No abstract

A multi-component polymer of methacrylic acid (MAA) and butyl acrylate (BA) grafted onto ethylene-propylene-diene (EPDM) terpolymer was synthesized in toluene using benzoyl peroxide (BPO) as initiator. The effect of EPDM/MAA-BA ratio and MAA/BA ratio on the grafting ratio of polymerization was investigated. The products were characterized by Fourier transform infrared (FTIR) spectroscopy, differential scanning calorimetry (DSC), surface energy, inherent viscosity, and atomic force microscopy (AFM). The results showed that the MAA and BA monomers were successfully grafted onto EPDM. Furthermore, after being grafted, the polarity of the surface of the EPDM-g-MAA-BA increased with increasing grafting ratio, and the morphology of its surface became more smooth.

A series of novel cotton cellulose-graft-polycaprolactone copolymers with different grafting contents were successfully prepared via ring-opening polymerization (ROP) in an ionic liquid 1-N-butyl-3methylimidazolium chloride ([Bmim]Cl). The structures of the grafting copolymers were systematically characterized by FTIR, CP/MAS 13 C-NMR, XRD, SEM and AFM, while thermal properties were investigated by DSC and TGA. Subsequently, Langmuir, Freundlich, Temkin, and Dubinin-Radushkevich (D-R) adsorption isotherms were representative to simulate adsorption isotherms of Cu(II) and Ni(II) ions in aqueous solution. From the comparison of different adsorption isotherm models, it was found that adsorption of Cu(II) by modified cellulose followed Langmuir, Freundlich and Temkin models, while that of Ni(II) followed the Freundlich model. The results of adsorption indicated that the selectivity sequence of metal ions on graft copolymers was Cu(II) > Ni(II) and the maximum removal capacities of Cu(II) andNi(II) ions were 98.7% and 35.6%, respectively. Hence, the graft copolymers exhibited significant potential to be an environmentally feasible biosorbent for removal of Cu(II) and Ni(II) ions from aqueous solution.

Background Dilated cardiomyopathy (DCM) is one of the most common cardiomyopathies in children, but we have no effective method to treat it. In recent years,the application of human umbilical cord mesenchymal stem cell (hucMSC) therapy in DCM has made a great progress, whileits mechanism remains unknown. The paracrine of hucMSCs has attracted attention as the main mechanism. In this study we explore the effect of the human umbilical cord mesenchymal stem cell-derived exosomes (hucMSC-Ex) on the cardiac function in rat models with DCM that is induced by Adriamycin. Methods Sprague-Dawley rats were intraperitoneally injected with Adriamycin to establish aDCM model. HucMSC-Ex were injected through the tail vein in the DCM group and phosphate-buffered saline (PBS) was injected in theDCMcontrolgroup.The rats were monitored for 2 weeks and thecardiac function was evaluated using thecardiac ultrasound.The pathological changes of the myocardium were observed usingimmunohistochemistry. Western blot and real-time fluorescent quantitative PCR were used to detect the expression of Smad3, alpha smooth muscle actin (α-SMA) and I type collagen (COLI)in the myocardial tissue amongthe groups of rats.Finally, the ultrastructure of the myocardium was observed using electron microscopy. High throughput sequencing was performed on the ventricular muscles in each group. Result High-throughput sequencing results show that after the treatment with hucMSC-Ex, the level of myocardial Scn5a in the myocardium significantly increased (P < 0.05). RT-PCR shows that the level of Lmod2 also significantly increased.The expression of Smad3,α-SMA and COL I was reduced(P < 0.05).The inflammation in the myocardial tissue decreased and the mitochondrial swelling was reduced.The left ventricular ejection function (LVEF) and left ventricular fractional shortening (LVFS)in the rats significantly increased (P < 0.05) and the cardiac function was significantly improved (P < 0.05). Conclusion The treatment with hucMSC-Ex through the tail vein can significantly improve thecardiac function and reduce the degree of myocardial fibrosis induced by Adriamycin.