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To meet the current requirements for absorbing materials with broadband, lower thickness, and lower density, the FeNi@C@Fe 3 O 4 magnetic powders with a density of 1.75 g/cm3 are constructed by the hydrothermal method and the liquid phase reduction method. The powders have good matching performance with air impedance in the band of 0.3 GHz ~ 18 GHz, and can consider both dielectric loss and magnetic loss-absorbing mechanisms. The loss tangent, tgδ, of the powders is 0.4–0.5. The powder coat is designed by using the interference absorption mechanism. When the thickness of the coat is 1.8 mm, the absorption peak of the coat is about − 30 dB. The coat has a maximum of effective absorption band for 12.2 GHz ~ 17.3 GHz, and the effective absorption bandwidth is 5.1 GHz. When the glass fiber/epoxy resin composite material of thickness 0.5 mm is coated on the FCFp coat of thickness 1.7 mm, the effective absorption band is further widened to 11.9 GHz ~ 17.6 GHz, and the effective absorption bandwidth reaches 5.7 GHz. The FeNi@C@Fe 3 O 4 powders have the characteristics of dielectric and magnetic loss-absorbing materials, and have the remarkable advantages of the wider effective absorption bandwidth and the lower density, which is a kind of high-efficiency absorbing material with outstanding comprehensive absorption performance. [Display omitted] [ABSTRACT FROM AUTHOR]

Liquid metal extraction (LME) is considered to be one of the alternatives for green production of rare earth elements from secondary resources. It leads to shift paradigm to eco-friendly economy to reduce carbon footprint and support sustainable development. However, separation of rare earths elements (REEs) from generated magnesium (Mg)-REEs after LME process is still remained as vacant technology due to lack of databases. In this work, fundamental investigation on the mechanism and kinetics for separation of REEs from Mg-REEs alloys by vacuum distillation is proposed. Experimental parameters of the process are thermodynamically designed at 2.0 × 10−5 atm in the range of 600 °C to 900 °C for selective distillation of Mg. Mg distillation is observed with gradual phase transformation from raw materials to phases including less Mg. 99.5 % yield of REEs and 99 % of pure Mg are successfully recovered as the metallic state, respectively. Interestingly, relatively rapid separation behavior of dysprosium (Dy) than neodymium (Nd) is observed and evaluated by variation Gibbs free energy and heat of mixing enthalpy based on the unique databases from practical experiments. It is indicated that the kinetics of phase transformation shows the different distillation behavior between individual REEs through thermodynamic and experimental assessments even if REEs group shares similar chemistry properties. This investigation can provide fundamental databases for grafting vacuum distillation after LME to secure sustainability for recycling industry. [Display omitted] • The vacuum distillation process is designed to separate REEs from Mg-REEs alloys based on the thermodynamic prediction. • Depending on the REEs, unexpected separation and recovery behaviors are observed due to relative affinity of compounds. • The derived results can provide fundamental databases for grafting vacuum distillation after LME for recycling industry. [ABSTRACT FROM AUTHOR]

Nebulized lidocaine has been suggested to be beneficial in asthma therapy, but the underlying mechanisms are little known. We aimed to investigate whether Toll-like receptor (TLR) 2 was involved in the protective effect of lidocaine on allergic airway inflammation. Female C57BL/6 mice were sensitized and challenged with ovalbumin (OVA). Meanwhile, some of the mice were treated with TLR2 agonist (Pam3CSK4, 100 μg) intraperitoneally in combination with OVA on day 0. Just after allergen provocation, mice were treated with inhaled lidocaine or vehicle for 30 min. In this model, we found that lidocaine markedly attenuated OVA-evoked airway inflammation, leukocyte recruitment and mucus production. Moreover, lidocaine abrogated the increased concentrations of T cytokines and TNF-α in bronchoalveolar lavage fluid (BALF) of allergic mice, as well as reducing the expression of phosphorylated nuclear factor (P-NF)-κBp65 and the NOD-like receptor pyridine containing 3 (NLRP3), which are important for the production of pro-inflammatory cytokines. In addition, our study showed that lidocaine dramatically decreased OVA-induced increased expression of TLR2 in the lung tissues. Furthermore, activation of TLR2 aggravated OVA-challenged airway inflammation, meanwhile, it also elevated OVA-induced expression of P-NF-κBp65 and NLRP3 in the lungs. However, lidocaine effectively inhibited airway inflammation and counteracted the expression of P-NF-κBp65 and NLRP3 in allergic mice pretreated with Pam3CSK4. Taken together, the present study demonstrated that lidocaine prevented allergic airway inflammation via TLR2 in an OVA-induced murine allergic airway inflammation model. TLR2/NF-κB/NLRP3 pathway may serve as a promising therapeutic strategy for allergic airway inflammation. [ABSTRACT FROM AUTHOR]

