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In this paper, randomly-directional beamforming (RDB) is considered for millimeter-wave (mmwave) multi-user (MU) multiple-input single-output (MISO) downlink systems. By using asymptotic techniques, the performance of RDB and the MU gain in mm-wave MISO are analyzed based on the uniform random line-of-sight (UR-LoS) channel model suitable for highly directional mm-wave radio propagation channels. It is shown that there exists a transition point on the number of users relative to the number of antenna elements for non-trivial performance of the RDB scheme, and furthermore sum rate scaling arbitrarily close to linear scaling with respect to the number of antenna elements can be achieved under the UR-LoS channel model by opportunistic random beamforming with proper user scheduling if the number of users increases linearly with respect to the number of antenna elements.The provided results yield insights into the most effective beamforming and scheduling choices for mm-wave MU-MISO in various operating conditions. Simulation results validate our analysis based on asymptotic techniques for finite cases. Index TermsMillimeter-Wave, Multi-User MIMO, Massive MIMO, Opportunistic Random Beamforming, RandomlyDirectional Beamforming † Corresponding authorThe authors are with

The Hippo signaling pathway controls nuclear accumulation and stability of the transcriptional coregulator YAP and its paralog TAZ. The activity of Hippo-YAP signaling is influenced not only by biochemical signals, but also by cell shape and mechanical tension transmitted through cell-cell junctions and cell-matrix adhesions. Data accumulated thus far indicates that the actin cytoskeleton is a key mediator of the regulation of Hippo-YAP signaling by means of a variety of biochemical and mechanical cues. In this review, we have outlined the role of actin dynamics and actin-associated proteins in the regulation of Hippo-YAP signaling. In addition, we discuss actin-mediated regulation of YAP/TAZ activity independent of the core Hippo kinases MST and LATS. Although our understanding of the link between Hippo-YAP signaling and the actin cytoskeleton is progressing rapidly, many open questions remain.

Recent studies have provided evidence that Zn 21 plays a crucial role in ischemia-and seizure-induced neuronal death. However, the intracellular signaling pathways involved in Zn 21-induced cell death are largely unknown. In the present study, we investigated the roles of mitogen-activated protein kinases (MAPKs), such as c-Jun N-terminal kinase (JNK), p38 MAPK and extracellular signal-regulated kinase (ERK), and of reactive oxygen species (ROS)