Inelastic deformation micromechanism and modified fragmentation model for silicon carbide under dynamic compression

The underlying micromechanism remains to be clarified for the bulk inelastic behaviour of specific ceramics under impact loads. In this study, the silicon carbide materials were subjected to the split-Hopkinson pressure bar compression in which the strain rate was not constant but increased to the dynamic level at high stresses. The inelastic deformation occurs in the high strain rate stage in compression, followed by the final transgranular fracture. The post-test fragments were examined in both the SEM and high resolution TEM. It was found that macroscopic inelastic behaviour is dominated by the dislocation motion and the localised amorphisation that arise at high strain rates. The damage and thus the degraded modulus in the dynamic inelastic deformation were incorporated to modify a dynamic fragmentation model to evaluate the fragment size as a function of strain rates. The modified model more accurately predicts the size of fragments produced at high strain rates

Finite element analysis of mechanical properties of 2.5D angle-interlock woven composites: Part 1— Full-cell model and its validation

A new parameterized micro-structural model of 2.5D angle-interlock woven composites, named ‘full-cell model’, has been established. In order to verify the validation of finite element model (FEM) based on the full-cell model, the effective elastic properties and the mechanical response of 2.5D woven composites are presented. Additionally, the effects of fibre aggregation density and thickness on the mechanical properties are also investigated in detail. The experimental results are compared with the values of FEM based on the full-cell model and inner-cell model

Estimation of Earth's reflectivity from low orbit satellite data

PresentationFirst author draf

GCS overexpression is associated with multidrug resistance of human HCT-8 colon cancer cells

<p>Abstract</p> <p>Purpose</p> <p>Multidrug resistance is one of the main impediments to the successful treatment of colon cancer. Glucosylceramide synthase (GCS) which is related to multidrug resistance (MDR) can reduce the level of ceramide and can help cells escape from the ceramide-induced cell apoptosis. However, the underlying mechanism is still unclear.</p> <p>Methods</p> <p>The cell proliferation and cell toxicity were measured with Cell Counting Kit-8 (CCK-8). The mRNA levels of GCS and MDR1 were detected by semiquantitative reverse transcription-PCR amplification, the protein levels of GCS, caspase-3 and P-gp proteins were indicated by Western blotting. The apoptosis rates of cells were measured with flow cytometry.</p> <p>Results</p> <p>The relative mRNA levels of GCS in HCT-8, HCT-8/VCR, HCT-8/VCR- sh-mock and HCT-8/VCR-sh-GCS were 71.4 ± 1.1%, 95.1 ± 1.2%, 98.2 ± 1.5%, and 66.6 ± 2.1% respectively. The mRNA levels of MDR1 were respectively 61.3 ± 1.1%, 90.5 ± 1.4%, 97.6 ± 2.2% and 56.1 ± 1.2%. The IC50 of Cisplatin complexes were respectively 69.070 ± 0.253 μg/ml, 312.050 ± 1.46 μg/ml, 328.741 ± 5.648 μg/ml, 150.792 ± 0.967 μg/ml in HCT-8, HCT-8/VCR, HCT-8/VCR-sh-mock and HCT-8/VCR-sh-GCS. The protein levels of caspase-3 were 34.2 ± o.6%, 93.0 ± 0.7%, 109.09 ± 0.7%, 42.7 ± 1.3% respectively. The apoptosis rates of cells were 8.77 ± 0.14%, 12.75 ± 0.54%, 15.39 ± 0.41% and 8.49 ± 0.23% respectively.</p> <p>Conclusion</p> <p>In conclusion, our research indicated that suppression of GCS restores the sensitivity of multidrug resistance colon cancer cells to drug treatment.</p