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Experiments on the relationship between temperature and vapor phase composition (T-y curve) of the Cu-Te and Pb-Te binary systems at 5 Pa were carried out, with distillation temperatures in the range of 900–1370 K and 724–920 K, respectively. The experimental results indicate that copper and lead can be satisfactorily removed from crude tellurium. The recovery rate of tellurium is relatively low due to the formation of a high melting point compound in the liquid phase. The activities of Cu and Pb of the Cu-Te and Pb-Te systems were obtained by function fitting and G-D equation, which are used to predict vapor phase composition. The results show good agreement with the experimental data. The activities and T-y curve of the Fe-Te binary system were calculated using the same method and believed to be reliable. A possible high-purity tellurium production cycle combined with vacuum distillation was also discussed. • Experiments of the Cu-Te and Pb-Te binary systems at 5 Pa were carried out. • The activities of components for the Cu-Te, PbTe and Fe-Te systems were correlated with the Gibbs-Duhem equation. • The temperature vs vapor phase composition curves for the three systems are presented. • The effect of high melting point compounds on tellurium evaporation is discussed. [ABSTRACT FROM AUTHOR]

• Echinacea Polysaccharide (EP) alleviated LPS-induced lung injury. • EP decreased LPS-induced inflammation in vivo and in vitro. • EP inhibited LPS-induced cell apoptosis. • EP might suppress the activation of TLR4/NF-κB signaling pathway. Lung injury is a common critical life-threatening syndrome. Inflammation is a key factor in the pathogenesis of lung injury. It is reported that Echinacea Polysaccharides (EP) has anti-inflammatory activity. However, the effect of EP on lung injury remains unclear. In our study, murine model of lung injury was induced with 2.5 mg/kg LPS before administration of 5 mg/kg or 10 mg/kg EP. EP ameliorated LPS-induced lung pathological damage, along with reduction in lung wet/dry weight ratio and myeloperoxidase activity. EP decreased the number of leukocytes, eosinophils, neutrophils, lymphocytes and macrophages in bronchoalveolar lavage fluid, and the release of tumour necrosis factor-α (TNF-α), interleukin-6 (IL-6) and interleukin-1β (IL-1β) in LPS-treated lung. EP suppressed LPS-induced apoptosis along with down-regulation of Bcl2-associated X (Bax) and cleaved caspase-3 (CC3), and elevated B-cell lymphoma-2 (Bcl-2). Besides, RAW 264.7 cells were treated with EP 100 μg/ml for 1 h and then incubated with 1 μg/ml LPS for 24 h. TNF-α, IL-6 and IL-1β levels were lowered by treatment of EP in LPS-treated RAW 264.7 cells. Moreover, EP down-regulated the expression of toll-like receptor 4 (TLR4), myeloid differentiating factor 88 (MyD88), p-IκBα, nuclear factor kappa-B (NF-κB), p-NF-κB, and up-regulated the inhibitor of NF-κB (IκBα) in vivo and in vitro following LPS induction, which is consistent with the effect of TAK-242. In conclusion, EP may alleviate LPS-induced lung injury via inhibiting inflammation, apoptosis and activation of TLR4/NF-κB signal pathway. [ABSTRACT FROM AUTHOR]