33 research outputs found

    Crocs: Cross-Technology Clock Synchronization for WiFi and ZigBee

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    Clock synchronization is a key function in embedded wireless systems and networks. This issue is equally important and more challenging in IoT systems nowadays, which often include heterogeneous wireless devices that follow different wireless standards. Conventional solutions to this problem employ gateway-based indirect synchronization, which suffers low accuracy. This paper for the first time studies the problem of cross-technology clock synchronization. Our proposal called Crocs synchronizes WiFi and ZigBee devices by direct cross-technology communication. Crocs decouples the synchronization signal from the transmission of a timestamp. By incorporating a barker-code based beacon for time alignment and cross-technology transmission of timestamps, Crocs achieves robust and accurate synchronization among WiFi and ZigBee devices, with the synchronization error lower than 1 millisecond. We further make attempts to implement different cross-technology communication methods in Crocs and provide insight findings with regard to the achievable accuracy and expected overhead

    Transcriptional suppression of breast cancer resistance protein (BCRP) by wild-type p53 through the NF-魏B pathway in MCF-7 cells

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    AbstractBreast cancer resistance protein (BCRP) has been shown to confer multidrug resistance, but the mechanisms of its regulation are poorly understood. Here, we investigate the effects of wild-type and mutant p53, and nuclear factor kappa-B (NF-魏B) (p50) on BCRP promoter activity in MCF-7 cells. Our results demonstrated that wild-type p53 markedly suppressed BCRP activity and enhanced the chemosensitivity of cells to mitoxantrone, whereas mutant p53 had little inhibitory effect. After inhibition of NF-魏B, similar results were obtained. Following knockdown of endogenous p53, BCRP and p50 expressions were increased, and the chemosensitivity of the cells to mitoxantrone was decreased. We conclude that wild-type p53 acts as a negative regulator of BCRP gene transcription

    Quasi-4-dimension ionospheric modeling and its application in PPP

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    The version of record of this article, first published in Satellite Navigation, is available online at Publisher鈥檚 website: http://dx.doi.org/10.1186/s43020-022-00085-zIonospheric delay modeling is not only important for GNSS based space weather study and monitoring, but also an efficient tool to overcome the long convergence time of PPP. In this study, a novel model, denoted as Q4DIM (Quasi-4-dimension ionospheric modeling) is proposed for wide-area high precision ionospheric delay correction. In Q4DIM, the LOS (line of sight) ionospheric delay from a GNSS station network is divided into different clusters according to not only latitude and longitude, but also elevation and azimuth. Both GIM (global ionosphere map) and SID (slant ionospheric delay) that traditionally used for wide-area and regional ionospheric delay modeling, respectively, can be regarded as special case of Q4DIM by defining proper grids in latitude, longitude, elevation and azimuth. Thus, Q4DIM presents a resilient model that is capable for both wide-area coverage and high precision. Then four different sets of clusters are defined to illustrate the properties of Q4DIM based on 200 EPN stations. The results suggested that Q4DIM is compatible with the widely acknowledged GIM products. Moreover, it is proved that by inducting the elevation and azimuth angle dependent residuals, the precision of the 2-dimensional GIM-like model, i.e., Q4DIM-2D, is improved from around 1.5 TECU to better than 0.5 TECU. In addition, by treating Q4DIM as a 4-dimensional matrix in latitude, longitude, elevation and azimuth, its sparsity is less than 5%, thus guarantees its feasibility in a bandwidth-sensitive applications, e.g., satellite-based PPP-RTK service. Finally, the advantage of Q4DIM in single frequency PPP over the 2-dimensional models is demonstrated with one month鈥檚 data from 30 EPN stations.Peer ReviewedPostprint (published version

    Development of o-aminobenzamide salt derivatives for improving water solubility and anti-undifferentiated gastric cancer

