N-modified carbon-coated NaTi2(PO4)3 as an anode with high capacity and long lifetime for sodium-ion batteries.

NASICON-type NaTi2(PO4)3 is recognized as a promising energy storage anode due to its high ionic conductivity and low cost. In this work, N-modified carbon-coated sodium titanium phosphate (NTPGN) composites were prepared by the sol-gel method by using sodium glutamate as a source of nitrogen and partial carbons. The addition of sodium glutamate forms a loose structure of nano-spherical flowers on the surface of sodium titanium phosphate, which shows a higher specific capacity, better rate performance, and excellent cycling performance compared to the carbon-coated titanium phosphate derived only from citric acid. The discharge capacities of NTPGN at 0.1 C, 5 C, 10 C, 20 C, and 30 C are 132.8, 132, 131.4, 105.9, and 98.2 mA h g-1, respectively. In particular, after 1000 cycles at 20 C, the discharge capacity is 102.6 mA h g-1 with a capacity retention rate of 96%. This work reveals that the combination of carbon coating and nitrogen doping using sodium glutamate improves the electrochemical performance of electrode materials.

An overview of the preparation and application of counter electrodes for DSSCs.

Dye-sensitized solar cells (DSSCs) are potential products for the next generation of photovoltaic technology, which is one of the research hotspots in photovoltaics. The counter electrode in DSSCs collects electron in the external circuit and catalyzes the reduction of the redox electrolyte and hole transport in the solid electrolyte. Thus, it undoubtedly has an important impact on the photovoltaic performance, long-term stability, and cost of DSSCs. In this work, the materials of counter electrodes are classified into metals, carbon materials, conductive polymers, and inorganic compounds. The preparation, mechanism, conversion efficiency, and properties of counter electrodes are reviewed.

Multiwalled carbon nanotube network connected Mg0.5Ti2(PO4)3 composites to improve sodium storage performance.

The research on sodium-ion batteries (SIDs) has aroused intensive attention. In this work, the Mg0.5Ti2(PO4)3 (MTP) composite material with NASICON structure has been studied as an anode material in SIDs. The sol-gel method is used to synthesize the Mg0.5Ti2(PO4)3 with a conductive network that can be constructed by using carbon nanotubes (CNTs) and phenolic resin as the amorphous source of carbon coating. The CNT network is used not only to improve the outcome of electrolyte penetration and reduce the internal resistance to diffusion but also to create a fast path for electron transport, thereby elevating the level of electronic conductivity. The phenolic resin is generated on the surface of MTP which extends its cycle life. The carbon-coated Mg0.5Ti2(PO4)3 with 0.10 g CNTs (MTP-CNT10) displays optimal performance as an anode material in SIDs, and shows a discharge capacity of 298.8 mA h g-1, 258.3 mA h g-1 and 254.8 mA h g-1 at 0.1C, 0.5C and 1C, respectively. Besides, the capacity retention rate reaches 92% after 300 cycles at 10C. This study contributes an effective solution to improving the electrochemical performance of electrode materials through the introduction of carbon coating and highly conductive materials.

Thermal Activation of Coal Gangue with Low Al/Si Ratio as Supplementary Cementitious Materials.

To effectively utilize coal gangue (CG) with low Al/Si ratio, the thermal activation method was used. The activated CG, as supplementary cementitious materials (SCMs), was added into ordinary Portland cement (OPC) to study its physical properties. The XRD results show that CG undergoes a phase transition from kaolinite to metakaolinite during activation. The NMR tests reveal that the low polymerization state Q3 is continuously broadened, and the Al coordination gradually changes from Al VI to Al V and Al IV. The CG particles are scale-like and glassy with a loose structure. By mixing the activated CG (under 800 °C) with cement (mass ratio = 3:7), the water demand of normal consistency increases by 7.2% and the initial and final setting times extend by 67 min and 81 min, respectively. The rough surface and loose structure of activated CG are the main factors contributing to the higher water demand of normal consistency. The micro-aggregate effect of the activated CG reduces the contact rate between the cement particles and water, and the interparticles, thus slowing down the process of hydration reaction, and leading to longer setting times.

Interleukin-38 overexpression prevents bleomycin-induced mouse pulmonary fibrosis.

Pulmonary fibrosis is a kind of pulmonary disorder with chronic inflammation and excessive collagen deposition, and its etiology is not clear. Interleukin (IL)-38 is a new member of IL-1 family cytokines, but its role in pulmonary fibrosis has not been elucidated. In this study, a lentivirus expressing IL-38 was injected into the nasal cavity of mice with bleomycin-induced pulmonary fibrosis. We found that IL-38 overexpression reduced the body weight loss and improved the survival of mice induced by bleomycin. Furthermore, IL-38 expression attenuated the pulmonary inflammation and fibrosis damage induced by bleomycin, decreased the production of pro-inflammatory and pro-fibrotic cytokines such as IL-1ß, IL-6, IL-17A, monocyte chemoattractant protein-1, and tumor necrosis factor-α, but increased the release of anti-inflammatory cytokine IL-1 receptor antagonist (IL-1Ra) in the lungs of bleomycin-challenged mice. Our data suggest that IL-38 may inhibit bleomycin-induced pulmonary inflammation and fibrosis through its anti-inflammatory effect and regulation of IL-1ß/IL-1Ra balance, and IL-38 may be a new strategy for the treatment of pulmonary fibrosis.

Interleukin-37 Attenuates Bleomycin-Induced Pulmonary Inflammation and Fibrosis in Mice.

