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The traditional RFID reader module relies on a discrete original design. This design integrates a microcontroller, high-frequency RFID reader IC and other multiple chips onto a PCB board, leading to bottlenecks in cost, power consumption, stability and reliability. To align with the trend towards high integration, miniaturization and low power consumption in RFID reader, this paper introduces a fully integrated RFID Reader SoC. The SoC employs the open-source Cortex-M0 core to integrate the RF transceiver, analog circuits, baseband protocol processing, memory and interface circuits into one chip. It's compatible with ISO/IEC 14443 A-type and B-type and ISO/IEC 15693 transmission protocols and rates. Manufactured using a 0.18 μ m process, the chip is compatible with multiple standards. The optimized design of the digital baseband control circuit results in a chip area of only 11.95 mm 2 offering clear advantages in both area and integration compared to similar work. [ABSTRACT FROM AUTHOR]

For 3d1 (V4+) impurity in 30PbO‐5Bi2O3‐(65‐x)SiO2 glass systems with different concentrations x of V2O5, the defect structures and gyromagnetic factors are theoretically investigated by using the perturbation formulas of g factors for a tetragonally compressed octahedral 3d1 group. The concentration dependences of d‐d transition band and g factors are suitably explained from the Fourier type concentration functions of the cubic crystal field parameter Dq, covalency factor N and relative tetragonal compression ratio ρ. The above concentration dependences of these quantities are suitably illustrated by the modifications of the local crystal field strength and electron cloud distribution with increasing x. The concentration variations of the electrical conductivity and dielectric relaxation are further analyzed from the stability of the systems in view of two competitive factors (increasing network polymerization and bulk stability at low concentrations and decreasing former SiO2 and stability at high concentrations). [ABSTRACT FROM AUTHOR]

Background: Inflammatory reactions induced by spinal cord injury (SCI) are essential for recovery after SCI. Atractylenolide III (ATL‐III) is a natural monomeric herbal bioactive compound that is mainly derived in Atractylodes macrocephala Koidz and has anti‐inflammatory and neuroprotective effects. Objective: Here, we speculated that ATL‐III may ameliorate SCI by modulating microglial/macrophage polarization. In the present research, we focused on investigating the role of ATL‐III on SCI in rats and explored the potential mechanism. Methods: The protective and anti‐inflammatory effects of ATL‐III on neuronal cells were examined in a rat SCI model and lipopolysaccharide (LPS)‐stimulated BV2 microglial line. The spinal cord lesion area, myelin integrity, and surviving neurons were assessed by specific staining. Locomotor function was evaluated by the Basso, Beattie, and Bresnahan (BBB) scale, grid walk test, and footprint test. The activation and polarization of microglia/macrophages were assessed by immunohistofluorescence and flow cytometry. The expression of corresponding inflammatory factors from M1/M2 and the activation of relevant signaling pathways were assessed by Western blotting. Results: ATL‐III effectively improved histological and functional recovery in SCI rats. Furthermore, ATL‐III promoted the transformation of M1 into M2 and attenuated the activation of microglia/macrophages, further suppressing the expression of corresponding inflammatory mediators. This effect may be partly mediated by inhibition of neuroinflammation through the NF‐κB, JNK MAPK, p38 MAPK, and Akt pathways. Conclusion: This study reveals a novel effect of ATL‐III in the regulation of microglial/macrophage polarization and provides initial evidence that ATL‐III has potential therapeutic benefits in SCI rats. [ABSTRACT FROM AUTHOR]

Abstract Background Transplantation of oligodendrocyte precursor cells (OPCs) is an attractive therapy for demyelinating diseases. Cyclosporin A (CsA) is one of the foremost immunosuppressive agents and has widespread use in tissue and cell transplantation. However, whether CsA affects survival and differentiation of engrafted OPCs in vivo is unknown. In this study, the effect of CsA on morphological, functional and immunological aspects, as well as survival and differentiation of engrafted OPCs in injured spinal cord was explored. Results We transplanted green fluorescent protein (GFP) expressed OPCs (GFP-OPCs) into injured spinal cords of rats treated with or without CsA (10 mg/kg). Two weeks after cell transplantation, more GFP-positive cells were found in CsA-treated rats than that in vehicle-treated ones. However, the engrafted cells mostly differentiated into astrocytes, but not oligodendrocytes in both groups. In the CsA-treated group, a significant decrease in spinal cord lesion volume along with increase in spared myelin and neurons were found compared to the control group. Such histological improvement correlated well with an increase in behavioral recovery. Further study suggested that CsA treatment could inhibit infiltration of T cells and activation of resident microglia and/or macrophages derived from infiltrating monocytes in injured spinal cords, which contributes to the survival of engrafted OPCs and repair of spinal cord injury (SCI). Conclusions These results collectively indicate that CsA can promote the survival of engrafted OPCs in injured spinal cords, but has no effect on their differentiation. The engrafted cells mostly differentiated into astrocytes, but not oligodendrocytes. The beneficial effect of CsA on SCI and the survival of engrafted cells may be attributed to its neuroprotective effect.

