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To improve the oxidation resistance of carbon/carbon (C/C) composites in 1473–1973 K, a HfSi 2 -HfB 2 -SiC coating was prepared on the surface of SiC-coated C/C composites by a combined method of slurry dipping and oxidation sintering at low temperature (below 1473 K). The Hf-Si-O multiphase layer generated by the oxidation of the coating acted as oxygen barriers at 1473–1973 K in air. The in-situ formed HfSiO 4 particles enhanced the thermal stability of the SiO 2 glass, terminated propagation of the crack, and relieved CTE mismatch between the inner and outer coating. Besides, B 2 O 3 filled pores in the early stage of oxidation and then SiO 2 took the place of the B 2 O 3 as a new filler with the increase time of oxidation. As a result, the coating can protect C/C composites for 516 h at 1473 K, 744 h at 1773 K, and 64 h at 1973 K with a mass gain of 0.63 wt%, 1.41 wt% and −1.91 wt%, respectively. [ABSTRACT FROM AUTHOR]

To improve the oxidation resistance of carbon/carbon (C/C) composites in a wide temperature range (1173–1773 K), a composite coating containing rich B 2 O 3 glass was prepared on SiC-coated C/C composites by slurry dipping-densifying at low temperature. Borosilicate and SiO 2 glasses acted as oxygen barriers at low and medium-high temperatures, respectively. Besides, Hf-oxides (HfO 2 , HfSiO 4) ceramic particles improved the thermal stability of the glass and enhanced the crack resistance of glass layer. Therefore, the composite coating can effectively protect C/C composites against oxidation for 403 h at 1173 K, 723 h at 1473 K and 403 h at 1773 K with the mass gain of 3.77 g·m−2, 21.41 g·m−2 and 0.42 g·m−2, respectively. After 50 times thermal cycles between room temperature and 1773 K, the mass gain of the coated sample was 3.95 g·m−2 and the mass retention rate was up to 98.19 % during the thermos-gravimetric test from room temperature to 1773 K. [ABSTRACT FROM AUTHOR]

HfB 2 -SiC coatings with 30–60 wt% HfB 2 additions were prepared by slurry-dipping on SiC-coated C/C composites for investigating their oxidation behavior at low (1173 K) and high (1773 K) temperatures. With the increase of HfB 2 content, more B 2 O 3 glass was produced in the coating and the coating became denser during oxidation at 1173 K. 50 wt% HfB 2 -SiC coating can protect C/C composites for 494 h against oxidation, which was attributed to the formation of the dense borosilicate glass with high thermal stability as an oxygen barrier layer. After oxidation at 1773 K, 30 wt% HfB 2 -SiC coating provided the longest protection time (460 h) for C/C composites among 30–60 wt% HfB 2 -SiC coatings. A few Hf-oxides inhibited the volatilization of SiO 2 glass as the main phase in the 30 wt% HfB 2 -SiC coating after oxidation. As for other coatings with higher content of HfB 2 , the violent oxidation of HfB 2 particles made more bubbles produced, resulting in the poor oxidation resistance at 1773 K. [ABSTRACT FROM AUTHOR]

To evaluate the in vitro and in vivo anti-metastasis efficacy of Jianpi Yangzheng (JPYZ) decoction against gastric cancer (GC) and its potential mechanisms. The distant metastasis of GC cells administered via tail vein injection was assessed using the pre-metastatic niche (PMN) model. 16S rRNA sequencing and GC–MS/MS were applied to determine the component of the gut microbiota and content of short-chain fatty acids (SCFAs) in feces of mice, respectively. The proportion of myeloid-derived suppressor cells (MDSCs) in the lung was evaluated by flow cytometry and immunofluorescence. Serum or tissue levels of inflammation factors including IL-6, IL-10 and TGF-β were determined by ELISA or Western blot respectively. Injecting GC cells into the tail vein of mice led to the development of lung metastases and also resulted in alterations in the composition of gut microbiota and the levels of SCFAs produced. Nevertheless, JPYZ treatment robustly impeded the effect of GC cells administration. Mechanically, JPYZ treatment not only prevented the alteration in gut microbiota structure, but also restored the SCFAs content induced by GC cells administration. Specifically, JPYZ treatment recovered the relative abundance of genera Moryella, Helicobacter, Lachnoclostridium, Streptococcus, Tuzzerella, GCA-900066575, uncultured_Lachnospiraceae, Rikenellaceae_RC9_gut_group and uncultured_bacterium_Muribaculaceae to near the normal control levels. In addition, JPYZ abrogated MDSCs accumulation in the lung tissue and blocked inflammation factors overproduction in the serum and lung tissues, which subsequently impede the formation of the immunosuppressive microenvironment. Correlation analysis revealed that the prevalence of Rikenellaceae in the model group exhibited a positive correlation with MDSCs proportion and inflammation factor levels. Conversely, the scarcity of Muribaculaceae in the model group showed a negative correlation with these parameters. This suggests that JPYZ might exert an influence on the gut microbiota and their metabolites, such as SCFAs, potentially regulating the formation of the PMN and consequently impacting the outcome of GC metastasis. These findings suggest that GC cells facilitate metastasis by altering the gut microbiota composition, affecting the production of SCFAs, and recruiting MDSCs to create a pro-inflammatory pre-metastatic niche. JPYZ decoction counteracts this process by reshaping the gut microbiota structure, enhancing SCFA production, and inhibiting the formation of the pre-metastatic microenvironment, thereby exerting an anti-metastatic effect. [Display omitted] [ABSTRACT FROM AUTHOR]