Chlorogenic acid (CGA), an ester with various pharmacological effects, is important in cancer therapy. However, the specific antitumor mechanism of CGA is not entirely clear, especially with respect to its suppression of non-small cell lung cancer (NSCLC). The present study was carried out to assess the effect of CGA on NSCLC, and the mechanism involved. Cell viability assay and colony formation assay revealed that CGA blocked the proliferative capacity of NSCLC cells in vitro. Results from the migration assay suggested that CGA also inhibited the migration of A549 cells. Other assays further revealed that CGA strongly and selectively inhibited histone deacetylase 6 (HDAC6) activity and suppressed the activity of matrix metalloproteinase-2 (MMP-2) through decreased expression of Ac-NF-κB. Tumorigenicity assay showed that CGA also inhibited the proliferation and metabolism of NSCLC in vivo. These results indicate that CGA significantly suppresses the proliferation of NSCLC by regulating the activity of histone deacetylase 6.

Creep tests of 2D-C/SiC in a wet oxidizing atmosphere were implemented for six samples. The loading process was monitored by acoustic emission (AE). Principal component analysis and a fuzzy clustering algorithm were used to perform pattern recognition of the AE data. All of the AE events were divided into four clusters and labelled as matrix cracking, interfacial damage, fiber breakage and fiber-bundle breakage respectively, according to their physical origin. It was found C/SiC has very scattered rupture lifetimes even under the same test conditions, and the evolution of AE events corresponding to fiber failure is quite different. With increasing rupture lifetime, the AE energy of fiber-bundle breakage is higher, while the number of these events is less. Thus, it is concluded that local oxidation and damage development is the controlling failure mechanism for short-lived specimens and uniform oxidation and damage development is the controlling failure mechanism for long-lived specimens.

Dropped-weight impact tests were carried out to investigate the coating damage behavior of SiC coated plainwoven C/SiC composites under low velocity impact (LVI). The oxidation performance after impact was evaluated in a wet oxygen environment. The relationships between coating damage area, oxidizing weight loss and the flexural strength after oxidation with the impact energy were analyzed. It was concluded from the test results that 0.5J was the impact energy corresponding to damage initiation of the coating, where the oxidation loss was 2.49% and the strength retention ratio was 94.92%, almost the same as the untreated coating. Between 0.5J and 2J, the weight loss of oxidation increased with impact energy, and the oxidation mechanism gradually changed from a diffusion-controlled local oxidation to a reaction-controlled uniform oxidation. When the impact energy was larger than 2J, although the coating damage still increased with impact energy, weight loss and residual flexural strength remained almost constant. The residual strength remaining was no more than 8% of the non-oxidized C/SiC, indicating that the coating totally loses its anti-oxidation function.

The acoustic emission data collected during room temperature tensile test of 2D-C/SiC composites were analyzed by hierarchical clustering and unsupervised pattern recognition method based on an improved genetic algorithm. Combined with the SEM observation on the fracture surface, five damage modes were identified and their typical acoustic emission characteristics were obtained. According to the analysis of energy distribution, cumulative event number and cumulative energy of different damage modes, the damage evolution process of C/SiC composites can be divided into four stages. The first stage (damage initiation stage) shows mainly matrix microcracks and interface debonding. In the second stage, matrix crack reaches saturated and then causes a considerable quantity of interlaminar delamination and fiber failure. The third stage is a gradual damage development stage and all kinds of damage keep occurring except the breakage of fiber bundles. In the last stage, a large amount of fiber bundles break and the sample eventually fails.

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