Metal-Organic Frameworks for Ammonia-Based Thermal Energy Storage.

Recently, the application of metal-organic frameworks (MOFs) in thermal energy storage has attracted increasing research interests. MOF-ammonia working pairs have been proposed for controlling/sensing the air quality, while no work has yet been reported on the immense potential of MOFs for thermal energy storage up till now. Herein, the feasibility of thermal energy storage using seven MOF-ammonia working pairs is experimentally assessed.

Mechanism of hysteresis for composite multi-halide and its superior performance for low grade energy recovery.

Sorption hysteresis commonly exists for different sorbents and has a great impact on the performance, and recently it was found that the multi-halide sorbents could reduce the hysteresis phenomena. Here we report the mechanism of the sorption hysteresis for multi-halide under equilibrium/non-equilibrium conditions and its superior performance for low grade energy recovery. We find that the inner reaction among different halides does not happen and contribute to sorption hysteresis in sorption/desorption phases under equilibrium conditions.

Targeted migration of bone marrow mesenchymal stem cells inhibits silica-induced pulmonary fibrosis in rats.

Background: Silicosis is a common occupational disease, characterized by silicotic nodules and diffuse pulmonary fibrosis. We demonstrated an anti-fibrotic effect of bone marrow mesenchymal stem cells (BMSCs) in silica-induced lung fibrosis. In the present study, we sought to clarify the homing ability of BMSCs and the specific mechanisms for their effects.

MicroRNA-29b inhibits supernatants from silica-treated macrophages from inducing extracellular matrix synthesis in lung fibroblasts.

Silicosis is pathologically characterized by diffused pulmonary fibrosis and abundant deposition of extracellular matrix (ECM) components. The ECM is mainly secreted by myofibroblasts which are the activated state of fibroblasts. MicroRNA-29b (miR-29b) is one of the well-known microRNAs involved in fibrosis, but its roles in silicosis have not been specified.

Bone marrow mesenchymal stem cells attenuate silica-induced pulmonary fibrosis via paracrine mechanisms.

The purpose of this study was to investigate the anti-fibrotic effect and possible mechanism of bone marrow mesenchymal stem cells (BMSCs) in silica-induced lung injury and fibrosis in vivo and in vitro. In vivo, rats were exposed to 50mg/ml silica intratracheally. The rats were sacrificed on day 15 or day 30 after intravenous injection of BMSCs.

Anti-fibrotic effects of bone morphogenetic protein-7-modified bone marrow mesenchymal stem cells on silica-induced pulmonary fibrosis.

Silicosis is an occupational lung disease caused by exposure to small particles of crystalline silica, which ultimately results in diffuse pulmonary fibrosis. Evidence indicates an anti-fibrotic role of bone morphogenetic protein-7 (BMP-7) and bone marrow mesenchymal stem cells (BMSCs) in lung diseases. Therefore, strategies incorporating genetic engineering and stem cell biology might have a tremendous potential to treat critical injuries and diseases.

SB203580 inhibits epithelial-mesenchymal transition and pulmonary fibrosis in a rat silicosis model.

To investigate the role of p38 MAPK in silicosis, we explored the effects of SB203580 as a specific inhibitor of p38 MAPK in the silicosis model in rats. Rats were exposed to 50mg/ml silica intratracheally. From the first day after instillation, rats were injected with SB203580 1mg/kg/d.

Bone morphogenetic protein-7 prevented epithelial-mesenchymal transition in RLE-6TN cells.

Bone morphogenetic protein-7 (BMP-7) plays an important role in the epithelial-mesenchymal transition (EMT) process, and has been identified as the most potent factor that can promote mesenchymal-epithelial transition (MET) and reduce organ fibrosis. Here we examined the important role of BMP-7 in silica-induced EMT and investigated the relationship between BMP-7 and the balance of EMT/MET. We found that silica induced EMT and decreased the expression of BMP-7 and , while silica activated the p38 MAPK/transcription factor signaling pathway in RLE-6TN cells.

BMP-7 attenuated silica-induced pulmonary fibrosis through modulation of the balance between TGF-β/Smad and BMP-7/Smad signaling pathway.

Objective: To investigate the anti-fibrotic effects and possible mechanisms of bone morphogenetic protein-7 (BMP-7) on silica induced fibrosis in RLE-6TN cells, and compare the preventive treatment of experimental silicosis with BMP-7 with therapeutic treatment of silicosis in vitro models.

Methods: RLE-6TN cells were incubated with the supernatant of RAW264.7, treated by 50 μg/mL silica in either presence or absence of BMP-7 in different phases.