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In order to improve the reliability of selective leakage protection of power network in mine, a hardware circuit using pulse broadening to realize selective leakage protection of zero-sequence current direction was proposed. Its test on 660 V test device and waveform on TEK DPO2014 oscilloscope proved that the proposed circuit is correct and reliable. Leakage protection devices with the proposed circuit have been successfully applied in coal mines.

An environmentally benign electrochemical approach has been developed for the α-hydroxymethylation of ketones using N,N-dimethylformamide as the carbon source for the construction of β-hydroxy ketones. This method does not require metal catalysts or chemical oxidants and proceeded smoothly at room temperature to demonstrate tolerance of a broad range of functional groups. [ABSTRACT FROM AUTHOR]

Steel fiber reinforced concrete (SFRC) is widely applied in the construction industry. Numerical elastoplastic analysis of the macroscopic behavior is complex. This typically involves a piecewise linear failure curve including corner singularities. This paper presents a single smooth biaxial failure curve for SFRC based on a semianalytical approximation. Convexity of the proposed model is guaranteed so that numerical problems are avoided. The model has sufficient flexibility to closely match experimental results. The failure curve is also suitable for modeling plain concrete under biaxial loading. Since this model is capable of simulating the failure states in all stress regimes with a single envelope, the elastoplastic formulation is very concise and simple. The finite element implementation is developed to demonstrate the conciseness and the effectiveness of the model. The computed results display good agreement with published experimental data. CE Database subject headings: Fiber reinforced materials; Concrete; Steel; Failure modes; Elastoplasticity; Construction materials.

In this study, two new coordination polymers (CPs),{[(CH3)2NH2][Zn(FDA)(TZ)2]}n (1, H2FDA = furan-2,5-dicarboxyl acid, TZ = 1,2,3-triazole) and {[Ni2(H2O)3(HTTCA)]·H2O}n (2, H4TTCA = [1,1':2',1''-terphenyl]-3,3'',4',5'-tetracarboxylic acid), have been prepared under solvothermal conditions and characterized by single-crystal X-ray diffraction analyses successfully. Furthermore, the protective effect of the compounds in vitro and in vivo was evaluated. Firstly, the bacterial growth curves were measured after treatment with the compounds. Besides, the inflammatory cytokines in the blood was detected with enzyme linked immunosorbent assay (ELISA) detection kit. Two new coordination polymers (CPs) have been prepared under solvothermal conditions and characterized by single-crystal X-ray diffraction analyses successfully. Furthermore, the protective effect of the compounds in vitro and in vivo was evaluated. Firstly, the bacterial growth curves were measured after treatment with the compounds. Besides, the inflammatory cytokines in the blood was detected with enzyme linked immunosorbent assay (ELISA) detection kit. [ABSTRACT FROM AUTHOR]

Two-dimensional (2D) transition metal dichalcogenides (TMDCs) such as tungsten diselenide (WSe2) have spead many interesting physical properties, which may become ideal candidates to develop new generation electronic and optoelectronic devices. In order to reveal essential features of 2D TMDCs, it is necessary to fabricate high-quality devices with reliable electrical contact. We systematically analyze the effect of graphene and metal contacts on performance of multi-layered WSe2 field effect transistors (FETs). The temperature-dependent transport characteristics of both devices are tested. Only graphene-contacted WSe2 FETs are observed with the metal-insulator transition phenomenon which mainly attributes to the ultra-clean contact interface and lowered contact barrier. Further characterization on contact barrier demonstrates that graphene contact enables lower contact barrier with WSe2 than metal contact, since the Fermi level of graphene can be modulated by the gate bias to match the Fermi level of the channel material. We also analyze the carrier mobility of both devices under different temperatures, revealing that graphene contact can reduce the charge scattering of the device caused by ionized impurities and phonon vibrations in low and room temperature regions, respectively. This work is expected to provide reference for fabricating 2D material devices with decent performances. [ABSTRACT FROM AUTHOR]

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A painful return to developmental NMDAR activity: Neuronal sensitivity is mediated, in part, by NMDA receptor (NMDAR) signaling, and increased abundance of GluN2B-containing NMDARs in sensory neuronal synapses is associated with enhanced nociception and pain. Using rodents, Zhang et al. found that GluN2B content in the sensory neurons of the spine is progressively restricted during early development and maintained at low abundance by the E3 ubiquitin ligase Cbl-b during adulthood. However, peripheral inflammation induced the dephosphorylation of Cbl-b and impaired its interaction with GluN2B, and the increase in GluN2B abundance enhanced NMDAR activity and neuronal sensitivity to touch. Identifying a way to target this mechanism might be therapeutic in patients suffering from inflammatory peripheral neuropathy. N-methyl-d-aspartate (NMDA) glutamate receptors (NMDARs) containing GluN2B subunits are prevalent early after birth in most brain regions in rodents. Upon synapse maturation, GluN2B is progressively removed from synapses, which affects NMDAR function and synaptic plasticity. Aberrant recruitment of GluN2B into mature synapses has been implicated in several neuropathologies that afflict adults. We found that the E3 ubiquitin ligase Cbl-b was enriched in the spinal cord dorsal horn neurons of mice and rats and suppressed GluN2B abundance during development and inflammatory pain. Cbl-b abundance increased from postnatal day 1 (P1) to P14, a critical time period for synapse maturation. Through its N-terminal tyrosine kinase binding domain, Cbl-b interacted with GluN2B. Ubiquitination of GluN2B by Cbl-b decreased the synaptic transmission mediated by GluN2B-containing NMDARs. Knocking down Cbl-b in vivo during P1 to P14 led to sustained retention of GluN2B at dorsal horn synapses, suggesting that Cbl-b limits the synaptic abundance of GluN2B in adult mice. However, peripheral inflammation induced by intraplantar injection of complete Freund's adjuvant resulted in the dephosphorylation of Cbl-b at Tyr363, which impaired its binding to and ubiquitylation of GluN2B, enabling the reappearance of GluN2B-containing NMDARs at synapses. Expression of a phosphomimic Cbl-b mutant in the dorsal horn suppressed both GluN2B-mediated synaptic currents and manifestations of pain induced by inflammation. The findings indicate a ubiquitin-mediated developmental switch in NMDAR subunit composition that is dysregulated by inflammation, which can enhance nociception. [ABSTRACT FROM AUTHOR]

Inhibitory glycinergic transmission in adult spinal cord is primarily mediated by glycine receptors (GlyRs) containing the α1 subunit. Here, we found that α1ins, a longer α1 variant with 8 amino acids inserted into the intracellular large loop (IL) between transmembrane (TM)3 and TM4 domains, was expressed in the dorsal horn of the spinal cord, distributed at inhibitory synapses, and engaged in negative control over nociceptive signal transduction. Activation of metabotropic glutamate receptor 5 (mGluR5) specifically suppressed α1ins-mediated glycinergic transmission and evoked pain sensitization. Extracellular signal-regulated kinase (ERK) was critical for mGluR5 to inhibit α1ins. By binding to a D-docking site created by the 8-amino–acid insert within the TM3–TM4 loop of α1ins, the active ERK catalyzed α1ins phosphorylation at Ser380, which favored α1ins ubiquitination at Lys379 and led to α1ins endocytosis. Disruption of ERK interaction with α1ins blocked Ser380 phosphorylation, potentiated glycinergic synaptic currents, and alleviated inflammatory and neuropathic pain. These data thus unraveled a novel, to our knowledge, mechanism for the activity-dependent regulation of glycinergic neurotransmission. [ABSTRACT FROM AUTHOR]