The interpretation of gas adsorption behavior on a coal surface is an important theoretical basis for gas injection to enhance the recovery of coalbed methane. In order to further explore the adsorption properties of different gases (CH 4 /CO 2 /N 2 ) on the coal surface, the thermodynamic parameters of adsorption were revealed using a molecular simulation method. The results show that the Langmuir−Freundlich model is more accurate to represent gas adsorption on anthracite coal than the Langmuir model and Freundlich model, which reveal that the gas adsorption on the coal surface is heterogeneous. Also, thermodynamic parameters indicate that gas adsorption on anthracite coal is a thermodynamically spontaneous (ΔG < 0) and exothermic physisorption (0 < ΔH < 10 kcal/mol) process, and the gas molecules tend to be in an ordered state (ΔS > 0). According to adsorption affinity and thermodynamic parameters, the adsorption capacity of these three gases on a coal surface follows the sequence of CO 2 > CH 4 > N 2 . This research can provide foundational knowledge for further interpretation of gas adsorption behavior on a coal surface.
BackgroundSalvia miltiorrhiza is used extensively to treat cardiovascular diseases. SAA is a major bioactive component in Salvia miltiorrhiza and mediates myocardial ischemia (MI). However, the industrial production of SAA is limited due to low yields. In addition, the direct targets of SAA are unknown. Here we explore cardioprotective mechanisms and targets of SAA in the cardiovascular system.MethodsTransgelin and actin were identified as targets of SAA using a chemical biology method and were validated by Biacore analysis, microscale thermophoresis and single-molecule imaging. Studies of transgelin (−/−) knockout mice further verify the target. Cardioprotective mechanisms and targets of SAA were studied in cultured vascular smooth muscle cells and transgenic mice.FindingsIn WT mice, SAA targeted transgelin and had a protective effect on myocardium but did not have the same protective effect on transgelin (−/−) mice. SAA stabilizes the transgelin-actin complex, modulates the reorganization of the actin cytoskeleton, facilitates F-actin bundling, further enhances the contractility and blood flows of coronary arteries, and improves outcomes of myocardial ischemia. Based on the target, a more active SAA derivative offering myocardial protection, SAA-30, was obtained.InterpretationWe report on the direct targets of SAA and mechanisms of myocardial ischemia treatment. We also find that transgelin may act as a novel therapeutic target of myocardial ischemia. Furthermore, a more effective derivative of SAA provides the basis for further clinical translational research.
Composites that can rapidly self-healing their structure and function at room temperature have broad application prospects. However, in view of the complexity of composite structure and composition, its self-heal is facing challenges. In this article, supramolecular effect is proposed to repair the multistage structure, mechanical and thermal properties of composite materials. A stiff and tough supramolecular frameworks of 2-[[(butylamino)carbonyl]oxy]ethyl ester (PBA)–polydimethylsiloxane (PDMS) were established using a chain extender with double amide bonds in a side chain to extend prepolymers through copolymerization. Then, by introducing the copolymer into a folded graphene film (FGf), a highly thermally conductive composite of PBA–PDMS/FGf with self-healing capacity was fabricated. The ratio of crosslinking and hydrogen bonding was optimized to ensure that PBA–PDMS could completely self-heal at room temperature in 10 min. Additionally, PBA–PDMS/FGf exhibits a high tensile strength of 2.23 ± 0.15 MPa at break and high thermal conductivity of 13 ± 0.2 W m−1 K−1; of which the self-healing efficiencies were 100% and 98.65% at room temperature for tensile strength and thermal conductivity, respectively. The excellent self-healing performance comes from the efficient supramolecular interaction between polymer molecules, as well as polymer molecule and graphene. This kind of thermal conductive self-healing composite has important application prospects in the heat dissipation field of next generation electronic devices in the future.
Oleanolic acid exhibits extensive pharmacologic activities and takes significant antitumor effects. Its pharmacologic mechanism, however, still remained to be further clarified. In this study, we demonstrated that oleanolic acid attenuated the migration and invasion abilities, resulting in the suppression of the epithelial-mesenchymal transition (EMT) process in liver cancer cells, and inhibited the tumor growth of the peritoneal lymphocytes-bearing mice. We further proved that inducible nitric oxide synthase (iNOS) may be the potential target of oleanolic acid. We confirmed that oleanolic acid could pro-mote the dimerization of iNOS, activating it, and subsequently increasing the production of nitric oxide. Further experiments indicated that oleanolic acid promoted the nitration of specific proteins and consequently suppressed their EMT-related biological functions. Furthermore, it has been confirmed that oleanolic acid enhanced the antitumor effects of regorafenib in liver cancer treatment. These results deepened our understanding of the pharmacologic mechanism of the antitumor effect oleanolic acid, and the importance of nitric oxide synthetase as a therapeutic target for liver cancer treatment.
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