack of Pam in zebrafish recapitulates the lethal edematous phenotype observed in Pam−/− mice and reveals additional defects. The pam−/− zebrafish embryos display an initial striking loss of microvilli and subsequently impaired ciliogenesis in the pronephros. In multiciliated mouse tracheal epithelial cells, vesicular PAM staining colocalizes with apical actin, below the microvilli. In PAM-deficient Chlamydomonas, the actin cytoskeleton is dramatically reorganized, and expression of an actin paralogue is upregulated. Biochemical assays reveal that the cytosolic PAM C-terminal domain interacts directly with filamentous actin but does not alter the rate of actin polymerization or disassembly. Our results point to a critical role for PAM in organizing the actin cytoskeleton during development, which could in turn impact both microvillus formation and ciliogenesis.This study was supported by grants DK032949 (to BAE and REM), DK044464 (to JDG) and GM051293 (to SMK) from the National Institutes of Health