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Lithium-sulfur (Li-S) batteries have become a research hotspot due to their high energy density, environment friendliness and low-cost. But commercial applications are hampered by rapid capacity fading and low sulfur content. Herein, the composite of integrating manganese oxide on graphene was prepared by a facile redox reaction between potassium permanganate (KMnO4) and graphene in acidic aqueous solution to solve the problems of the Li-S batteries. X-ray Diffraction (XRD), Scanning Electron Microscope (SEM) and transmission electron microscopy (TEM) and X-ray photoelectron spectroscopy (XPS) analysis show that sulfur was uniformity coated on G/MnO2 composite. TG indicated that the G/MnO2/S composites contained 76.56 wt% active sulfur. The prepared cathode of G/MnO2/S composites exhibited excellent rate performance and cycle stability. At a high rate of 1 C, its maximum discharge capacity reached 908 mA h g−1 and its average capacity decreasing rate was only 0.105%/cycle when running over 500 cycles. The interaction mechanism of MnO2 with polysulfides was investigated by adsorption tests and XPS analysis. The excellent electrochemical performance might be due to a combination of adsorption or catalytic properties of MnO2, and the conductivity network of graphene.

Introduction Lipopolysaccharide (LPS) has been implicated in mesenchymal stem cell differentiation processes. Wnt5a, one of the “non-canonical” Wnt family members, is important in signaling stem cell differentiation and in the inflammatory responses of immune cells. Here we studied whether LPS can regulate the expression of Wnt5a in human dental pulp stem cells (hDPSCs) and investigated the intracellular signaling pathways activated by LPS. Methods Wnt5a mRNA and protein expression changes in hDPSCs were investigated by real-time polymerase chain reaction analysis and enzyme-linked immunosorbent assay. In addition, real-time polymerase chain reaction, enzyme-linked immunosorbent assay, and luciferase activity assays were used to determine whether toll-like receptor 4 (TLR4), myeloid differentiating factor 88 (MyD88), nuclear factor kappa B (NF-kB), or the phosphatidylinositol 3-OH kinase (PI3K)/AKT pathways are involved in LPS-induced Wnt5a expression. The activation of PI3K and AKT in hDPSCs was measured by Western blot analysis. Results Wnt5a mRNA and protein expression was rapidly increased in response to LPS in a time- and dose-dependent manner. LPS-induced Wnt5a expression was effectively attenuated by administration of a TLR4 neutralizing antibody, MyD88 inhibitory peptide, PI3-kinase inhibitors (LY294002 and wortmannin), an AKT inhibitor, or NF-κB inhibitor (pyrrolidine dithiocarbamate), IκBa phosphorylation inhibitor (Bay 117082), or IκB protease inhibitor (L-1-tosylamido-2-phenylethyl chloromethyl ketone). Treatment of hDPSCs with LPS activated PI3-kinase (p85) and AKT signaling in a time-dependent manner. Moreover, LPS-mediated increases in κB-luciferase activity were diminished by the overexpression of dominant negative mutants of TLR4, MyD88, p85, AKT, and IκBa. Conclusions These results demonstrated that LPS-induced Wnt5a expression was mediated through the TLR4/MyD88/PI3-kinase/AKT pathway, which then initiated NF-κB activation in hDPSCs.

