Room-temperature Magnetic Thermal Switching by Suppressing Phonon-Magnon Scattering

Thermal switching materials, whose thermal conductivity can be controlled externally, show great potential in contemporary thermal management. Manipulating thermal transport properties through magnetic fields has been accomplished in materials that exhibit a high magnetoresistance. However, it is generally understood that the lattice thermal conductivity attributed to phonons is not significantly impacted by the magnetic fields. In this study, we experimentally demonstrate the significant impact of phonon-magnon scattering on the thermal conductivity of the rare-earth metal gadolinium near room temperature, which can be controlled by a magnetic field to realize thermal switching. Using first-principles lattice dynamics and spin-lattice dynamics simulations, we attribute the observed change in phononic thermal conductivity to field-suppressed phonon-magnon scattering. This research suggests that phonon-magnon scattering in ferromagnetic materials is crucial for determining their thermal conductivity, opening the door to innovative magnetic-field-controlled thermal switching materials

Quantification of growth factors in different platelet concentrates

Concentrated growth factor (CGF), a new generation of platelet concentrate product, appears to have more abundant growth factors because of its special centrifugation process. However, there are few studies supporting this. This study was designed to evaluate the contents of major growth factors in CGF and compare them with those found in PRP (platelet-rich plasma) and PRF (platelet-rich fibrin). PRP, PRF, and CGF were obtained from the same samples of peripheral blood. Concentrations of five representative growth factors in platelets were measured with enzyme-linked immunosorbent assay (ELISA): platelet-derived growth factor-BB (PDGF-BB), transforming growth factor β-1 (TGF-β1), insulin-like growth factor-1 (IGF-1), vascular endothelial growth factor (VEGF), and basic fibroblast growth factor (bFGF). The results showed that the bFGF levels in CGF and PRF were significantly higher than that in activated PRP. For other growth factors, such as PDGF-BB, TGF-β1, IGF-1, and VEGF, the levels did not differ significantly among activated PRP, PRF, and CGF. Our findings extended the currently available data on the release and measurement of growth factors in CGF and other platelet gels. In future studies, we need more data to find the proper therapeutic doses for platelet concentrates suitable for different clinical applications

STAT1/SOCS1/3 Are Involved in the Inflammation-Regulating Effect of GAS6/AXL in Periodontal Ligament Cells Induced by Porphyromonas gingivalis Lipopolysaccharide In Vitro

Periodontitis involves chronic inflammation of the tissues around the teeth caused by plaque and the corresponding immune response. Growth arrest-specific protein 6 (GAS6) and AXL receptor tyrosine kinase (AXL) are known to be involved in inflammatory diseases, while signal transducer and activator of transcription-1 (STAT1) and suppressor of cytokine signaling (SOCS) are related to inflammatory processes. Moreover, miRNA34a directly targets AXL to regulate the AXL expression. However, the specific roles of GAS6 and AXL in periodontitis remain unclear. This study was designed to explore the effect and mechanism of AXL on the expression of inflammatory cytokines induced by Porphyromonas gingivalis lipopolysaccharide (P. gingivalis LPS) in human periodontal ligament cells (hPDLCs). The effects of different concentrations of P. gingivalis LPS on the expression of GAS6/AXL in hPDLCs were observed. Additionally, the effect of LPS on AXL was investigated by transfection of the miRNA34a inhibitor. AXL was knocked down or overexpressed to observe the release of inflammatory cytokines interleukin- (IL-) 8 and IL-6. The results showed that the expression levels of GAS6 and AXL decreased after P. gingivalis LPS infection. Transfection of a miR-34a inhibitor to hPDLCs demonstrated a role of miR-34a in the downregulation of AXL expression induced by LPS. Moreover, AXL knockdown or overexpression influencing the expression of IL-8 and IL-6 was investigated under LPS stimulation. AXL knockdown decreased the expression of STAT1 and SOCS1/3. Overall, these results demonstrate that AXL inhibits the expression of LPS-induced inflammatory cytokines in hPDLCs and that STAT1 and SOCS1/3 are involved in the regulation of inflammation by GAS6/AXL

Auto-Encoder-Extreme Learning Machine Model for Boiler NOx Emission Concentration Prediction

An automatic encoder (AE) extreme learning machine (ELM)-AE-ELM model is proposed to predict the NOx emission concentration based on the combination of mutual information algorithm (MI), AE, and ELM. First, the importance of practical variables is computed by the MI algorithm, and the mechanism is analyzed to determine the variables related to the NOx emission concentration. Then, the time delay correlations between the selected variables and NOx emission concentration are further analyzed to reconstruct the modeling data. Subsequently, the AE is applied to extract hidden features within the input variables. Finally, an ELM algorithm establishes the relationship between the NOx emission concentration and deep features. The experimental results on practical data indicate that the proposed model shows promising performance compared to state-of-art models.Comment: Accepted by Energ

Effect of nicotine on the expression of pro-inflammatory mediators in HUVECs.

<p>HUVECs were stimulated with nicotine (10 µM-10 mM), and the expression levels of ICAM-1 (A), VCAM-1 (B), E-selectin (C), MCP-1 (D), and IL-8 (E) were measured by qPCR. GAPDH was used as endogenous control gene. Each value represents mean ±SEM of three independent assays. Non-stimulated HUVECs were used as a control ( = 1). The expression levels of pro-inflammatory mediators were not analyzed after stimulation with 10-mM nicotine for 24 and 72 h because the cells were not viable.</p

Effect of nicotine and <i>P. gingivalis</i> LPS on the proportion of viable HUVECs.

<p>HUVECs were stimulated with nicotine (10 µM-10 mM) and/or <i>P. gingivalis</i> LPS, and the proportion of viable cells was measured using a flow cytometry apoptosis assay after 4 (A), 24 (B), and 72 (C) h. Viable cells were those negative for annexin V and propidium iodide. Data are presented as mean ±SD of three independent experiments. * – significantly lower compared to control group, p<0.05.</p

Effect of nicotine and <i>P. gingivalis</i> LPS on HUVEC migration measured in the microchemotaxis chamber.

<p>HUVEC migration through a polycarbonate membrane with pore size of 8 µm over 8 h was assessed in a 48-well microchemotaxis chamber. The y-axis represents mean ±SD of cells per microscope field of four different wells of one representative experiment. * – significantly different between groups, p<0.05.</p

Effect of nicotine on the <i>P. gingivalis</i> LPS-induced protein expression of pro-inflammatory mediators in HUVECs.

<p>HUVECs were stimulated by <i>P. gingivalis</i> LPS in the presence or absence of nicotine (10 µM–10 mM) for 4, 24, and 72 h. After stimulation, the surface expression levels of ICAM-1 (A), VCAM-1 (B), and E-selectin (C) were measured by flow cytometry, and the quantity of MCP-1 (D) and IL-8 (E) in conditioned media was measured by ELISA. Each value represents mean ±SD of three independent assays. Non-stimulated HUVECs were used as a control. The protein expression levels of pro-inflammatory mediators were not analyzed after stimulation with 10-mM nicotine for 24 and 72 h because the cells were not viable. * – significantly different between groups, p<0.05. † – significantly higher compared to controls, p<0.05.</p