131 research outputs found
Design of fl uid pipeline leakage signal acquisition system
Fluid, namely liquid and gas, is a necessary resource in national production and life, so fl uid plays a pivotal role in the
progress of the whole society and the development of human civilization. If the fl uid leaks, and is not found and treated in time, it will cause
huge material losses and waste of resources, what is more, it will cause irreversible environmental damage. This paper takes fl uid pipeline
leakage detection as the main research object, the main research is as follows: According to the steady-state pipeline as the main analysis
goal, C8051F040 single chip microcomputer as the main processor, DS18B20 temperature sensor, CEMPX221 pressure sensor, LWGY-C
model turbine fl owmeter for data acquisition, and the collected data through the CAN interface, RS485 interface to the host computer
Waveform-Domain Adaptive Matched Filtering: A Novel Approach to Suppressing Interrupted-Sampling Repeater Jamming
The inadequate adaptability to flexible interference scenarios remains an
unresolved challenge in the majority of techniques utilized for mitigating
interrupted-sampling repeater jamming (ISRJ). Matched filtering system based
methods is desirable to incorporate anti-ISRJ measures based on prior ISRJ
modeling, either preceding or succeeding the matched filtering. Due to the
partial matching nature of ISRJ, its characteristics are revealed during the
process of matched filtering. Therefore, this paper introduces an extended
domain called the waveform domain within the matched filtering process. On this
domain, a novel matched filtering model, known as the waveform-domain adaptive
matched filtering (WD-AMF), is established to tackle the problem of ISRJ
suppression without relying on a pre-existing ISRJ model. The output of the
WD-AMF encompasses an adaptive filtering term and a compensation term. The
adaptive filtering term encompasses the adaptive integration outcomes in the
waveform domain, which are determined by an adaptive weighted function. This
function, akin to a collection of bandpass filters, decomposes the integrated
function into multiple components, some of which contain interference while
others do not. The compensation term adheres to an integrated guideline for
discerning the presence of signal components or noise within the integrated
function. The integration results are then concatenated to reconstruct a
compensated matched filter signal output. Simulations are conducted to showcase
the exceptional capability of the proposed method in suppressing ISRJ in
diverse interference scenarios, even in the absence of a pre-existing ISRJ
model
Ionic liquid-assisted synthesis of Yb3+-Tm3+ codoped Y7O6F9 petal shaped microcrystals with enhanced upconversion emission
Petal-like Yb3+-Tm3+ codoped Y7O6F9 microparticles were achieved via ionic liquid-assisted (IL) hydrothermal process. The emission efficiency of Y7O6F9:Yb3+/Tm3+ powders is much stronger than that of Y2O3:Yb3+/Tm3+ sample. Under excitation at 980 nm with an unfocused laser beam under weak pump density of ∼0.1 W/cm2 (pump power 10 mW), the UC emission of the sample can been seen clearly. Four emission bands at 477, 540, 647 and 692 nm are observed and correspond to the 1G4 state to 3H6 state, 1D2 state to 3H5 state, 1G4 sate to 3F4 state, and 3F3 state to 3H6 state transition of Tm3+ ions. The enhanced UC emission is related to high crystallinity and lower effective phonon energy of oxyfluorides. The ionic liquid (IL) of [BMIM][BF4] is used both as the reaction medium and the source of F−
Wogonin induces cell cycle arrest and erythroid differentiation in imatinib-resistant K562 cells and primary CML cells
Wogonin, a flavonoid derived from Scutellaria baicalensis Georgi, has been demonstrated to be highly effective in treating hematologic malignancies. In this study, we investigated the anticancer effects of wogonin on K562 cells, K562 imatinib-resistant cells, and primary patient-derived CML cells. Wogonin up-regulated transcription factor GATA-1 and enhanced binding between GATA-1 and FOG-1, thereby increasing expression of erythroid-differentiation genes. Wogonin also up-regulated the expression of p21 and induced cell cycle arrest. Studies employing benzidine staining and analyses of cell surface markers glycophorin A (GPA) and CD71 indicated that wogonin promoted differentiation of K562, imatinib-resistant K562, and primary patient-derived CML cells. Wogonin also enhanced binding between GATA-1 and MEK, resulting in inhibition of the growth of CML cells. Additionally, in vivo studies showed that wogonin decreased the number of CML cells and prolonged survival of NOD/SCID mice injected with K562 and imatinib-resistant K562 cells. These data suggested that wogonin induces cycle arrest and erythroid differentiation in vitro and inhibits proliferation in vivo
Surface modification of NiCo2Te4 nanoclusters: a highly efficient electrocatalyst for overall water-splitting in neutral solution
