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. From ammonia sorption stability and sorption thermodynamics results, it is found that MIL-101(Cr) exhibits both high ammonia sorption stability and the largest sorption capacity of ≈0.76 g g-1 . Compared with MIL-101(Cr)-water working pair, MIL-101(Cr)-ammonia working pair improves the sorption capacity by over three times with evaporation temperature lower than 8.4 °C. Due to stable ammonia sorption stability and negligible hysteresis, MIL-101(Cr) and ZIF-8(Zn) are tested at condensation/evaporation temperature of 30 °C/10 °C. The thermal energy storage density (reaching over 1200 kJ kg-1 ) and coefficient of performance of MIL-101(Cr)-based system are both higher than ZIF-8(Zn)-based one due to larger average isosteric enthalpy and cycle sorption capacity. This experimental work paves the way for developing the high efficient and stable thermal energy storage system with MOF-ammonia working pairs especially for critical conditions with low evaporation temperature and high condensation temperature.

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. Therefore, we modified BMSCs to overexpress the BMP-7 gene (BMP-7-BMSCs) by lentivirus transduction, and then evaluated whether fibrotic processes were inhibited by these cells in vivo. Wistar rats were divided into four groups: control, silica, BMSCs, and BMP-7-BMSCs. The control group received saline, the silica group received silica and saline, the BMSCs group received silica and BMSCs, and the BMP-7-BMSCs group received silica and BMP-7-BMSCs. Rats were sacrificed on days 15 or 30 after silica instillation. Hematoxylin and eosin, and Masson's trichrome staining were performed for histological examination. The severity of fibrosis was evaluated by the levels of hydroxyproline, fibronectin (FN), and transforming growth factor (TGF)-ß1. Restoration of the alveolar epithelium was detected by the epithelial marker surfactant protein (SP)-C and aquaporin (AQP)-5. Histopathological results showed that BMP-7-BMSCs could remarkably block the progression of silica-induced fibrosis. Hydroxyproline, FN, and TGF-ß1 contents in the BMP-7-BMSCs-treated group were significantly lower than those in the BMSCs group (P<0.05). Furthermore, the expression of SP-C and AQP-5 in the BMP-7-BMSCs-treated group was significantly higher than those in the BMSCs group (P<0.05). In conclusion, the pulmonary fibrosis induced by silica in rats was significantly reduced by treatment with BMP-7-BMSCs and BMSCs. The anti-fibrotic effect of BMSCs can be strengthened by BMP-7. Treatment with BMP-7-BMSCs might be a potential therapeutic intervention for silicosis.

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. While under non-equilibrium conditions, multi-halide sorbents reduce the hysteresis significantly (the average hysteresis temperature difference decreases from 23.4 °C to 7.8 °C at 4.41 bar). The phenomena is studied, and results show that the continuous reaction within different halides under heterothermic condition leads to an operable multi-stage reaction property, which corresponds to better flexibility and faster response to heat source. The utilization of solar energy as heat source for a cloudy day is analyzed, and multi-halide sorbent has much larger average refrigeration power (improved by 43%) and could work efficiently most of the time. Such characteristics are also prospective for other thermochemical reaction technologies, such as de-NOx and energy storage because of lower energy input and higher energy output features.

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. METHODS AND RESULTS: The biodistribution of BMSCs was identified by near-infrared fluorescence (NIRF) imaging in vivo and in vitro. The results showed that BMSCs labeled with NIR-DiR dyes targeted silica-injured lung tissue, wherein they reached a peak at 6 h post-injection and declined dramatically by day 3. Based on these findings, a second injection of BMSCs was administered 3 days after the first injection. The injected BMSCs migrated to the injured lungs, but did not undergo transformation into specific lung cell types. Interestingly, the injection of BMSC-conditioned medium (BMSCs-CM) significantly attenuated silica-induced pulmonary fibrosis. The collagen deposition and number of nodules were decreased in lung tissues of BMSCs-CM-treated rats. In parallel with these findings, the mRNA levels of collagen I, collagen III, and fibronectin, and the content of transforming growth factor (TGF)-ß1 and hydroxyproline were decreased in the BMSCs-CM-treated group compared with the silica group. In addition, alveolar epithelial markers were upregulated by BMSCs-CM treatment. CONCLUSIONS: BMSCs migrated to injured areas of the lung after silica instillation and attenuated pulmonary fibrosis. The anti-fibrotic effects of BMSCs were mainly exerted in paracrine manner, rather than through their ability to undergo differentiation.