Pulmonary fibrosis is a disease with chronic inflammation and excessive collagen deposition for which there is no effective treatments. Interleukin (IL)-37 is a newly identified anti-inflammatory cytokine but its role in pulmonary fibrosis remains unclear. In this study, we investigated the effect of IL-37 on bleomycin-induced pulmonary fibrosis in mice. A lentivirus expressing IL-37 was administered intranasally to bleomycin-induced C57BL/6 mice. We found that IL-37 improved the survival of mice and reduced the body weight loss of mice caused by bleomycin. Furthermore, IL-37 significantly attenuated pulmonary inflammatory infiltration and collagen deposition and decreased the hydroxyproline content in bleomycin-treated mice. Finally, IL-37 treatment inhibited the expression of monocyte chemoattractant protein-1, IL-6, and tumor necrosis factor-α, but increased the expression of interferon-γ in lung tissues from bleomycin-challenged mice. Taken together, these results suggest that in vivo expression of IL-37 is useful in preventing pulmonary fibrosis induced by bleomycin and provides a possible therapeutic approach to pulmonary fibrosis diseases.

IL-38 alleviates concanavalin A-induced liver injury in mice.

Interleukin (IL)-38 is a poorly characterized cytokine of the IL-1 family with anti-inflammatory activity. The role of IL-38 in liver injury remains unknown. We have investigated the potential effect of hydrodynamic-based gene delivery to express human IL-38 in mice with concanavalin A (Con A)-induced liver injury. Transfer of plasmid DNA encoding IL-38 significantly reduced hepatic toxicity and serum levels of aspartate aminotransferase and alanine aminotransferase compared with administration of a control plasmid. Moreover, IL-38 expression dramatically reduced serum levels of several pro-inflammatory cytokines, such as tumor necrosis factor-α, interferon-γ, IL-6, IL-17, and IL-22, but not levels of the anti-inflammatory cytokine IL-10. These results suggest that in vivo expression of human IL-38 in mice has hepatoprotective effects against Con A-induced liver injury by inhibition of inflammatory cytokine production.

Lentivirus expressing soluble ST2 alleviates bleomycin-induced pulmonary fibrosis in mice.

It has been shown that the expression of ST2, a receptor of interleukin (IL)-33, is elevated in the lungs of idiopathic pulmonary fibrosis patients and bleomycin-induced mouse models, however its contribution to the development of pulmonary fibrosis has yet to be tested. In the present study, we treated mice by intranasal instillation of lentivirus expressing soluble ST2 and evaluated lung inflammation and fibrosis in the bleomycin-induced pulmonary fibrosis mouse model. We found that ST2 lentivirus treatment significantly improved survival rate and reduced weight loss compared with controls treated with empty lentivirus. Furthermore, ST2 treatment profoundly attenuated the pulmonary inflammatory cell infiltration and fibrotic changes. Finally, ST2 treatment markedly lowered the levels of IL-4, IL-6, IL-13, IL-33, monocyte chemoattractant protein-1, and transforming growth factor-ß1, whereas it increased the levels of interferon-γ in bronchoalveolar lavage fluid. The results indicate that ST2 might prevent bleomycin-induced pulmonary fibrosis possibly through downregulating proinflammatory and profibrotic mediators. This study suggests that lentivirus expressing soluble ST2 might represent an effective therapeutic approach in the treatment of pulmonary fibrotic diseases.

Role of IL-38 and its related cytokines in inflammation.

Interleukin- (IL-) 38 is a recently discovered cytokine and is the tenth member of the IL-1 cytokine family. IL-38 shares structural features with IL-1 receptor antagonist (IL-1Ra) and IL-36Ra. IL-36R is the specific receptor of IL-38, a partial receptor antagonist of IL-36. IL-38 inhibits the production of T-cell cytokines IL-17 and IL-22. IL-38 also inhibits the production of IL-8 induced by IL-36γ, thus inhibiting inflammatory responses. IL-38-related cytokines, including IL-1Ra and IL-36Ra, are involved in the regulation of inflammation and immune responses. The study of IL-38 and IL-38-related cytokines might provide new insights for developing anti-inflammatory treatments in the near future.

Adenovirus expressing IFN-λ1 (IL-29) attenuates allergic airway inflammation and airway hyperreactivity in experimental asthma.

BACKGROUND: Asthma is thought to result from the generation of T helper type 2 (Th2) responses, leading to bronchial inflammation. IFN-λ1 (also known as IL-29) is a recently described member of the IFN-λ family and has been shown to decrease production of Th2 cytokines in vitro. However, the role and mechanism of IFN-λ1 in asthma remain unknown. OBJECTIVES: The aim of this study was to clarify the importance of IFN-λ1 in allergen-induced airway hyperresponsiveness (AHR) and inflammation. METHODS: We used a murine model for ovalbumin (OVA)-induced asthma to examine the effect of intranasal delivery of recombinant adenovirus expressing human IFN-λ1 (Ad-hIFN-λ1) on AHR and allergic airway inflammation. RESULTS: Intranasal instillation of Ad-hIFN-λ1 before airway antigen challenge in OVA-immunized mice significantly decreased the severity of AHR and numbers of eosinophils and levels of IL-4, IL-5, and IL-13, but not IL-10 and IFN-γ; both in vivo, in the bronchoalveolar lavage fluid and in vitro, following stimulation of lymphocytes from spleens with OVA, compared with administration of a control virus (Ad-mock). Furthermore, Ad-hIFN-λ1 treatment inhibited serum IgE secretion and increased numbers of splenic CD4(+)CD25(+)FOXP3(+) Treg cells. Histological studies showed that Ad-hIFN-λ1 attenuated OVA-induced lung tissue eosinophilia. CONCLUSIONS: These results demonstrate that delivery of the Ad-hIFN-λ1 can mitigate allergic airway inflammation in experimental asthma. The potent immunoregulatory action of IFN-λ1 may offer a novel therapeutic approach to treat allergic asthma.