In this paper, we for the first time report the catalytic activity and durability of nickel cobaltite telluride (NiCo2Te4) nanocluster bifunctional catalysts can be significantly boosted by surface modification with perylene-tetracarboxylic-dianhydride for overall water-splitting in neutral solution. We reveal that tuning energy distribution of nanoclusters via a simple surface ligand can drastically increase the catalytic activity towards efficient hydrogen and oxygen evolution reaction simultaneously. A two-electrode based water electrolysis cell using this newly developed nanocluster catalyst operates at a low bias voltage of 1.55 V to achieve a current density of 10 mA·cm-2 in near-neutral pH solution for overall water-splitting. This, to the best of our knowledge, represents the most efficient mixed-transition-metal-based electrode that has so far been reported for electrochemical water splitting
Electric Vehicle Revolution and Implications: Ion Battery and Energy
As record high heat waves sweep globally, global warming (caused by environmental pollution and greenhouse gas emissions) has turned into the primary concern, which put the non-renewable petrochemical energy and fuel vehicles on the chopping block. The development of new energy electric vehicles (EVs) leading by USA, EU and China has the potential to achieve zero-emissions. The innovation technologies of the corresponding rechargeable ion battery play the keys role. Thus, the EVs have profound impact on traditional energy, vehicles industries and the daily life
Oroxylin a Inhibits the Protection of Bone Marrow Microenvironment on CML Cells Through CXCL12/CXCR4/P-gp Signaling Pathway
Imatinib (IM) resistance could have significant impact on the survival time of the CML-patients treated with IM. Previous studies have shown that the protective effects of the bone marrow stroma cells (BMSCs) on CML cells are achieved by the secretion of CXCL12. The aim of this study was to investigate whether Oroxylin A could reverse the protective effect of BMSCs on CML cells and illuminate the underlying mechanisms. The results showed that CXCL12 could enhance the resistance potential of K562 and KU812 cells to IM by increasing the expression of CXCR4, thus promoting the translocation of β-catenin into nucleus and subsequently increasing the expression of P-gp in K562 and KU812 cells. What's more, IM resistance could also be partially reversed by CXCR4 siRNA transfection. Moreover, the reverse effect of IM resistance by Oroxylin A was demonstrated by the inhibition of β-catenin/P-gp pathway via the decrease of CXCR4 in vitro. The in vivo study also showed that Oroxylin A could decrease the expression of P-gp and β-catenin in mice bone marrow with low toxicity, which could be consistent with the mechanisms verified in vitro studies. In conclusion, all these results showed that Oroxylin A improved the sensitivity of K562 and KU812 cells to IM in BM microenvironment by decreasing the expression of CXCR4 and then inhibiting β-catenin/P-gp pathway
ESX Secretion-Associated Protein C From Mycobacterium tuberculosis Induces Macrophage Activation Through the Toll-Like Receptor-4/Mitogen-Activated Protein Kinase Signaling Pathway
Mycobacterium tuberculosis, as a facultative intracellular pathogen, can interact with host macrophages and modulate macrophage function to influence innate and adaptive immunity. Proteins secreted by the ESX-1 secretion system are involved in this relationship. Although the importance of ESX-1 in host-pathogen interactions and virulence is well-known, the primary role is ascribed to EsxA (EAST-6) in mycobacterial pathogenesis and the functions of individual components in the interactions between pathogens and macrophages are still unclear. Here, we investigated the effects of EspC on macrophage activation. The EspC protein is encoded by an espA/C/D cluster, which is not linked to the esx-1 locus, but is essential for the secretion of the major virulence factors of ESX-1, EsxA and EsxB. Our results showed that both EspC protein and EspC overexpression in M. smegmatis induced pro-inflammatory cytokines and enhanced surface marker expression. This mechanism was dependent on Toll-like receptor 4 (TLR4), as demonstrated using EspC-treated macrophages from TLR4−/− mice, leading to decreased pro-inflammatory cytokine secretion and surface marker expression compared with those from wild-type mice. Immunoprecipitation and immunofluorescence assays showed that EspC interacted with TLR4 directly. Moreover, EspC could activate macrophages and promote antigen presentation by inducing mitogen-activated protein kinase (MAPK) phosphorylation and nuclear factor-κB activation. The EspC-induced cytokine expression, surface marker upregulation, and MAPK signaling activation were inhibited when macrophages were blocked with anti-TLR4 antibodies or pretreated with MAPK inhibitors. Furthermore, our results showed that EspC overexpression enhanced the survival of M. smegmatis within macrophages and under stress conditions. Taken together, our results indicated that EspC may be another ESX-1 virulence factor that not only modulates the host innate immune response by activating macrophages through TLR4-dependent MAPK signaling but also plays an important role in the survival of pathogenic mycobacteria in host cells
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