An Overview on IEEE 802.11bf: WLAN Sensing

With recent advancements, the wireless local area network (WLAN) or wireless fidelity (Wi-Fi) technology has been successfully utilized to realize sensing functionalities such as detection, localization, and recognition. However, the WLANs standards are developed mainly for the purpose of communication, and thus may not be able to meet the stringent requirements for emerging sensing applications. To resolve this issue, a new Task Group (TG), namely IEEE 802.11bf, has been established by the IEEE 802.11 working group, with the objective of creating a new amendment to the WLAN standard to meet advanced sensing requirements while minimizing the effect on communications. This paper provides a comprehensive overview on the up-to-date efforts in the IEEE 802.11bf TG. First, we introduce the definition of the 802.11bf amendment and its formation and standardization timeline. Next, we discuss the WLAN sensing use cases with the corresponding key performance indicator (KPI) requirements. After reviewing previous WLAN sensing research based on communication-oriented WLAN standards, we identify their limitations and underscore the practical need for the new sensing-oriented amendment in 802.11bf. Furthermore, we discuss the WLAN sensing framework and procedure used for measurement acquisition, by considering both sensing at sub-7GHz and directional multi-gigabit (DMG) sensing at 60 GHz, respectively, and address their shared features, similarities, and differences. In addition, we present various candidate technical features for IEEE 802.11bf, including waveform/sequence design, feedback types, as well as quantization and compression techniques. We also describe the methodologies and the channel modeling used by the IEEE 802.11bf TG for evaluation. Finally, we discuss the challenges and future research directions to motivate more research endeavors towards this field in details.Comment: 31 pages, 25 figures, this is a significant updated version of arXiv:2207.0485

Cdx4 and Menin Co-Regulate Hoxa9 Expression in Hematopoietic Cells

BACKGROUND: Transcription factor Cdx4 and transcriptional coregulator menin are essential for Hoxa9 expression and normal hematopoiesis. However, the precise mechanism underlying Hoxa9 regulation is not clear. METHODS AND FINDINGS: Here, we show that the expression level of Hoxa9 is correlated with the location of increased trimethylated histone 3 lysine 4 (H3K4M3). The active and repressive histone modifications co-exist along the Hoxa9 regulatory region. We further demonstrate that both Cdx4 and menin bind to the same regulatory region at the Hoxa9 locus in vivo, and co-activate the reporter gene driven by the Hoxa9 cis-elements that contain Cdx4 binding sites. Ablation of menin abrogates Cdx4 access to the chromatin target and significantly reduces both active and repressive histone H3 modifications in the Hoxa9 locus. CONCLUSION: These results suggest a functional link among Cdx4, menin and histone modifications in Hoxa9 regulation in hematopoietic cells

A Fault-Line Selection Method for Small-Current Grounded System Based on Deep Transfer Learning

Usually, data-driven methods require many samples and need to train a specific model for each substation instance. As different substation instances have similar fault features, the number of samples required for model training can be significantly reduced if these features are transferred to the substation instances that lack samples. This paper proposes a fault-line selection (FLS) method based on deep transfer learning for small-current grounded systems to solve the problems of unstable training and low FLS accuracy of data-driven methods in small-sample cases. For this purpose, fine-turning and historical averaging techniques are proposed for use in transfer learning to extract similar fault features from other substation instances and transfer these features to target substation instances that lack samples to improve the accuracy and stability of the model. The results show that the proposed method obtains a much higher FLS accuracy than other methods in small-sample cases; it has a strong generalization ability, low misclassification rate, and excellent application value

Deletion of the Men1 Gene Prevents Streptozotocin-Induced Hyperglycemia in Mice

Diabetes ultimately results from an inadequate number of functional beta cells in the islets of Langerhans. Enhancing proliferation of functional endogenous beta cells to treat diabetes remains underexplored. Here, we report that excision of the Men1 gene, whose loss-of-function mutation leads to inherited multiple endocrine neoplasia type 1 (MEN1), rendered resistant to streptozotocin-induced hyperglycemia in a tamoxifen-inducible and temporally controlled Men1 excision mouse model as well as in a tissue-specific Men1 excision mouse model. Men1 excision prevented mice from streptozotocin-induced hyperglycemia mainly through increasing the number of functional beta cells. BrdU incorporation by beta cells, islet size, and circulating insulin levels were significantly increased in Men1-excised mice. Membrane localization of glucose transporter 2 was largely preserved in Men1-excised beta cells, but not in Men1-expressing beta cells. Our findings suggest that repression of menin, a protein encoded by the Men1 gene, might be a valuable means to maintain or increase the number of functional endogenous beta cells to prevent or ameliorate diabetes

Harnessing the Hidden Antitumor Power of the MLL-AF4 Oncogene to Fight Leukemia

It is unclear whether the antiproliferative/proapoptotic activity of oncogenes can be pharmacologically reactivated in cancer cells. In this issue of Cancer Cell, Liu and colleagues report that a proteasome inhibitor reactivates an MLL-AF4 controlled antitumor program to kill leukemia cells in an oncogene dose- and cell type-dependent manner

Critical Role of Smad and AP-1 Complexes in TGF-β-Dependent Apoptosis

Transforming growth factor-β1 (TGF-β1) induces not only cell growth inhibition but also apoptosis in hepatocytes, myeloid cells, and epithelial cells. Smad complexes (Smad2-Smad4 and Smad3-Smad4) are identified as key signaling molecules which transmit TGF-β1 signal for growth inhibition from the TGF-β receptors to the nucleus (1, 2). However, their roles are unclear in the induction of apoptosis. Our results show here that both Smad and AP-1 complexes play a critical role in TGF-β1 signaling for apoptosis.National Institutes of Health (U.S.) (Grant CA63260

Squamosamide Derivative FLZ Protects Pancreatic β-Cells from Glucotoxicity by Stimulating Akt-FOXO1 Pathway

Chronic hyperglycemia increases apoptosis and reduces glucose-stimulated insulin secretion. Although protective agents have been searched extensively, none has been found so far. Here we tested FLZ, a synthetic derivative of squamosamide from a Chinese herb, as a potential candidate for antiglucotoxicity in INS-1E cells and mouse islets. Chronic culture of β-cells in 30 mM glucose caused progressive reduction of cell viability, accompanied with increased apoptosis and reduced insulin secretion. These effects on apoptosis and insulin were reversed by FLZ in a dose-dependent manner. FLZ treatment also increased forkhead box O1 protein phosphorylation and reduced its nuclear location. On the contrary, FLZ increased pancreatic and duodenal homeobox-1 expression and its nuclear localization, an effect mediated by increased p-Akt. Consistently, Akt selective inhibitor MK-2206 completely abolished antiglucotoxicity effect of FLZ. Furthermore, FLZ treatment increased cytosolic ATP/ADP ratio. Taken together, our results suggest that FLZ could be a potential therapeutic agent to treat the hyperglycemia-induced β-cell failure