Bluetooth Low Energy Interference Awareness Scheme and Improved Channel Selection Algorithm for Connection Robustness

Bluetooth Low Energy (BLE) is a popular wireless communication protocol heavily used in Internet of Things applications. Nowadays, robustness is considered a key requirement in wireless communication. However, radio interference from various sources may affect the performance of BLE devices, leading to channel congestion. Therefore, there is a broadly recognized need of methodologies capable of sensing and avoiding interference. In this paper, two improvements at the data link layer for interference detection and channel selection are proposed to enhance the BLE connection robustness. This paper also presents a wide range of experimental evaluations aiming at validating the improvements and providing insights on both these improvements. Particularly, the communication performance of the BLE link layer is assessed in terms of channel usage distribution, supervision timeout ratio (STR) and packet loss rate (PLR) under different interference environments. Results from these experiments (reliability over 97% and 99% under two different harsh environments) highlight the effects of both improvements on the BLE robustness. Meanwhile, the authority of scheduling the whole mechanism is given to the link layer and even the higher application layer. This paper provides a set of solutions for BLE confronting interference in link layer

The transcription factor EGR2 is indispensable for tissue-specific imprinting of alveolar macrophages in health and tissue repair

Alveolar macrophages are the most abundant macrophages in the healthy lung where they play key roles in homeostasis and immune surveillance against air-borne pathogens. Tissue-specific differentiation and survival of alveolar macrophages relies on niche-derived factors, such as granulocyte-macrophage colony stimulating factor 2 (GM-CSF) and transforming growth factor beta (TGF-β). However, the nature of the downstream molecular pathways that regulate the identity and function of alveolar macrophages and their response to injury remains poorly understood. Here, we identify that the transcription factor EGR2 is an evolutionarily conserved feature of lung alveolar macrophages and show that cell-intrinsic EGR2 is indispensable for the tissue-specific identity of alveolar macrophages. Mechanistically, we show that EGR2 is driven by TGF-β and GM-CSF in a PPAR-γ-dependent manner to control alveolar macrophage differentiation. Functionally, EGR2 was dispensable for regulation of lipids in the airways, but crucial for the effective handling of the respiratory pathogen Streptococcus pneumoniae. Finally, we show that EGR2 is required for repopulation of the alveolar niche following sterile, bleomycin-induced lung injury and demonstrate that EGR2-dependent, monocyte-derived alveolar macrophages are vital for effective tissue repair following injury. Collectively, we demonstrate that EGR2 is an indispensable component of the transcriptional network controlling the identity and function of alveolar macrophages in health and disease