A biobased flame retardant towards improvement of flame retardancy and mechanical property of ethylene vinyl acetate

A new biobased flame retardant(MHPA)with remarkable compatibility was synthesized via a facile and low-cost neutralization reaction of magnesium hydroxide(MH)and phytic acid(PA).By blending the prepared MHPA into ethylene vinyl acetate(EVA),the fire retardancy,smoke suppression and mechanical properties of the composites were significantly improved.When 50 wt%of MH was added into EVA matrix,the value of limiting oxygen index(LOI)reached 26.1%.Whereas,when 10 wt%MH in the EVA composites(with initial 50 wt%MH)was replaced by MHPA,the resulted EVA composites had a LOI value of 30.8%,indicating high efficiency of addition of MHPA to improve flame retardancy.Moreover,the heat release rate(HRR)and total smoke production(TSP)of the EVA composites reduced by 54.4%and 27.6%,respectively,suggesting that incorporation of MHPA could effectively hinder rapid degradation of EVA composites during burning process.The fire-retardant mechanism may reside in that the MHPA combined with MH can present the excellent carbonization and expansion effects.This study illustrates that the biobased MHPA has a broad application prospect to develop flame-retardant EVA composites.

Taurocholic acid inhibits the response to interferon-αtherapy in patients with HBeAg-positive chronic hepatitis B by impairing CD8^(+)T and NK cell function

Pegylated interferon-alpha (PegIFNα) therapy has limited effectiveness in hepatitis B e-antigen (HBeAg)-positive chronic hepatitis B (CHB) patients. However, the mechanism underlying this failure is poorly understood. We aimed to investigate the influence of bile acids (BAs), especially taurocholic acid (TCA), on the response to PegIFNα therapy in CHB patients. Here, we used mass spectrometry to determine serum BA profiles in 110 patients with chronic HBV infection and 20 healthy controls (HCs). We found that serum BAs, especially TCA, were significantly elevated in HBeAg-positive CHB patients compared with those in HCs and patients in other phases of chronic HBV infection. Moreover, serum BAs, particularly TCA, inhibited the response to PegIFNα therapy in HBeAg-positive CHB patients. Mechanistically, the expression levels of IFN-γ, TNF-α, granzyme B, and perforin were measured using flow cytometry to assess the effector functions of immune cells in patients with low or high BA levels. We found that BAs reduced the number and proportion and impaired the effector functions of CD3^(+)CD8^(+) T cells and natural killer (NK) cells in HBeAg-positive CHB patients. TCA in particular reduced the frequency and impaired the effector functions of CD3^(+)CD8^(+) T and NK cells in vitro and in vivo and inhibited the immunoregulatory activity of IFN-α in vitro. Thus, our results show that BAs, especially TCA, inhibit the response to PegIFNα therapy by impairing the effector functions of CD3^(+)CD8^(+) T and NK cells in HBeAg-positive CHB patients. Our findings suggest that targeting TCA could be a promising approach for restoring IFN-α responsiveness during CHB treatment.