The dynamic response of a high-density polyethylene slow-release structure under launching overload

Based on the 60 mm artillery grenade,a slow-release structure was designed to reduce the severity of ammunitions response to accidental thermal stimulation and improve the thermal stability of ammunitions.The slow-release structure was made of high-density polyethylene(HDPE) and connected the fuse and the projectile body through internal and external threads.To study the safety of the slowrelease structure under artillery launching overload,mechanical analysis of the slow-release structure was simulated via finite element analysis(FEA).The impacts of various factors(e.g.,fuse mass,number of threads,and nominal diameter of internal threads of the slow-release structure) on the connection strength of the slow-release structure were studied.A strength-prediction model based on the fuse mass and internal thread parameters was established by fitting the maximum effective stress of the slowrelease structure.This led to good prediction results.In conclusion,this study provides references and theoretical support for the design of thermal protection structures insensitive to ammunition.

Berberine mitigates nonalcoholic hepatic steatosis by downregulating SIRT1-FoxO1-SREBP2 pathway for cholesterol synthesis

Objective:To investigate effects of berberine(BBR)on cholesterol synthesis in HepG2 cells with free fatty acid(FFA)-induced steatosis and to explore the underlying mechanisms.Methods:A steatosis cell model was induced in HepG2 cell line fed with FFA(0.5 mmol/L,oleic acid:-palmitic acid=2:1),and then treated with three concentrations of BBR;cell viability was assessed with cell counting kit-8 assays.Lipid accumulation in cells was observed through oil red O staining and total cholesterol(TC)content was detected by TC assay.The effects of BBR on cholesterol synthesis mediators were assessed by Western blotting and quantitative polymerase chain reaction.In addition,both silent information regulator 1(SIRT1)and forkhead box transcription factor O1(FoxO1)inhibitors were employed for validation.Results:FFA-induced steatosis was successfully established in HepG2 cells.Lipid accumulation and TC content in BBR groups were significantly lower(P<0.05,P<0.01),associated with significantly higher m RNA and protein levels of SIRT1(P<0.05,P<0.01),significantly lower sterol regulatory elementbinding protein 2(SREBP2)and 3-hydroxy 3-methylglutaryl-Co A reductase levels(P<0.05,P<0.01),as well as higher Acetyl-FoxO1 protein level(P<0.05,P<0.01)compared to the FFA only group.Both SIRT1 inhibitor SIRT1-IN-1 and FoxO1 inhibitor AS1842856 blocked the BBR-mediated therapeutic effects.Immunofluorescence showed that the increased SIRT1 expression increased FoxO1 deacetylation,and promoted its nuclear translocation.Conclusion:BBR can mitigate FFA-induced steatosis in HepG2 cells by activating SIRT1-FoxO1-SREBP2 signal pathway.BBR may emerge as a potential drug candidate for treating nonalcoholic hepatic steatosis.