Integration on acceleration signals by adjusting with envelopes

Direct integration of acceleration often causes unrealistic drifts in velocity and displacement. A method of integration on acceleration data to acquire realistic velocity and displacement is proposed. In this approach, drifts are estimated by using the mean of the upper and lower envelopes of signals after integration from acceleration into velocity and displacement. The experimental results obtained by using simulated data and real world signals are presented to demonstrate the effectiveness of the method

Application of Cross-Linked Polyborosiloxanes and Organically Modified Boron Silicate Binders in Silicon-Containing Anodes for Lithium-Ion Batteries

To determine the effect of cross-linking in polymer binders on gravimetric capacity and retention in charge/discharge cycling of lithium-ion batteries containing silicon anodes, polymers with a varied chemiophysical characters have been studied as electrode binders. Here we report the utilization of cross-linked polyborosiloxanes and a boron-modified organosilicate as binders for nanoparticulate silicon-containing anodes for lithium-ion batteries. We show that highly cross-linked binders enable a large degree of capacity to be accessed and that capacity retention is greater when the electrodes are cycled in half cells. More extensive analysis of the boron-modified organosilicate is further explored

The audio auditor: user-level membership inference in Internet of Things voice services

With the rapid development of deep learning techniques, the popularity of voice services implemented on various Internet of Things (IoT) devices is ever increasing. In this paper, we examine user-level membership inference in the problem space of voice services, by designing an audio auditor to verify whether a specific user had unwillingly contributed audio used to train an automatic speech recognition (ASR) model under strict black-box access. With user representation of the input audio data and their corresponding translated text, our trained auditor is effective in user-level audit. We also observe that the auditor trained on specific data can be generalized well regardless of the ASR model architecture. We validate the auditor on ASR models trained with LSTM, RNNs, and GRU algorithms on two state-of-the-art pipelines, the hybrid ASR system and the end-to-end ASR system. Finally, we conduct a real-world trial of our auditor on iPhone Siri, achieving an overall accuracy exceeding 80%. We hope the methodology developed in this paper and findings can inform privacy advocates to overhaul IoT privacy

Mesenchymal stromal cells-exosomes: a promising cell-free therapeutic tool for wound healing and cutaneous regeneration

Cutaneous regeneration at the wound site involves several intricate and dynamic processes which require a series of coordinated interactions implicating various cell types, growth factors, extracellular matrix (ECM), nerves, and blood vessels. Mesenchymal stromal cells (MSCs) take part in all the skin wound healing stages playing active and beneficial roles in animal models and humans. Exosomes, which are among the key products MSCs release, mimic the effects of parental MSCs. They can shuttle various effector proteins, messenger RNA (mRNA) and microRNAs (miRNAs) to modulate the activity of recipient cells, playing important roles in wound healing. Moreover, using exosomes avoids many risks associated with cell transplantation. Therefore, as a novel type of cell-free therapy, MSC-exosome -mediated administration may be safer and more efficient than whole cell. In this review, we provide a comprehensive understanding of the latest studies and observations on the role of MSC-exosome therapy in wound healing and cutaneous regeneration. In addition, we address the hypothesis of MSCs microenvironment extracellular vesicles (MSCs-MEVs) or MSCs microenvironment exosomes (MSCs-MExos) that need to take stock of and solved urgently in the related research about MSC-exosomes therapeutic applications. This review can inspire investigators to explore new research directions of MSC-exosome therapy in cutaneous repair and regeneration

School bullying among migrant children in China: A cross-sectional study

BackgroundBullying is a serious public health concern affecting the physical and mental health of children. Migrant children are at higher risk of developing health problems. We conducted this study to investigate the prevalence of school bullying and its possible influencing factors of migrant children.MethodsA cross-sectional study was carried out in Hunan Province, China from April to July 2018. Multi-stage cluster sampling was adopted to achieve a representative sample covering both urban and rural areas. Migrant children are defined as those who migrate with one or both parents to other places and who do not have a hukou in their city of residence. The Chinese version of Olweus Bully/Victim Questionnaire was applied to measure children’s involvement in school bullying.ResultsA total of 7,607 students were surveyed, including 995 migrant children and 6,612 non-migrant children. The prevalence of school bullying was significantly higher in migrant children than in non-migrant children (χ2 = 22.740; p < 0.001). Binary regression analysis showed that male, middle school identity, more times of playing violent games, more social friends owning and being beaten by parents or caregivers may increase the risk of involvement of school bullying in migrant children.ConclusionMigrant children showed a higher prevalence of school bullying than non-migrant children. Gender, grade, frequency of playing violent games, number of social friends and being beaten by parents or caregivers were associated with school bullying in migrant children

Efficient FPGA implementation of high-throughput mixed radix multipath delay commutator FFT processor for MIMO-OFDM

This article presents and evaluates pipelined architecture designs for an improved high-frequency Fast Fourier Transform (FFT) processor implemented on Field Programmable Gate Arrays (FPGA) for Multiple Input Multiple Output Orthogonal Frequency Division Multiplexing (MIMO-OFDM). The architecture presented is a Mixed-Radix Multipath Delay Commutator. The presented parallel architecture utilizes fewer hardware resources compared to Radix-2 architecture, while maintaining simple control and butterfly structures inherent to Radix-2 implementations. The high-frequency design presented allows enhancing system throughput without requiring additional parallel data paths common in other current approaches, the presented design can process two and four independent data streams in parallel and is suitable for scaling to any power of two FFT size N. FPGA implementation of the architecture demonstrated significant resource efficiency and high-throughput in comparison to relevant current approaches within literature. The proposed architecture designs were realized with Xilinx System Generator (XSG) and evaluated on both Virtex-5 and Virtex-7 FPGA devices. Post place and route results demonstrated maximum frequency values over 400 MHz and 470 MHz for Virtex-5 and Virtex-7 FPGA devices respectively