An electrochemical oxidative cross-coupling reaction between 2.5-substituted-pyrazolin-5-ones and ammonium thiocyanate has been developed, which resulted in a series of unprecedented cross-coupling products under metal catalyst-, exogenous-oxidant-, and exogenous-electrolyte-free conditions. It is worth noting that since the resulting cross-coupling products are nearly insoluble in MeCN, the pure product could be afforded without silica gel column purification. In addition, the prepared ammonium oxides are versatile building blocks for synthesizing functionalized pyrazole derivatives. [ABSTRACT FROM AUTHOR]

Previous studies have shown that caspase-1 plays an important role in the acute inflammatory response of spinal cord injury (SCI). VX-765, a novel and irreversible caspase-1 inhibitor, has been reported to effectively intervene in inflammation. However, the effect of VX-765 on genome-wide transcription in acutely injured spinal cords remains unknown. Therefore, in the present study, RNA-sequencing (RNA-Seq) was used to analyze the effect of VX-765 on the local expression of gene transcription 8 h following injury. The differentially expressed genes (DEGs) underwent enrichment analysis of functions and pathways by Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analyses, respectively. Parallel analysis of western blot confirmed that VX-765 can effectively inhibit the expression and activation of caspase-1. RNA-Seq showed that VX-765 treatment resulted in 1,137 upregulated and 1,762 downregulated DEGs. These downregulated DEGs and their associated signaling pathways, such as focal adhesion, cytokine-cytokine receptor interaction, leukocyte transendothelial migration, extracellular matrix-receptor interaction, phosphatidylinositol 3-kinase-protein kinase B, Rap1 and hypoxia inducible factor-1 signaling pathway, are mainly associated with inflammatory response, local hypoxia, macrophage differentiation, adhesion migration and apoptosis of local cells. This suggests that the application of VX-765 in the acute phase can improve the local microenvironment of SCI by inhibiting caspase-1. However, whether VX-765 can be used as a therapeutic drug for SCI requires further exploration. The sequence data have been deposited into the Sequence Read Archive (https://www.ncbi.nlm.nih.gov/sra/PRJNA548970). [ABSTRACT FROM AUTHOR]

This paper presents a fully integrated high-frequency (HF) radio-frequency identification (RFID) tag chip based on the ISO/IEC 15693 and discusses a series of design techniques, including analog and digital control circuits. In order to get a more coupled power supply, an amplitude shift keying demodulator with very low modulation index is proposed. Moreover, modulator, limiter, and electrostatic discharge circuit are mentioned to make the tag IC work effectively and reliably. Besides, digital control circuit with 2-kbit EEPROM memory is designed to help the tag operate correctly under a very low magnetic field. The proposed RFID tag IC was fabricated using a 0.18-μm 2P6M CMOS technology with an area of 926 μm by 855 μm and a power consumption of less than 120 μA. Data rates of 6.62–52.97 kb/s are supported. The tag can operate under a minimum magnetic field of 0.12 A/m and a minimum modulation index of 2.33% which is far less than 10% required by the RFID standard. Compared with the prior references, the proposed tag IC has better performances especially in the aspect of low modulation index. [ABSTRACT FROM AUTHOR]

Previous studies by our group have demonstrated that the transplantation of exogenous platelet-derived growth factor (PDGF)-AA-overexpressing oligodendrocyte progenitor cells (OPCs) promotes tissue repair and recovery of neurological function in a rat model of spinal cord injury (SCI). However, it remains unclear whether treatment with PDGF-AA also affects endogenous oligodendrocytes (OLs) or even neurons, thus promoting further functional recovery after SCI. In the present study, we evaluated the therapeutic potential of PDGF-AA treatment by direct subcutaneous injection of PDGF-AA immediately after SCI. We demonstrated that PDGF-AA injection resulted in increased tissue sparing, myelination and functional recovery in rats following SCI. Further experimentation confirmed that PDGF-AA increased the survival of endogenous OPCs and OLs, and promoted the proliferation of OPCs and their differentiation into OLs. Moreover, PDGF-AA also protected motor neurons from death in the injured spinal cord. These results indicated that PDGF-AA administration may be an effective treatment for SCI. [ABSTRACT FROM AUTHOR]

After the advent of the quartz crystal microbalance (QCM) technology, various QCM-based sensing systems have got certain applications in many science and technology fields and resulted in dramatic progress in these fields. The core advantage of QCM is its high mass sensitivity which leads to high accuracy and low detection limit. For a QCM, the mass sensitivity is determined by the diameter and thickness of the electrode to a certain extent when the frequency of the quartz wafer is already determined. Theoretical approximate calculation reveals that there is an optimum electrode diameter corresponding to the maximum sensitivity. This is different from the traditional opinion that the smaller the electrode, the higher the mass sensitivity. A plating experiment was carried out using 28 QCMs with different electrode diameters, and the experimental results verified the existence of the optimum diameter. This study is helpful to obtain higher mass sensitivity by optimizing electrode parameters. [ABSTRACT FROM AUTHOR]

