Free-radical grafting of glycidyl methacrylate (GMA ) onto polypropylene (PP) powder was studied in a batch mixer. The reaction temperature was below the melting point of PP so that PP was modified in the solid phase. The graft yield of GMA obtained under various experimental conditions allowed for a good appreciation of the effects of chemical parameters (the concentration of monomer, initiator, and interfacial agent) and those of processing parameters (reaction time and temperature). Toluene was used as an interfacial agent to etch the surface of PP powder to provide more sites for reaction. Quantitative determination of the graft level was performed by wet chemical methods. The results showed that the solid-phase grafting could take place over a temperature range of 100-140ЊC in the initiation of benzoyl peroxide (BPO). The ultimate GMA grafting level achieved was higher than that obtained in the melt state with dicumyl peroxide (DCPO) as a radical initiator. The grafting of GMA affected the crystalline morphology of PP and speeded up the crystallization process. The energy of activation and initial decomposition temperature of grafted samples were higher than those of ungrafted PP.
Necrotizing enterocolitis (NEC) is a major cause of mortality and morbidity in newborns, characterized by inflammatory intestinal necrosis. Sirtuin-1 (SIRT1), a NAD-dependent deacetylase, is involved in multiple biological functions. It has been reported that SIRT1 was downregulated in NEC tissues. However, the precise role of SIRT1 in NEC progress remains unknown. In this study, we found that SIRT1 was decreased in serum samples of NEC patients, associated with an inflammation response. an in vitro model was established by using LPS-induced NEC-like cell in this study. The results indicate that overexpression of SIRT1 inhibited the cell apoptosis induced by LPS. Besides, overexpression of SIRT1 suppressed the high expression of proinflammatory factors (IL-6, IL-8, and TNF-α), the decrease of transepithelial electrical resistance (TEER), and the decline expression of tight junction proteins (ZO-1, ZO-2, and Claudin-4) induced by LPS in Caco-2 cells. What is more, serum HIF-1α was increased in NEC patients. SIRT1 overexpression suppressed the expression and activity of HIF-1a, while knockdown of SIRT1 made the opposite effect. In summary, this study indicates that overexpression of SIRT1 alleviates the inflammation response and intestinal epithelial barrier dysfunction through regulating the expression and inactivation of HIF-1a.
A hierarchical nanostructural coating of amorphous SN on a PEEK surface was prepared by ICPECVD which exhibited excellent cytocompatibility and antibacterial activity.
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