Maslinic acid potentiates the anti-tumor activity of tumor necrosis factor α by inhibiting NF-κB signaling pathway

<p>Abstract</p> <p>Background</p> <p>Tumor necrosis factor alpha (TNFα) has been used to treat certain tumors in clinic trials. However, the curative effect of TNFα has been undermined by the induced-NF-κB activation in many types of tumor. Maslinic acid (MA), a pharmacological safe natural product, has been known for its important effects as anti-oxidant, anti-inflammatory, and anti-viral activities. The aim of this study was to determine whether MA potentiates the anti-tumor activity of TNFα though the regulation of NF-κB activation.</p> <p>Results</p> <p>In this study, we demonstrate that MA significantly enhanced TNFα-induced inhibition of pancreatic cancer cell proliferation, invasion, and potentiated TNFα-induced cell apoptosis by suppressing TNFα-induced NF-κB activation in a dose- and time-dependent manner. Addition of MA inhibited TNFα-induced IκBα degradation, p65 phosphorylation, and nuclear translocation. Furthermore, MA decreased the expression levels of NF-κB-regulated genes, including genes involved in tumor cell proliferation (Cyclin D1, COX-2 and c-Myc), apoptosis (Survivin, Bcl-2, Bcl-xl, XIAP, IAP-1), invasion (MMP-9 and ICAM-1), and angiogenesis (VEGF). In athymic nu/nu mouse model, we further demonstrated that MA significantly suppressed pancreatic tumor growth, induced tumor apoptosis, and inhibited NF-κB-regulated anti-apoptotic gene expression, such as Survivin and Bcl-xl.</p> <p>Conclusions</p> <p>Our data demonstrate that MA can potentiate the anti-tumor activities of TNFα and inhibit pancreatic tumor growth and invasion by activating caspase-dependent apoptotic pathway and by suppressing NF-κB activation and its downstream gene expression. Therefore, MA together with TNFα could be new promising agents in the treatment of pancreatic cancer.</p

Nonresonant valence-to-core x-ray emission spectroscopy of niobium

The valence-to-core (V2C) portion of x-ray emission spectroscopy (XES) measures the electron states close to the Fermi level. These states are involved in bonding, thus providing a measure of the chemistry of the material. In this article, we show the V2C XES spectra for several niobium compounds. The K β ′′ peak in the V2C XES results from the transition of a ligand 2 s electron into the 1 s core-hole of the niobium, a transition allowed by hybridization with the niobium 4 p . This location in energy of this weak peak shows a strong ligand dependence, thus providing a sensitive probe of the ligand environment about the niobium

Effects of Melanocortin 3 and 4 Receptor Deficiency on Energy Homeostasis in Rats

Melanocortin-3 and 4 receptors (MC3R and MC4R) can regulate energy homeostasis, but their respective roles especially the functions of MC3R need more exploration. Here Mc3r and Mc4r single and double knockout (DKO) rats were generated using CRISPR-Cas9 system. Metabolic phenotypes were examined and data were compared systematically. Mc3r KO rats displayed hypophagia and decreased body weight, while Mc4r KO and DKO exhibited hyperphagia and increased body weight. All three mutants showed increased white adipose tissue mass and adipocyte size. Interestingly, although Mc3r KO did not show a significant elevation in lipids as seen in Mc4r KO, DKO displayed even higher lipid levels than Mc4r KO. DKO also showed more severe glucose intolerance and hyperglycaemia than Mc4r KO. These data demonstrated MC3R deficiency caused a reduction of food intake and body weight, whereas at the same time exhibited additive effects on top of MC4R deficiency on lipid and glucose metabolism. This is the first phenotypic analysis and systematic comparison of Mc3r KO, Mc4r KO and DKO rats on a homogenous genetic background. These mutant rats will be important in defining the complicated signalling pathways of MC3R and MC4R. Both Mc4r KO and DKO are good models for obesity and diabetes research

Metformin represses bladder cancer progression by inhibiting stem cell repopulation via COX2/PGE2/STAT3 axis

Cancer stem cells (CSCs) are a sub-population of tumor cells playing essential roles in initiation, differentiation, recurrence, metastasis and development of drug resistance of various cancers, including bladder cancer. Although multiple lines of evidence suggest that metformin is capable of repressing CSC repopulation in different cancers, the effect of metformin on bladder cancer CSCs remains largely unknown. Using the N-methyl-N-nitrosourea (MNU)-induced rat orthotropic bladder cancer model, we demonstrated that metformin is capable of repressing bladder cancer progression from both mild to moderate/severe dysplasia lesions and from carcinoma in situ (CIS) to invasive lesions. Metformin also can arrest bladder cancer cells in G1/S phases, which subsequently leads to apoptosis. And also metformin represses bladder cancer CSC repopulation evidenced by reducing cytokeratin 14 (CK14+) and octamer-binding transcription factor 3/4 (OCT3/4+) cells in both animal and cellular models. More importantly, we found that metformin exerts these anticancer effects by inhibiting COX2, subsequently PGE2 as well as the activation of STAT3. In conclusion, we are the first to systemically demonstrate in both animal and cell models that metformin inhibits bladder cancer progression by inhibiting stem cell repopulation through the COX2/PGE2/STAT3 axis