Aim To investigate the effects of CpG ODN (CpG oligodeoxynucleotides) to model the action of bacterial challenge on pulpal matrix metalloproteinase-13 (MMP-13) expression and elucidate the associated intracellular signalling pathways. Methodology Real-time PCR was used to detect the effects of CpG ODN on MMP-13 mRNA expression levels in a murine odontoblast-lineage cell line (OLCs). The possible involvement of TLR9/MyD88, NF-κB or MAPK pathways involved in the CpG ODN-induced MMP-13 expression was examined by real-time PCR, transient transfection, luciferase activity assay and ELISA. Western blotting was performed to assay the phosphorylation of ERK at a range of time points. Results MMP-13 was constitutively expressed in OLCs, and their exposure to CpG ODN significantly increased MMP-13 expression. Pre-treatment of OLCs with the inhibitory peptide MyD88, or chloroquine, attenuated the CpG ODN-induced expression of MMP-13. Treatment of the OLCs with CpG ODN increased NF-κB-luciferase activity. This activity was decreased by the over-expression of a nondegrading mutant of IκBα (IκBαSR), although enhanced by the over-expression of NF-κB p65. MMP-13 expression induced by CpG ODN was markedly suppressed by NF-κB inhibitors (pyrrolidine dithiocarbamate, PDTC), IκBα phosphorylation inhibitors (Bay 117082) or IκB protease inhibitor (L-1-tosylamido-2-phenylethyl chloromethyl ketone, TPCK). The inhibitor of ERK1/2, U0126, but not inhibitors of p38 MAPK and JNK, SB203580 and SP600125, decreased CpG ODN-mediated MMP-13 expression. Conclusion The CpG ODN-induced MMP-13 expression in OLCs is mediated through TLR9, NF-κB and the ERK pathway indicating that potentially the recognition of CpG ODN by TLR9 on odontoblasts may regulate the remodelling of injured dental pulp and hard tissues by inducing MMP-13 expression.

A new millimeter wave spatial power combiner based on broadband multi-way ridged waveguides is designed. The device is composed of a multi-step impedance transformer and eight ridged waveguides. Since the ridged waveguides provide a consistent impedance transformation and a broad band working frequency, a millimeter wave solid-state power amplifier based on the combiner demonstrates an output power of more than 5 W at 40 GHz and greater than 10 W over the 30 GHz to 34 GHz band. Measured results show that all the ridged waveguides have the high uniformity of amplitude and phase, and the combiner has demonstrated operation over a broadband of 30 GHz to 40 GHz with more than 10 dB return loss and less than 0.8 dB insertion loss.

Determination of tides using reflected signals is an important aspect of GNSS application technique at the present. For the problem of remote sensing the tide heights, a method of retrieving the height of sea surface is proposed from the power of the interference signals obtained by a coastal GPS receiver with singular antenna. An experiment was carried out at the coast of Qingdao. Results of the receiving antenna height over the sea surface from observed interference signals are presented. Compared to tide gauges, the results show its validity of the method based on GPS interference measurements using right-hand circular polarization antenna.

Runx2, of the Runx family, is an essential transcription factor that controls bone and tooth development by regulating osteoblast and odontoblast differentiation. However, the function of Runx2 in late stage odontoblast differentiation is not clear. We studied the function of Runx2 in dentinogenesis by generating transgenic mice expressing Runx2 specifically in odontoblasts. We observed dentin formation in postnatal day 3 (P3), P7 and P28 mice and measured the expression levels of Runx2 and matrix proteins in dentin. The odontoblasts in transgenic mice (Tg) lost their tall columnar shape and polarization and dentinal tubules were absent. The dental pulp chamber was dramatically enlarged and the dentin in Tg mice was thinner. Osteoblast-like cells were seen instead of normal odontoblasts and were embedded in a bone-like matrix, indicating that dentin formation was replaced with bone. Predentin was disorganized possessing lacunae that contained odontoblasts. The mandibular molars of Tg mice showed noticeable defects by Micro-CT. Using quantitative real-time PCR, the expression of dentin matrix proteins, particularly dentin sialophosphoprotein (DSPP), was found to be upregulated in 3-day-old Tg mice and downregulated at 1 month of age. These findings indicate that Runx2 inhibited odontoblast terminal differentiation and induced transdifferentiation of odontoblasts to osteoblasts at the late cell differentiation stage. Therefore, Runx2 should be inhibited in odontoblasts to encourage normal cell maturation, differentiation and dentinogenesis.