Aims Glucocorticoids are the most effective anti-inflammatory agent in treating pulmonary diseases typically accompanied by hypoxia. Our previous study has demonstrated that glucocorticoid receptor α (GRα) expression is reduced in hypoxia but the underlying mechanism remains elusive. In this study we aim to identify the signaling pathway involved in hypoxia-induced down-regulation of GRα, and whether hypoxia affects nuclear translocation of GRα. Main methods Female C57BL/6 mice were sensitized with saline or ovalbumin (OVA) as the in vivo model. Mice were divided into control and OVA groups, and their lung histology and the expression of hypoxia inducible factor (HIF-1) and GRα were examined. A549 cells were exposed to chemical hypoxia as the in vitro model, where mitogen-activated protein kinases (MAPKs) were inhibited specifically by SB203580. Next, under normal or hypoxic conditions, the expression of GRα, MAPKs and HIF-1 signal protein were determined by Western blot analysis, and GRα translocation were observed through live-cell imaging. Key findings In OVA challenged mice the expression of GRα was down-regulated whereas HIF-1 was up-regulated. Hypoxia caused a time-dependent decrease of GRα expression, and activated multiple signaling pathways including MAPKs and HIF-1. Moreover, GRα expression increased with MAPK inhibition. Interestingly, only MAPK inhibitor SB203580, but not JNK inhibitor SP600125 or ERK inhibitor U0126 improved the expression of GRα under hypoxic condition. GRα nuclear translocation was also significantly inhibited by hypoxia. Significance Hypoxia down-regulated the expression of GRα through p38 signaling pathway, as well as inhibited GRα nuclear translocation significantly. [ABSTRACT FROM AUTHOR]

• A glucan (18.3 kDa) from purple sweet potato is composed of →4)Glc p (1→ glycosyls. • It branches at O -2, O -3, and O -6 positions with α- d -Glc p (1→ residue as side chain. • Its particle size is concentrated at 230 nm and has no triple-helix conformation. • Its height and width rangs from 1.0 to 6.1 nm and 65 to 210 nm, respectively. • Its maximum ring diameter and chain length is ∼800 nm and ∼7.0 μm, respectively. A novel glucan PSPP-1 (18.3 kDa) was purified from the foot tuber of purple sweet potato Ipomoea Batatas (L.) Lam. Its backbone was composed of →4)-α- d -Glc p (1→ glycosyl, and branching at the O -2, O -3, and O -6 positions with α- d -Glc p (1→ residues. X-ray diffraction experiment showed that PSPP-1 existed as an amorphous form. Its microstructure was detected via scanning electron microscopy. Its particle size was mainly concentrated at 230 nm in water. Congo red and circular dichroism experiments showed there was no triple-helix conformation. Atomic force microscopy data suggested that its height and width ranged from 1.0 to 6.1 nm and 65 to 210 nm, respectively; its maximum ring diameter and chain length was ∼800 nm and ∼7.0 μm, respectively. Furthermore, it exhibited inhibitory activities on HepG2, LOVO, and MCF-7 cells. Collectively, our data are useful for understanding the structural characteristics of sweet potato polysaccharides, and their application in foods and pharmaceutical areas. [ABSTRACT FROM AUTHOR]

Numerous studies indicate that toll-like receptor 2 (TLR2) led to divergent effects in asthma. The occurrence of autophagy in asthma pathogenesis is still incompletely understood. Here, we aimed to investigate the role of TLR2 and the underlying mechanisms in allergic airway inflammation and autophagy activation. C57BL/6 and TLR2 knockout (TLR2−/−) mice were subjected to an ovalbumin (OVA)-immunized allergic airway model, and were treated with SP600125. Differential cell counts in bronchoalveolar lavage fluid were determined by Wright's staining. Histological analysis of airway inflammation was determined by haematoxylin and eosin (H&E) and periodic acid-Schiff (PAS) staining. The levels of OVA-specific immunoglobulin E (IgE), tumor necrosis factor α (TNF-α) and interleukin 10 (IL-10) were detected by enzyme-linked immunosorbent assay (ELISA). Proteins expression in lung tissues was detected by western blot, expression of TLR2 was further observed by immunofluorescence. Autophagy activation was determined by western blot and transmission electron microscopy (TEM). TLR2 expression was increased upon OVA challenge, and TLR2 deficiency was associated with decreased allergic airway inflammation. Meanwhile, TLR2 deficiency weakened autophagy activation. Moreover, inhibition of c-Jun N-terminal kinase (JNK) by SP600125 also suppressed OVA-induced allergic airway inflammation and autophagy activation. Interestingly, treating TLR2−/− mice with SP600125 showed similar OVA-induced allergic airway inflammation and autophagy activation compared to that in vehicle-treated TLR2−/− mice. TLR2 might contribute to the maintenance of allergic airway inflammation through JNK signaling pathway accompanying with autophagy activation. These findings may provide a novel signal target for prevention of allergic airway inflammation. [ABSTRACT FROM AUTHOR]