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BtPDR: Bluetooth and PDR-Based Indoor Fusion Localization Using Smartphones
( Yingbiao Yao ),( Qiaojing Bao ),( Qi Han ),( Ruili Yao ),( Xiaorong Xu ),( Junrong Yan ) 한국인터넷정보학회 2018 KSII Transactions on Internet and Information Syst Vol.12 No.8
This paper presents a Bluetooth and pedestrian dead reckoning (PDR)-based indoor fusion localization approach (BtPDR) using smartphones. A Bluetooth and PDR-based indoor fusion localization approach can localize the initial position of a smartphone with the received signal strength (RSS) of Bluetooth. While a smartphone is moving, BtPDR can track its position by fusing the localization results of PDR and Bluetooth RSS. In addition, BtPDR can adaptively modify the parameters of PDR. The contributions of BtPDR include: a Bluetooth RSS-based Probabilistic Voting (BRPV) localization mechanism, a probabilistic voting-based Bluetooth RSS and PDR fusion method, and a heuristic search approach for reducing the complexity of BRPV. The experiment results in a real scene show that the average positioning error is < 2m, which is considered adequate for indoor location-based service applications. Moreover, compared to the traditional PDR method, BtPDR improves the location accuracy by 42.6%, on average. Compared to state-of-the-art Wireless Local Area Network (WLAN) fingerprint + PDR-based fusion indoor localization approaches, BtPDR has better positioning accuracy and does not need the same offline workload as a fingerprint algorithm.
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TRIM24-Mediated Acetylation of STAT6 Suppresses Th2-Induced Allergic Rhinitis
Yue Liyan,Jia Qiaojing,Dong Jinhui,Wang Jianxing,Ren Xiumin,Xu Ou 대한천식알레르기학회 2023 Allergy, Asthma & Immunology Research Vol.15 No.5
Purpose: Allergic rhinitis (AR) is a T helper type 2 (Th2)-mediated inflammatory disease. The E3 ligase tripartite motif-containing 24 (TRIM24) regulates the recruitment of acetyltransferase CREB-binding protein (CBP) to signal transducer and activator of transcription 6 (STAT6). CBP mediates the acetylation of STAT6 and decreases its activity. To date, the precise role of TRIM24 in AR has not been fully interpreted. Herein, our study aimed to explore the functions of TRIM24 in AR. Methods: The expression of TRIM24 in peripheral blood mononuclear cells (PBMCs) and CD4+ T cells from patients with AR was measured. TRIM24-conditional knockout mice with TRIM24 deficiency in CD4+ T cells were generated. Wide-type (WT) AR mice and TRIM24-conditional knockout AR mice were established. Then, AR symptoms and interleukin (IL)-4 levels were compared. Further, the proliferation, activation and polarization of CD4+ T cells from WT mice and TRIM24 knockout mice after stimulation were determined. The effects of TRIM24 deficiency on STAT6 activities were also evaluated. Results: Downregulated TRIM24 expression was detected in PBMCs and CD4+ T cells from patients with AR. TRIM24 conditional knockout mice had more sever AR symptoms with elevated IL-4 production. TRIM24-knockout CD4+ T cells had similar proliferation and activation when compared to WT CD4+ T cells, while they had enhanced Th2 polarization. TRIM24-knockout CD4+ T cells had decreased acetylation of STAT6 and enhanced STAT6 activities after IL-4 stimulation. The regulation of STAT6 activities by TRIM24 depended on TRIM24 N terminal RIGN domain and Lys383 acetylation site of STAT6. Conclusions: TRIM24 suppresses Th2-mediated AR by regulating the acetylation of STAT6.
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