Investigation of Parameter Sensitivity and the Physical Mechanism for the Formation of a Core-Skin-Core (CSC) Structure in Two-Stage Co-Injection Molding.

One of the main challenges in co-injection molding is how to predict the skin to core morphology accurately and then manage it properly, especially after skin material has been broken through. In this study, the formation of the Core-Skin-Core (CSC) structure and its physical mechanism in a two-stage co-injection molding has been studied based on the ASTM D638 TYPE V system by using both numerical simulation and experimental observation. Results showed that when the skin to core ratio is selected properly (say 30/70), the CSC structure can be observed clearly at central location for 30SFPP/30SFPP system. When the skin to core ratio and operation conditions are fixed, regardless of material arrangement (including 30SFPP/30SFPP; PP/PP; 30SFPP/PP; and PP/30SFPP systems), the morphologies of the CSC structures are very close for all systems. This CSC structure can be further validated by using µ-CT scan and image analysis technologies perfectly. Furthermore, the influences of various operation parameters on the CSC structure variation have been investigated. Results exhibited that the CSC structure does not change significantly irrespective of the flow rate changing, melt temperature varying, or even mold temperature being modified. Moreover, the mechanism to generate the CSC structure can be derived using the melt front movement of the numerical simulation. It is worth noting that after the skin material was broken through, the core material travelled ahead with fountain flow to occupy the flow front. In the same period, the proper amount of skin material with certain inertia of enough kinetic energy will keep going to penetrate the new coming core material to travel until the end of filling. It ends up with this special CSC structure.

[Construction of PTEN eukaryotic expression plasmid and its effects on breast carcinoma cell line MDA468].

OBJECTIVE: To investigate the effects of exogenous wild PTEN gene stably transfection on growth of breast cancer cells in vitro. METHODS: At first, a recombinant eukaryotic expression plasmid pcDNA3.1-PTEN was constructed. Human breast cancer cell line MDA468 was transfected with pcDNA3.1-PTEN or mock transfected plasmid pcDNA3.1(-) with lipofectamine. RT-PCR, immunohistochemical staining and Western blot were used to determine target gene expression. Cell viability was tested by MTT assay. Apoptosis was determined by flow cytometry with a double-staining method using FITC-conjugated annexin V and PI. RESULTS: The PTEN stably transfected cells demonstrated the integration of the exogenous target gene and corresponding mRNA and protein over-expression. There was a significant decline in cell viability of pcDNA3.1-PTEN transfected MDA468 cells in comparison with the mock-transfected ones (P < 0.01). The PTEN-trasfected MDA468 cells also showed an increase in the rate of apoptosis, compared with parental and mock-trasfected cells (P < 0.001). CONCLUSION: Stable expression of exogenous PTEN can suppress the malignant phenotypes of the human breast cancer cell line MDA468.