Interferon-induced transmembrane protein 1 (IFITM1) is a member of the IFITM family that is associated with some acute-phase cytokine-stimulated response. Recently, we demonstrated that IFITM1 was significantly upregulated in the injured spinal cords at the mRNA level. However, its expression and cellular localization at the protein level is still unclear. Here, a rat model of spinal cord injury (SCI) was performed to investigate the spatio-temporal expression of IFITM1 after SCI. IFITM1 mRNA and protein were assessed by quantitative reverse transcription-PCR and western blot, respectively. IHC was used to identify its cellular localization. We revealed that IFITM1 could be found in sham-opened spinal cords and gradually increased after SCI. It reached peak at 7 and 14 days postinjury (dpi) and still maintained at a relatively higher level at 28 dpi. IHC showed that IFITM1 expressed in GFAP+ and APC+ cells in sham-opened spinal cords. After SCI, in addition to the above-mentioned cells, it could also be found in CD45+ and CD68+ cells, and its expression in CD45+, CD68+, and GFAP+ cells was increased significantly. These results demonstrate that IFITM1 is mainly expressed in astrocytes and oligodendroglia in normal spinal cords, and could rapidly increase in infiltrated leukocytes, activated microglia, and astrocytes after SCI. [ABSTRACT FROM AUTHOR]

This work centered on the double-toggle clamping mechanism with diagonal-five points for the high-speed precise plastic injection machine. Based on Lagrange equations, the differential equations of motion for the beam elements are established, in a rotating coordinate system and an absolute coordinate system, respectively. 43 generalized coordinates and a model matrix for the mechanism are created and some coordinate matrices are derived. By coupling the coordinate transformation and matrix manipulation, a high nonlinear and strong time-variant elastic dynamic model is obtained. Based on the dynamic model, a Kineto-Elasto Dynamics (KED) analysis and a Kineto-Elasto Static (KES) analysis are carried out, respectively. By comparing and analyzing the simulation results of KED and KES, the regularity of elastic vibration of the clamping mechanism in high-speed clamping process has been revealed. [ABSTRACT FROM AUTHOR]

Objective The objective of this study was to investigate whether cytosolic phospholipase A2 (cPLA2), an important isoform of PLA2 that mediates the release of arachidonic acid, plays a role in the pathogenesis of spinal cord injury (SCI). Methods A combination of molecular, histological, immunohistochemical, and behavioral assessments were used to test whether blocking cPLA2 activation pharmacologically or genetically reduced cell death, protected spinal cord tissue, and improved behavioral recovery after a contusive SCI performed at the 10th thoracic level in adult mice. Results SCI significantly increased cPLA2 expression and activation. Activated cPLA2 was localized mainly in neurons and oligodendrocytes. Notably, the SCI-induced cPLA2 activation was mediated by the extracellular signal-regulated kinase signaling pathway. In vitro, activation of cPLA2 by ceramide-1-phosphate or A23187 induced spinal neuronal death, which was substantially reversed by arachidonyl trifluoromethyl ketone, a cPLA2 inhibitor. Remarkably, blocking cPLA2 pharmacologically at 30 minutes postinjury or genetically deleting cPLA2 in mice ameliorated motor deficits, and reduced cell loss and tissue damage after SCI. Interpretation cPLA2 may play a key role in the pathogenesis of SCI, at least in the C57BL/6 mouse, and as such could be an attractive therapeutic target for ameliorating secondary tissue damage and promoting recovery of function after SCI. ANN NEUROL 2014;75:644-658 [ABSTRACT FROM AUTHOR]

The previous studies suggested that some subpopulations of T lymphocytes against central nervous system (CNS) antigens, such as myelin basic protein (MBP), are neuroprotective. But there were few reports about the effect of these T cells on axon regeneration. In this study, the neonatally thymectomied (Tx) adult rats which contain few T lymphocytes were subjected to spinal cord hemisection and then passively immunized with MBP-activated T cells (MBP-T). The regeneration and dieback of transected axons of cortico-spinal tract (CST) were detected by biotin dextran amine (BDA) tracing. The behavioral assessments were performed using the Basso, Beattie, and Bresnahan locomotor rating scale. We found that passive transferring of MBP-T could attenuate axonal dieback. However, no significant axon regeneration and behavioral differences were observed among the normal, Tx and sham-Tx (sTx) rats with or without MBP-T passive immunization. These results indicate that passive transferring of MBP-T cells can attenuate axonal dieback and promote neuroprotection following spinal cord injury (SCI), but may not promote axon regeneration. [ABSTRACT FROM AUTHOR]

The complete mitochondrial genome sequence of Takydromus septentrionalis was determined by shotgun sequencing. The total length of mitogenome is 18,304 bp, and contains 13 protein-coding genes, 22 tRNA genes, 2 ribosome RNA genes, and 2 control regions. Most of the genes of T. septentrionalis were distributed on the H-strand, except for the ND6 subunit gene and eight tRNA genes which were encoded on the L-strand. The phylogenetic tree of T. septentrionalis and 8 other closely related species was reconstructed. The phylogenetic analyses based on these mitogenomes presented here will be useful for further insights on the evolutionary relationships of Takydromus. [ABSTRACT FROM AUTHOR]