37 research outputs found

    Embedded Based Miniaturized Universal Electrochemical Sensing Platform

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    We created an embedded sensing platform based on STM32 embedded system, with integrated carbon-electrode ionic sensor by using a self-made plug. Given ration of concentration-unknown nitrate liquid samples, this platform is able to measure the nitrate concentration in neutral environment. Response signals which were transmitted by the sensor can be displayed via a serial port to the computer screen or via Bluetooth to the smartphone. Processed by a fitting function, signals are transformed into related concentration. Through repeating the experiment many times, the accuracy and repeatability turned out to be excellent. The results can be automatically stored on smartphone via Bluetooth. We created this embedded sensing platform for field water quality measurement. This platform also can be applied for other micro sensors’ signal acquisition and data processing

    Compressive-Sensing-Enhanced First-Principles Calculation of Photoluminescence Spectra in Color Centers: A Comparison between Theory and Experiment for the G Center in Silicon

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    Photoluminescence (PL) spectra are a versatile tool for exploring the electronic and optical properties of quantum defect systems. In this work, we investigate the PL spectra of the G center in silicon by combining first-principles computations with a machine-learned compressive-sensing technique and experiment. We show that the compressive-sensing technique provides a speed up of approximately 20 times compared with the finite-displacement method with similar numerical accuracy. We compare theory and experiment and show good agreement for the historically proposed configuration B of the G center. In particular, we attribute the experimentally observed E-line of the G center to a local vibration mode mainly involving two substitutional C atoms and one interstitial Si atom. Our theoretical results also well reproduce and explain the experimental E-line energy shifts originating from the carbon isotopic effect. In addition, our results demonstrate that some highly anharmonic modes that are apparent in computed spectra could be absent experimentally because of their short lifetime. Our work not only provides a deeper understanding of the G-center defect but also paves the way to accelerate the calculation of PL spectra for color centers

    DUSP4 inhibits autophagic cell death in PTC by inhibiting JNK-BCL2-Beclin1 signaling

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    DUSP4 is a prognostic marker and potential target of papillary thyroid carcinoma (PTC). However, the molecular mechanism underlying DUSP4-regulated PTC carcinogenesis is unclear. DUSP4 is a negative regulator of the autophagy promoter, JNK. This study aimed to explore the relationship between DUSP4 and JNK-mediated autophagic cell death in PTC. In this study, we explored the roles of DUSP4 in PTC using gain-of-function and loss-of-function assays. In addition, we further identified the significance of JNK-BCL2-Beclin1-autophagy signaling on DUSP4-regulated PTC carcinogenesis by combining DUSP4 silencing with JNK specific inhibitor (SP600125). We found that DUSP4 silencing promoted the phosphorylation of JNK and BCL2 in PTC cells and enhanced the release of Beclin1 from BCL2-Beclin1 complex. DUSP4 silencing promoted autophagy and death in PTC cells.The death and autophagy enhanced by DUSP4 silencing was reversed by JNK inhibitor. We further extended the in vitro experiments by injecting K1 cells transduced with DUSP4-silencing vector subcutaneously into nude mice. In vivo assays showed that DUSP4 silencing not only inhibited tumor growth, but also promoted JNK and BCL2 phosphorylation and LC3II expression.Overall, DUSP4 inhibits BCL2-Beclin1- autophagy signaling through negatively regulating JNK activity, thus inhibiting PTC oncogenesis.This study provides more potential clues for the prevention and cure of PTC.The accepted manuscript in pdf format is listed with the files at the bottom of this page. The presentation of the authors' names and (or) special characters in the title of the manuscript may differ slightly between what is listed on this page and what is listed in the pdf file of the accepted manuscript; that in the pdf file of the accepted manuscript is what was submitted by the author

    DUSP4 inhibits autophagic cell death in PTC by inhibiting JNK–BCL2–Beclin1 signaling

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    Dual specificity phosphatase 4 (DUSP4) is a prognostic marker and potential target of papillary thyroid carcinoma (PTC); however, the molecular mechanism underlying DUSP4-regulated PTC carcinogenesis is unknown. DUSP4 is a negative regulator of the autophagy promoter, JNK. This study explored the relationship between DUSP4 and JNK-mediated autophagic cell death in PTC, and the roles of DUSP4 in PTC using gain-of-function and loss-of-function assays. In addition, we further identified the significance of the JNK–BCL2–Beclin1–autophagy signaling pathway on DUSP4-regulated PTC carcinogenesis by combining knockdown of DUSP4 with a JNK-specific inhibitor (SP600125). We found that knockdown of DUSP4 promoted the phosphorylation of JNK and BCL2 in PTC cells, and enhanced the release of Beclin1 from the BCL2–Beclin1 complex. Knockdown of DUSP4 promoted autophagy and the death of PTC cells. The death and autophagy enhanced by knockdown of DUSP4 was reversed by the JNK inhibitor. We further extended the in-vitro experiments by subcutaneously injecting nude mice with K1 cells transfected with DUSP4-silencing vector. In-vivo assays showed that knockdown of DUSP4 not only inhibited tumor growth, but also promoted the phosphorylation of JNK and BCL2 and the expression of LC3II. In conclusion, DUSP4 inhibits BCL2–Beclin1–autophagy signaling by negatively regulating JNK activity, thus inhibiting PTC oncogenesis. The data from this study contribute to the prevention and cure of PTC. </jats:p

    mRNA Transcriptome Analysis of Bone in a Mouse Model of Implant-Associated Staphylococcus aureus Osteomyelitis

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    To investigate the molecular pathogenesis of bone with osteomyelitis, we developed implant-associated osteomyelitis (IAOM) models in mice. An orthopedic stainless pin was surgically placed in the right femoral midshaft of mice, followed by an inoculation of Staphylococcus aureus into the medullary cavity. </jats:p

    A versatile strategy for uniform hybrid nanoparticles and nanocapsules

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    A novel and versatile strategy for uniform organo-silica hybrid nanoparticles and nanocapsules was developed. The key to our strategy is the implementation of spherical star-like homopolymers and diblock copolymers with well-controlled molecular weights that form unimolecular micelles in solution as nanoreactors.</p
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