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. In this study, we hypothesized that miR-29b might play a protective role in the progression of silicosis. MTT assay, qRT-PCR, immunofluorescence and western blotting were applied. The results demonstrated that the supernatants from silica-treated macrophages not only caused the proliferation of fibroblasts (NIH-3T3 and MRC-5) but were also involved in the down-regulation of miR-29b. Meanwhile they could induce fibroblast activation, increasing the expression of ECM components such as collagen1 and collagen3, in a silica dose-dependent manner. Furthermore, overexpression of miR-29b by transfecting mimics markedly reduced the expression of ECM components and inhibited ECM synthesis. These findings indicate that miR-29b inhibits the supernatants from silica-treated macrophages from inducing extracellular matrix synthesis, thus miR-29b might have a strong anti-fibrotic capacity in silicosis and serve as a potential therapeutic agent for the treatment.

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. Histopathological examination demonstrated that BMSCs decreased the blue areas of collagen fibers and the number of nodules. Alveolar epithelium was damaged by silica, but it was restored by BMSCs. In vitro, BMSCs co-cultured with RLE-6TN cells in 6-Transwell plates were evaluated to determine the possible mechanism. The results demonstrated that BMSCs downregulated the expression of collagen I and III. BMSCs reversed morphological abnormalities and reduced the proliferation of RLE-6TN cells. These data showed that BMSCs did not give rise to alveolar epithelial cells directly, while the levels of hepatocyte growth factor, keratinocyte growth factor and bone morphogenetic protein -7 increased and expression of tumor necrosis factor-α and transforming growth factor-ß1 decreased in the 6TN+Silica+BMSCs group compared with the 6TN+Silica group. Our results revealed that BMSCs exerted anti-fibrotic effects on silica-induced pulmonary fibrosis, which might be associated with paracrine mechanisms rather than differentiation.

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 in vivo and in vitro, while silica activated the p38 MAPK/transcription factor signaling pathway in RLE-6TN cells. Lentivirus mediated transfection was used to stably upregulate the expression of BMP-7. Exogenous BMP-7 brought on MET exceeded silica-induced EMT and restrained the p38 MAPK/transcription factor signaling pathway in RLE-6TN cells. Our results revealed that BMP-7 promoted MET above EMT induced by silica associated with inhibition of the p38 MAPK/transcription factor signaling pathway, and BMP-7 was a potential target for treatment of silicosis fibrosis.

BMP-7 attenuated silica-induced pulmonary fibrosis through modulation of the balance between TGF-ß/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. Morphological changes and the cellular wound-healing assays were used to evaluate the process of EMT. By using Western Blotting, the epithelial marker E-cadherin (E-cad), and the mesenchymal markers Vimentin (Vim), Snail, and fibronectin (FN) were detected as well as the Smad signaling pathway proteins, including phosphorylated Smad1/5(P-Smad1/5), phosphorylated Smad2/3(P-Smad2/3), and non-phosphorylated Smad1, Smad8, and Smad2. The progress of fibrosis was assessed by the content of hydroxyproline (Hyp) and collagen I and III protein levels. In addition, MTT assay was used to explore the toxic effects of silica as well as BMP-7. RESULTS: The EMT model of RLE-6TN cells was established successfully, the cells had a fibroblast-like morphology with increasing migration activity. The expressions of Vim, Snail, FN, collagen I and collagen III were up-regulated with the increase of silica concentration. BMP-7 could attenuate the decrease of P-Smad1/5 and the increase of P-Smad2/3, collagen I, collagen III, and FN via Smad signaling pathway. BMP-7 inhibited the mesenchymal-like responses in RLE-6TN cells, including cell migration, expression of fibrosis markers, and secretion of Hyp. Furthermore, the anti-fibrotic effects in the prevention group were more effective than treatment group. CONCLUSION: The restoration of BMP signaling with BMP-7 is associated with inhibiting silica-induced fibrosis through the mechanisms of activated BMP-7/Smad and suppressed TGF-ß/Smad pathways. Preventive treatment of pulmonary fibrosis progression with BMP-7 may expect to be the optimized strategy than therapeutic therapy of fibrosis.