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    Background: Gastric cancer is one of the cancers with wide incidence, difficult treatment and high mortality in the world, especially in Asia and Africa. In our previous work, a novel o-aminobenzamide analogue F8 was identified as an early preclinical candidate for treatment of undifferentiated gastric cancer (IC50 of 0.26聽渭M for HGC-27). However, the poor water solubility of compound F8 prevents its further progress in preclinical studies.Aim: To improve the water solubility and drug-likeness of F8 via salt formation.Method: Different acids and F8 were reacted to obtain different salt forms. Physicochemical property screening, pharmacokinetic property research, and antitumor biological activity evaluation in vitro and in vivo were used to obtain the optimal salt form with the best druggability.Results: our continuous efforts have finally confirmed F8路2HCl as the optimal salt form with maintained in vitro antitumor activity, improved water solubility and pharmacokinetic properties. Importantly, the F8路2HCl displayed superior in vivo antitumor efficacy (TGI of 70.1% in 75聽mg/kg) in HGC-27 xenograft model. The further immunohistochemical analysis revealed that F8路2HCl exerts an antitumor effect through the regulation of cell cycle-related protein (CDK2 and p21), apoptosis-related protein Cleaved Caspase-3, proliferation marker Ki67, and cell adhesion molecule E-cadherin. In addition, F8路2HCl showed acceptable safety in the in vivo acute toxicity assay.Conclusion: Salting is an effective means to improve the drug-like properties of compound F8, and F8路2HCl can serve as a promising therapeutic agent against undifferentiated gastric cancer

    OmniTrack: Orientation-aware RFID Tracking with Centimeter-level Accuracy

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    Anthocyanins from the Red Juvenile Leaves of Loropetalum Chinense聽var.聽rubrum (Chinese Fringe Flower) Identification and pH Sensing Behaviors

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    In this study, anthocyanins were extracted from the frozen juvenile leaves of Loropetalum Chinense var. rubrum with high efficiency using ethanol containing 0.1% HCl as extractant. After being purified with AB-8 resin, this extract was investigated with HPLC-DAD-MS/MS determination, and six anthocyanins were identified according to chromatogram, MS data and ratios of absorbance at 400-460 nm to that at absorption maximum (~520 nm), A400-460/A520. Besides cyanidin 3-O-glucoside, peonidin 3-O-glucoside, malvidin 3-O-glucoside, the most abundant malvidin 3,5-O-diglucoside was confirmed through preparative HPLC separation and 1 H NMR determination. However, two delphinidin- and petunidin-derived anthocyanins should be further clarified whether they are 3,5-O-diglucoside or 5-O-glucobioside. In addition, a novel anthocyanin, 2H-pyran[5,6]malvidin 3-O-glucobioside was also proposed yet need more data to confirm. Moreover, malvidin 3,5-O-diglucoside showed excellent pH sensing ability, displaying distinct color change from pink (pH 1.5) to colorlessness (pH 5.5), to blue (pH 6.8) and finally green (pH 8.8 to pH 10.5). All these should be helpful to evaluate this plant as natural pigment resource. </p

    MicroRNA-493 suppresses tumor growth, invasion and metastasis of lung cancer by regulating E2F1.

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    miRNAs have been proposed to be key regulators of progression and metastasis in cancer. However, an understanding of their roles and molecular mechanisms is needed to provide deeper insights for better therapeutic opportunities. In this study we investigated the role and mechanism of miR-493 in the development and progression of nonsmall-cell lung cancer (NSCLC). Our data indicated that the expression of miR-493 was markedly reduced in pulmonary carcinoma. The ectopic expression of miR-493 impaired cell growth and invasion in vitro and in vivo. Mechanically, miR-493 commonly directly targeted E2F1, which resulted in a robust reduction of the expression of mRNA and protein. This effect, in turn, decreased the growth, invasion and metastasis of lung cancer cells. Our findings highlight the importance of miR-493 dysfunction in promoting tumor progression, and implicate miR-493 as a potential therapeutic target in lung cancer
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